Lycium barbarum polysaccharide LBPF4-OL may be a new Toll-like receptor 4/MD2-MAPK signaling pathway activator and inducer
Xiao-rui Zhang a ,Chun-hui Qi a ,Jun-ping Cheng a ,Gang Liu a ,Lin-juan Huang b ,Zhong-fu Wang b ,Wen-xia Zhou a ,?,Yong-xiang Zhang a ,?
a
Beijing Institute of Pharmacology and Toxicology,Beijing 100850,China
b Key Laboratory of Resource and Biotechnology in Western China,Ministry of Education,Shaanxi Provincial Key Laboratory of Biotechnology,Life Science College,Northwest University,Xi'an 710069,China
a b s t r a c t
a r t i c l e i n f o Article history:
Received 24October 2013
Received in revised form 12December 2013Accepted 12January 2014
Available online 23January 2014Keywords:
Lycium barbarum polysaccharides TLR4/MD2complex Macrophages
Mitogen-activated protein kinase In ?ammatory factor Lymphocytes
Recognition of the utility of the traditional Chinese medicine Lycium barbarum L.has been gradually increasing in Europe and the Americas.Many immunoregulation and antitumor effects of L.barbarum polysaccharides (LBP)have been reported,but its molecular mechanism is not yet clear.In this study,we reported that the activity of the polysaccharide LBPF4-OL,which was puri ?ed from LBP,is closely associated with the TLR4–MAPK signaling pathway.We found that LBPF4-OL can signi ?cantly induce TNF-αand IL-1βproduction in peritoneal macro-phages isolated from wild-type (C3H/HeN)but not TLR4-de ?cient mice (C3H/HeJ).We also determined that the proliferation of LBPF4-OL-stimulated lymphocytes from C3H/HeJ mice is signi ?cantly weaker than that of lymphocytes from C3H/HeN mice.Furthermore,through a bio-layer interferometry assay,we found that LPS but not LBPF4-OL can directly associate with the TLR4/MD2molecular complex.Flow cytometry analysis indicat-ed that LBPF4-OL markedly upregulates TLR4/MD2expression in both peritoneal macrophages and Raw264.7cells.As its mechanism of action,LBPF4-OL increases the phosphorylation of p38-MAPK and inhibits the phos-phorylation of JNK and ERK1/2,as was observed through Western blot analysis.These data suggest that the L.barbarum polysaccharide LBPF4-OL is a new Toll-like receptor 4/MD2-MAPK signaling pathway activator and inducer.
?2014Elsevier B.V.All rights reserved.
1.Introduction
Lycium barbarum is an important traditional Chinese herbal medicine for the promotion of health and longevity and as a food supplement [1,2].In recent years,the health care functions of L.barbarum are gradu-ally gaining the interest of the US and Europe [3].Modern medicine found that the polysaccharide of L.barbarum (LBP)is the main active in-gredient of L.barbarum .Many bene ?cial health effects of LBPs,such as immune regulation,anti-stress,anti-colon cancer,neuroprotective,and anti-diabetic effects,have been reported [4–12].Several studies also found that LBPs exhibit myocardial protection,eye protection,anti-radiation damage,and anti-aging effects [4–12].However,the molecular mechanism of LBPs has not yet been elucidated.LBPs (100mg/mL)can increase the co-expression of I-A/I-E and CD11c and the secretion of IL-12p40in bone marrow-derived dendritic cells (BMDCs),which suggests that LBPs are capable of promoting both the phenotypic and functional maturation of murine BMDCs in vitro [13].LBPs can also up-regulate the DC expression of CD40,CD80,CD86,and MHC class H molecules,down-regulate the uptake of Ag by DCs,enhance the co-stimulatory
activity of DCs,and induce IL-12p40and p70production.Furthermore,LBPs induce the development of an enhanced Th1response,and LBP-treated DCs exhibited enhanced Th1and Th2responses in vitro and in vivo .Several studies have provided a rationale for the use of LBP under various clinical conditions to enhance host immunity and suggest the use of LBP as a potent adjuvant for the design of DC-based vaccines [14].We previously found that macrophages,rather than T and B cells,are the principal immunostimulatory target cells of the L.barbarum poly-saccharide LBPF4-OL.All of these results suggest that macrophages and dendritic cells are the primary target cells of LBPs [15].
At present,TLR4/2is generally believed to be the main receptor of polysaccharides.A Japanese scholar ?rst reported that saf ?ower poly-saccharides activate the transcription factor NF-kB via Toll-like receptor 4and induce cytokine production [16].More recently,South Korean and Chinese scholars began to report that the Toll-like receptor-mediated activation of B cells and macrophages by polysaccharides isolated from the cell culture of Acanthopanax senticosus and polysaccharides from Dioscorea batatas induce tumor necrosis factor-alpha secretion via Toll-like receptor 4-mediated protein kinase signaling pathways [17,18].Anti-TLR4monoclonal antibody blocking and the use of cells from TLR4-defective mice are two mainstream methods for revealing the molecular mechanism of active polysaccharides,but these methods do not directly indicate whether the polysaccharide is a ligand of TLR4.A
International Immunopharmacology 19(2014)132–141
?Corresponding authors at:Beijing Institute of Pharmacology and Toxicology,27TaiPing Avenue,Beijing 100850,China.Tel.:+861066931625;fax:+861068211656.
E-mail addresses:zhouwx@https://www.doczj.com/doc/8410151843.html, (W.Zhou),zhangyx@https://www.doczj.com/doc/8410151843.html, (Y.
Zhang).1567-5769/$–see front matter ?2014Elsevier B.V.All rights reserved.
https://www.doczj.com/doc/8410151843.html,/10.1016/j.intimp.2014.01.010
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large number of studies suggest that several polysaccharides can signif-icantly activate the TLR4–MAPK signaling pathway and induce TNF-α, IL-1β,and IFN-α/βproduction.However,it is currently unclear whether the LBP activity is related to the TLR4–MAPK signaling pathway and whether LBP can be directly combined with TLR4.In this study,we in-vestigated the molecular mechanism of the polysaccharide LBPF4-OL, which was extracted from LBP,in peritoneal macrophages and murine RAW264.7macrophage cells.
2.Material and methods
2.1.Animals
Six-week-old female BALB/c mice and C3H/HeN mice were pur-chased from Vital River Experimental Animal Center(Beijing,China) and were housed in a controlled environment(12-h light/12-h dark photoperiod,22±2°C,45–55%relative humidity).Female C3H/HeJ mice were obtained from The Jackson Laboratory.All of the mice were used at the age of8to10weeks.All of the experiments were conducted according to the National Guide for the Care and Use of Laboratory An-imals and were approved by the Bioethics Committee of the Beijing In-stitute of Pharmacology and Toxicology.
2.2.Reagents
Lipopolysaccharide(LPS from Escherichia coli,serotype055:B5)was purchased from Sigma-Aldrich(St.Louis,MO,USA).Ethylenediamine tetraacetic acid disodium salt(EDTA-Na2)was purchased from Sinopharm Chemical Reagent(Shanghai,China).TNF-αand IL-1βELISA kits were purchased from Dakewe Biotech(Beijing,China). Anti-mouse TLR4/MD2,anti-CR3,and anti-TLR2were purchased from BioLegend.Extracellular signal-regulated kinase(ERK),C-Jun N-terminal kinase(JNK),and p38mitogen-activated protein kinase (MAPK)were purchased from Cell Signaling Technology(Beverly,MA, USA).RPMI(Roswell Park Memorial Institute)1640medium was pur-chased from Gibco BRL(Life Technologies,USA).Fetal bovine serum (FBS)was purchased from Hyclone Laboratories,and3H-thymidine was obtained from GE Healthcare(Buckinghamshire,UK).
2.3.Preparation of LBPF4-OL
LBPF4-OL was isolated from L.barbarum fruit as described previously [6].First,crude LBP was isolated from L.barbarum fruit.Brie?y,dried L.barbarum fruit was extracted with water,and the water extract was precipitated with ethanol.The free proteins were removed using the Sevag reagent(CHCl3:n-BuOH=4:1).The crude LBP was obtained through dialysis and lyophilization.Second,the polysaccharide–protein complex LBPF4was isolated from LBP.Brie?y,LBP was separated through DEAE-cellulose ion exchange chromatography(successively eluted with water,followed by0.05M,0.1M,0.25M,and0.5M NaHCO3),and?ve homogenous fractions,designated LBPF1,LBPF2, LBPF3,LBPF4,and LBPF5,were obtained.LBPF4was then puri?ed main-ly through gel?ltration chromatography using a Sephadex G-100col-umn with0.1M sodium chloride–water solution as the eluent,and LBPF4was obtained.Third,LBPF4-OL was released from LBPF4.Brie?y, 80mg of LBPF4was dissolved in3.5mL of0.1N Tris–hydrochloric acid buffer(pH8.0)containing0.1%calcium chloride.Then,1%(g/g) Pronase E was added to the buffer,and the sample was allowed to digest for24h at37°C and then an additional48h with a supplement of0.5% (g/g)Pronase E.Then,100μL of methylbenzene was used to inhibit the growth of the bacterium.LBPF4-OL was?nally puri?ed using a Sephadex G-100column,and the polysaccharide LBPF4-OL released from LBPF4was obtained.The molecular weight of LBPF4-OL was181 kD,as determined by SDS-PAGE.The protein content was found to be ~0%,as determined through the Bradford method using a protein assay kit according to the manufacturer's protocol.LBPF4-OL was dis-solved in PBS or normal saline and?ltered through a0.22-μm?lter. 2.4.Isolation of peritoneal macrophages
Mice were injected i.p.with1mL of3%thioglycolate(Sigma-Aldrich). After three days,the peritoneum was washed with10mL of ice-cold PBS. The cells were incubated on24-well plates with DMEM(Invitrogen Life Technologies)containing10%FCS(HyClone Laboratories),100U/mL penicillin,100U/mL streptomycin,2mM L-glutamine,1mM sodium py-ruvate,and nonessential amino acids for3h at37°C in5%CO2.The nonadherent cells were removed by washing.
2.5.ELISA
The resident cells from the peritoneal cavity of mice were collected, and the macrophage population was enriched according to the method described by Shalev et al.[19].The levels of TNF-αand IL-1βin the su-pernatants were measured with precoated TNF-αand IL-1βELISA kits according to the manufacturer's instructions.The absorbance was mea-sured at450nm with a reference wavelength of570nm using a spec-trometer(BMG POLARStar Galaxy v4.0,Germany).
2.6.Cell line
RAW264.7is a tumor macrophage cell line derived from BALB/c mice(20)that retains phagocytic and Ag-presenting capabilities (21).RAW264.7cells were obtained from American Type Culture Collection(ATCC)and were raised in full medium at37°C in a5% CO2atmosphere.
2.7.Splenocyte proliferation assay
C3H/HeN and C3H/HeJ mice were sacri?ced.Their spleen was asep-tically removed and minced through a40-μm nylon cell strainer to achieve a single-cell suspension.The red blood cells were depleted with Tris–NH4Cl lysis buffer(0.144M NH4Cl,0.017M Tris–HCl).A total of5×105spleen cells were stimulated with LBPF4-OL at serial con-centrations,including5,10,50,100,and200μg/mL.The spleen cells were cultured in RPMI-1640medium supplemented with10%FBS,pen-icillin(100U/mL),and streptomycin(100μg/mL)at37°C in a5%CO2 humidi?ed incubator for72h and were pulsed with3H-thymidine (1μCi/well)during the last18h of incubation.The cells were harvested on glass?ber?lters using a Filtermate cell harvester(Packard).The amount of3H-thymidine incorporated into the cells was measured using aβ-scintillation counter(Beckman LS6500).The results are expressed as cpm(counters per minute)of the stimulated cells and cpm of the unstimulated cells.
2.8.Flow cytometry
The cells were washed with cold PBS containing0.1%NaN3and1% FBS.A total of106cells were incubated with PE-conjugated anti-mouse TLR4/MD2or isotype control IgG(BD Biosciences)for20min at room temperature.The cells were washed in PBS containing0.1% FBS and analyzed by?ow cytometry(BD Calibur?).
2.9.Western blot
The cells were washed in1×PBS and lysed in lysis buffer[10mM Tris–HCl(pH7.5),10mM NaH2PO4/NaHPO4(pH7.5),130mM NaCl, 1%Triton X-100,10mM NaPPi,1mM phenylmethylsulphonyl?uoride, and2μg/mL pepstatin A]for30min on ice.The lysates were then centri-fuged at30,000rpm and4°C for30min.The supernatant was collected, and the protein content was then measured using a Bio-Rad protein assay kit before its analysis.The cytoplasmic or nuclear protein samples
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were loaded at a concentration of10μg of protein/lane,separated by so-dium dodecyl sulfate-polyacrylamide gel electrophoresis(SDS-PAGE)in a10–15%gel,and transferred to polyvinylidene di?uoride membranes (Immun-Blot PVDF membrane,0.2μm;Bio-Rad).The membranes were blocked with5%nonfat powdered milk in1×Tris-buffered saline(TBS) containing0.1%Tween20for1h and then incubated with primary anti-bodies overnight at4°C.The membranes were then treated with horse-radish peroxidase-coupled secondary antibodies for1h at4°C and washed with T-TBS after each antibody binding reaction.The detection of each protein was performed using an enhanced chemiluminescence (ECL)kit(Millipore Co.,USA).
2.10.Bio-layer interferometry(BLI)
The kinetic estimates were obtained using the ForteBio Octet RED system(ForteBio).The octet analysis was performed at30°C in HBS-EP+0.1mg/mL BSA running buffer.Brie?y,the anti-human IgG Fc cap-ture(AHC)sensors from ForteBio were used to capture the TLR4/MD2-Fc onto the kinetic surface of the sensor.TLR4/MD2-Fc was loaded to saturation onto the anti-human Fc biosensors,washed in buffer(30s), and placed for3min in the wells containing LBPF4-OL,LPS,and FBS. The one-shot KD was calculated based on the1:1model,and the aver-age KD was extracted from the binding results obtained for?ve different concentrations of the analyses.
2.11.Statistical analysis
Unless speci?cally mentioned,all of the data are expressed as the means±S.D.The ANOVA procedure was used to assess the signi?cance of the differences between groups.For each signi?cant treatment effect, Dunnett-type multiple comparisons were used to compare the means of multiple groups.All of the statistical analyses were conducted using the SPSS12.0software package.A value of P b0.05was used as the thresh-old for signi?cance.
3.Results
3.1.Anti-TLR4/2treatment inhibits LBPF4-OL-induced TNF-a and IL-1βproduction
Our previous research study found that LBPF4-OL induces the pro-duction of multiple cytokines,including TNF-α,IL-1?,IL-2,IL-6,IL-8, IL-10,IL-12,and GM-CSF,in splenocytes in a dose-dependent manner [15].Of all of these cytokines,TNF-αand IL-1βwere the most signi?cant-ly up-regulated.To determine whether the reported polysaccharide-related receptors,including TLR4/2and CR3,are related to the activities of L.barbarum polysaccharides,macrophages were treated with anti-TLR4/2antibody,and the concentrations of TNF-αand IL-1βin the cell culture supernatants were examined.Treatment with LBPF4-OL for24 h stimulated TNF-αand IL-1βproduction compared with the medium control(Fig.1A).Anti-TLR4(0.31,0.62,1.25,and2.5μg/mL)treatment inhibited the LBPF4-OL(100μg/mL)-induced secretion of TNF-αand IL-1βin a concentration-dependent manner.Anti-TLR4(0.62μg)also signi?cantly inhibited the LPS(5μg/mL)-induced secretion of TNF-αand IL-1β(Fig.1B).We further found that anti-TLR2(0.31, 0.62,1.25,and2.5μg/mL)treatment partially inhibited the LBPF4-OL(100μg)-induced TNF-αand IL-1βsecretion,and anti-TLR2(0.62μg/mL)has no apparent effect on the LPS(5μg/mL)-induced TNF-αand IL-1βsecretion(Fig.1C).Neither anti-CD11b nor anti-CD18/anti-CD11b combined with anti-CD18had an effect on the LBPF4-OL-and LPS-induced TNF-αand IL-1βproduction(Fig.1D). These results suggest that the LBPF4-OL-induced TNF-αand IL-1βproduction is TLR4/2-related and not CR3-related.
3.2.Anti-TLR4/MD2treatment inhibits LBPF4-OL-induced lymphocyte proliferation
The immunoenhancement activity of LBP is mainly reported to stimulate mouse splenocyte proliferation[15,20,21]and to induce the phenotypic and functional maturation of DCs with strong immu-nogenicity[14].A recent study found that the water-soluble polysac-charide fraction LBP-IV isolated from L.barbarum leaves signi?cantly enhanced the proliferation of splenocytes stimulated by Con A or LPS [22].To investigate whether TLR4and CR3are related to the immu-nological enhancement activity of LBPF4-OL,we further observed the effect of LBPF4-OL on lymphocyte proliferation through antibody pretreatment.BALB/c splenocytes were prepared,and lymphocyte separation medium was used to obtain the lymphocytes.The lym-phocytes were pre-treated with anti-TLR4and anti-CR3antibody for1h in vitro,and the3H-TdR incorporation method was then used to analyze the LBPF4-OL-and LPS-induced lymphocyte prolifer-ation.Fig.2A shows that LBPF4-OL induces lymphocyte proliferation in a concentration-dependent manner,but the stimulation intensity is signi?cantly weaker than that obtained with LPS.Fig.2B and C shows that anti-TLR4can completely inhibit the LBPF4-OL-induced lymphocyte proliferation,but anti-CR3has no effect on the LBPF4-OL-induced lymphocyte proliferation.These results indicate that the LBPF4-OL-induced lymphocyte proliferation is TLR4-dependent and not CR3-dependent.
3.3.LBPF4-OL cannot induce TNF-αand IL-1βproduction in peritoneal macrophages from C3H/HeJ mice
The C3H/HeJ mouse is TLR4-defective[23].To further clarify wheth-er TLR4is a LBPF4-OL activity-related site and to determine whether the production of in?ammatory cytokines induced by LBPF4-OL is associat-ed with TLR4,the supernatant TNF-αand IL-1βconcentrations of peri-toneal macrophages from C3H/HeJ mice were analyzed.As shown in Fig.3,LBPF4-OL(50,100μg/mL)signi?cantly increased the TNF-αand IL-1βproduction by peritoneal macrophages from C3H/HeN mice but had no effect on the TNF-αand IL-1βproduction by macrophages from C3H/HeJ mice.In addition,we found that the TNF-αand IL-1βpro-duction by peritoneal macrophages from C3H/HeJ mice was obviously weaker than that obtained from C3H/HeN macrophages.The results show that TLR4is in fact an activity-association receptor of LBPF4-OL for the induction of TNF-ɑand IL-1βproduction,but it is unclear whether TLR4is a LBPF4-OL binding site.
3.4.LBPF4-OL-stimulated proliferation of lymphocytes from C3H/HeJ mice is weaker than that of lymphocytes from C3H/HeN mice
To determine whether the lymphocyte proliferation induced by LBPF4-OL is associated with TLR4,the in vitro proliferation rates of the lymphocytes from C3H/HeJ and C3H/HeN mice were compared through
Fig.1.Anti-TLR4/2treatment inhibits LBPF4-OL-induced TNF-ɑand IL-1βproduction.BALB/c mice were sacri?ced,and their spleen cells were prepared.The spleen cells(5×105)were stimulated with LPS(5μg/mL),Dextran(100μg/mL),anti-TLR4(0.31–2.5μg/mL),anti-TLR2(0.31–2.5μg/mL),anti-CR3(0.31–1.25μg/mL),and LBPF4-OL(10–100μg/mL)for24h.
(A)LBPF4-OL induced TNF-ɑand IL-1βproduction in peritoneal macrophages in vitro.*P b0.05compared with the medium control.(B)Anti-TLR4treatment inhibited LBPF4-OL (100μg/mL)-induced TNF-ɑand IL-1βproduction.**P b0.01compared with the medium control;##P b0.01compared with LPS;$$P b0.01compared with LBPF4-OL.(C)Anti-TLR2treat-ment inhibits LBPF4-OL(100μg/mL)-induced TNF-ɑand IL-1βproduction.**P b0.01compared with the medium control;##P b0.01compared with LBPF4-OL.(D)Anti-CR3treatment had no effect on LBPF4-OL(100μg/mL)-induced TNF-ɑand IL-1βproduction.**P b0.01compared with the medium control.The production of TNF-ɑand IL-1βwas measured by ELISA. The data represent the means±SD of four replicates.
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the 3H-TdR incorporation method.As shown in Fig.4,the effect of LBPF4-OL on the proliferation of C3H/HeN mouse splenocytes is obvi-ously weaker than that on the proliferation of C3H/HeJ mouse splenocytes,and this effect is dependent on the concentration (5to 200μg/mL)of LBPF4-OL.However,the proliferation of lymphocytes from C3H/HeJ mice induced by LBPF4-OL is signi ?cantly higher than that observed in the control group.The results show that TLR4is in fact an activity association receptor of LBPF4-OL for the induction of lymphocyte proliferation.The results also indicate that other receptors in addition to TLR4may participate in the LBPF4-OL-induced lympho-cyte proliferation.
3.5.LBPF4-OL cannot directly bind to TLR4in vitro
Many of the bioactivities of botanical polysaccharides are closely associated with TLR4;however,it has not yet been reported whether these polysaccharides can be directly combined with TLR4.LPS is a glycolipid located in the outer membrane of Gram-negative bacteria and is composed of an amphipathic lipid A component,hydrophilic polysaccharides in the core,and O-antigen.Lipid A represents the conserved molecular pattern of LPS and is the main inducer of the immunological responses to LPS [24].TLR4in association with MD-2is responsible for the physiological recognition of LPS [25].In this study,a new method based on bio-layer interferometry (BLI)was used to determine the binding and dissociation of LBPF4-OL and LPS with TLR4in vitro [26].As shown in Fig.5A,the AHC sensor
combined effectively with the FC fragment of human rat recombi-nant TLR4molecules,and the maximum response value was found to be 0.8nm.Fig.5B shows that LPS directly binds to TLR4and rapidly reached saturation within 10s in a concentration-dependent man-ner.Because we cannot acquire the molecular weight of LPS,it is im-possible to quantify the interactions through equilibrium binding analyses.This result shows that LPS can bind directly to TLR4in vitro .As a comparison,the association of LBPF4-OL with TLR4was tested under the same conditions,and we found that LBPF4-OL at different concentrations (31.25–500μg/mL)cannot bind to TLR4.These results suggest that LBPF4-OL cannot directly associate with TLR4.
3.6.LBPF4-OL increases TLR4expression on the membranes of peritoneal macrophages and RAW26
4.7cells
It has been reported that one of the molecular mechanisms of the immune-enhancing effect of polysaccharides is the induction of the expression of TLR4on the cytomembrane.Therefore,we further ob-served the effect of LBPF4-OL on the expression of TLR4on peritone-al macrophages and RAW264.7cells by ?ow cytometry.As indicated in Fig.6A,peritoneal macrophages stimulated with LBPF4-OL or LPS for 24h cannot induce the expression of TLR4on the cytomembrane,and a high expression of TLR4was observed in these cells after stim-ulation for 48h with both LPS and LBPF4-OL.A partial recovery of the TLR4expression was observed in cells stimulated with LBPF4-OL
for
Fig.2.Anti-TLR4/MD2treatment inhibits LBPF4-OL-induced lymphocyte proliferation.BALB/c mice were sacri ?ced,and their spleen cells were prepared.The spleen cells (5×105)were pretreated with anti-CR3(0.62μg/mL)and anti-TLR4/MD2(0.62μg/mL)and then stimulated with LPS (5μg/mL)and LBPF4-OL (100μg/mL)for 72h.(A)Anti-TLR4/MD2treatment inhibits the LBPF4-OL-induced proliferation of the spleen cells.*P b 0.05and **P b 0.01compared with the medium control;#P b 0.05and ##P b 0.01compared with LPS treatment.(B)Anti-CR3treatment has no effect on the LBPF4-OL-induced proliferation of spleen cells;*P b 0.05and **P b 0.01compared with the medium control.The cell proliferation was measured by 3H-thymidine incorporation assay.The data represented as mean the means ±SD of four replicates.
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72h.In contrast,the LPS-induced TLR4expression was completely recovered after 72h.In addition,we observed the effect of LBPF4-OL on TLR4expression in the macrophage cell line RAW264.7.In
contrast to its effect on peritoneal macrophages,the expression of TLR4on the RAW264.7membrane was signi ?cantly increased by both LBPF4-OL and LPS after 24h.Moreover,we found that
the
Fig.3.LBPF4-OL cannot induce TNF-αand IL-1βproduction by peritoneal macrophages from C3H/HeJ mice.Both C3H/HeN and C3H/HeJ mice were sacri ?ced,and their spleen cells were prepared.The spleen cells (5×105)were stimulated with LPS (5μg/mL),galactan (100μg/mL),and LBPF4-OL (10–100μg/mL)for 24h.(A)LBPF4-OL could not induce TNF-ɑproduction by the peritoneal macrophages from C3H/HeJ mice.(B)LBPF4-OL could not induce IL-1βproduction by the peritoneal macrophages from C3H/HeJ mice.*P b 0.01compared with the LPS-stimulated spleen cells from C3H/HeN mice;#P b 0.05and ##P b 0.01compared with the LBPF4-OL-stimulated spleen cells from C3H/HeN mice.The TNF-ɑand IL-1βproduction levels were measured by ELISA.The data represent the means ±SD of four replicates.
5
10
50
100
200
3
H -t h y m i d i n e i n c o p o r a t i o n (c p m )
2000
4000
6000
8000
LBPF4-OL(g/ml)
Fig.4.The LBPF4-OL-stimulated proliferation of lymphocytes from C3H/HeJ mice is weaker than that of lymphocytes from C3H/HeN mice.Both C3H/HeN and C3H/HeJ mice were sacri ?ced,and their spleen cells were prepared.The spleen cells (5×105)were stimulated with LBPF4-OL (5–200μg/mL)for 72h and pulsed with 3H-thymidine (1μCi/well)during the last 18h.The cells were harvested on glass ?ber ?lters using a Filtermate cell harvester.*P b 0.05and **P b 0.01compared with the LBPF4-OL-stimulated spleen cells from C3H/HeN mice.The 3H-thymidine incorporation method was used to determine the cell proliferation.The data represent the means ±SD of four replicates.
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expression of TLR4in LBPF4-OL-treated cells was recovered to a nor-mal level,but the TLR4expression in LPS-treated cells was signi ?-cantly lower than that observed in the control group after 48h.These results suggest that LBPF4-OL and LPS trigger different molec-ular mechanisms to induce TLR4expression.The above results also suggest that the immune-enhancing effect of LBPF4-OL is due to TLR4expression.
3.7.LBPF4-OL regulates the phosphorylation of MAPKs
Mitogen-activated protein kinase (MAPK)signal transduction path-ways are ubiquitous and highly evolutionarily conserved mechanisms of eukaryotic cell regulation [27].The multiple MAPK pathways present in all eukaryotic cells enable coordinated and integrated responses to di-verse stimuli.It is de ?nite that both LPS and the other
botanical
Fig.5.LPS and not LBPF4-OL can bind to TLR4on the octet platform.(A)Loading of label-free mouse TLR4(aa24–334)-Fc to immobilized anti-human IgG Fc capture (AHC)sensors in the octet,which was used to detect the molecular –molecular interactions via bio-layer interferometry.(B)LPS association and dissociation with mouse TLR4(aa24–334)show an increase in the saturation response with increasing concentration.(C)LBPF4-OL does not associate with mouse TLR4(aa24–334).Bio-layer interferometry (BLI)was used to analyze the association and dissociation of polysaccharides with TLR4.The experiment was repeated three times,and representative results are shown.
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polysaccharide can effectively evoke the MAPK signal pathway through TLR4.However,the effects of L.barbarum polysaccharides on MAPK sig-nal pathway have not yet been reported.In the present study,the effect of LBPF4-OL on p-38,ERK1/2,and SAPK/JNK phosphorylation was ob-served through the WB method (Fig.7).We found that phospho-p38was markedly increased after stimulation with LBPF4-OL at a concentra-tion of 100μg/mL for 30min,and the level of phospho-p38was recov-ered after 45min.In contrast,phospho-ERK1/2was signi ?cantly inhibited early during treatment (within 30min)with LBPF4-OL and returned to the normal level after 45min.LBPF4-OL has no effect on the level of SAPK over a period of 1h.We also found that LBPF4-OL markedly inhibits the phospho-JNK level within 1h.In contrast,we ob-served that the treatment of cells with LPS for 45min signi ?cantly en-hanced the levels of phos-p-38,phos-ERK1/2,and phospho-SAPK/JNK.These results indicate that LBPF4-OL can regulate the p-38,ERK1/2,and JNK MAPK signaling pathways in macrophages.4.Discussion
Immunomodulation and antitumor effects are one of the main activ-ities of L.barbarum polysaccharide.Previous studies have shown that the polysaccharide –protein complex from L.barbarum (LBP3p)can sig-ni ?cantly inhibit the growth of transplantable sarcoma S180and in-crease macrophage phagocytosis;in addition,the form of antibody secreted by spleen cells,spleen lymphocyte proliferation,CTL activity,and IL-2mRNA expression level were increased,and lipid peroxidation was reduced in S180-bearing mice [28].Moreover,L.barbarum polysac-charide (LBP),which was isolated with boiling water from L.barbarum fruits,can inhibit the proliferation of HeLa cells [29].The present study provides the ?rst demonstration that L.barbarum polysaccharide stimu-lates tumor necrosis factor-alpha (TNF-α)and IL-1βgeneration and promotes lymphocyte proliferation in a TLR4-dependent manner.TNF-α,a pro-in ?ammatory cytokine that was initially identi ?ed and named as a result of its anti-tumoral properties,is involved in the path-ogenesis of multiple chronic in ?ammatory or autoimmune diseases.TNF-αcan act on monocytes and macrophages in an autocrine manner to enhance various functional responses and induce the expression of other immunoregulatory and in ?ammatory mediators.IL-1βis involved in fever during the induction of the acute-phase protein response.In ad-dition,IL-1βcooperates with IFN-γand IL-12to induce tumor death by NK cells.It has been reported that,after an initial phase of growth,some murine tumor cells transduced with the TNF-αgene either completely regress or demonstrate decreased tumorigenicity.Consistently,Ganoderma atrum polysaccharide (PSG-1)can activate macrophages and increase TNF-α,IL-1β,and nitric oxide production via TLR4-dependent signaling pathways,improve immunity,and inhibit tumor growth [30].All of these results strongly suggest that TLR4plays an im-portant role in the immunomodulation and antitumor effects of L.barbarum polysaccharide LBPF4-OL.
In this study,we found that the underlying mechanisms induced by LBPF4-OL and LPS on the TLR4–MAPK signaling pathway are dif-ferent.First,we found that the anti-TLR4,anti-TLR2,and anti-CR3treatments resulted in markedly different effects on the LPS-and LBPF4-OL-induced secretion of in ?ammatory cytokines.As shown in Fig.1,both anti-TLR4and anti-TLR2treatments signi ?cantly inhibited the LBPF4-OL-induced TNF-αand IL-1βsecretion.Howev-er,anti-TLR4and not anti-TLR2inhibited the LPS-induced TNF-αand IL-1βproduction by macrophages.In addition,as shown in Fig.3,we found that LBPF4-OL markedly induced the secretion of TNF-αand IL-1βby C3H/HeN mice peritoneal macrophages but had no effect on the secretion of cytokines by macrophages from TLR4-defective C3H/HeJ mice.On the contrary,LPS signi ?cantly induced the secretion of TNF-αand IL-1βBy C3H/HeJ mouse peritoneal macrophages in vitro .These results are consistent with the activity characteristics of LPS.Studies have shown that the LPS –TLR4interaction requires the participation of many other molecules,such as CD14/LBP and HSP70,and this molecular community is known as the LPS receptor family [31–33].In addition,these receptors are clustered together and are involved in LPS-induced transmembrane signal transduction.Studies have also found that TLR4de ?ciency cannot fully reduce the activity of LPS.These results indicate that,in addition to TLR4,LBPF4-OL can induce the secretion of in ?amma-tory factors by TLR2,and LPS can induce the secretion of in ?ammatory factors through an unknown receptor.Second,there is a clear difference in the TLR4expression induced by LPS and LBPF4-OL.Vicky Sender found that LPS can signi ?cantly induce TLR4expression on the cell mem-brane of alveolar macrophages,and this expression peaks after 30
min
Fig.6.LBPF4-OL increases TLR4expression on the membranes of peritoneal macrophages and RAW264.7cells.Macrophages or Raw264.7cells were cocultured with LBPF4-OL and LPS for 24,36,and 48h,and the PE-conjugated anti-mouse TLR4/MD2complex (0.25μg per million cells in 100μL)was used for the ?ow cytometric analysis.(A)LBPF4-OL induces TLR4expres-sion in peritoneal macrophages from C3H/HeN mice.(B)LBPF4-OL induces TLR4expression in Raw264.7cells.
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and then gradually decreases [34].Our experimental results indicate that the LPS-induced TLR4expression on peritoneal macrophages continues to be higher than the normal levels after 12h and recovers to the normal levels after 24h.The TLR4expression induced by LBPF4-OL after 12and 24h is signi ?cantly higher than that obtained with LPS (Fig.6).These re-sults suggest that the LBPF4-OL-induced TLR4expression is signi ?cantly stronger than the effect induced by LPS.Finally,there are signi ?cant dif-ferences in the LPS-and LBPF4-OL-induced MAPK signaling pathway.Our results show that LPS signi ?cantly promotes the phosphorylation of P-38,ERK1/2,and JNK MAPKs.However,LBPF4-OL only promoted the phosphorylation of P-38and inhibited the phosphorylation of ERK1/2and JNK (Fig.7).These results indicate that LPS plays a facilitating role and LBPF4-OL plays a regulatory role in the MAPK signaling pathway.
Recent studies have shown that Goji berries can cause allergic re-actions in both exposed and unexposed food-allergic individuals,es-pecially those who are allergic to lipid-transfer proteins (LTPs)from other foods [35].However,it seems impossible that L.barbarum polysaccharide LBPF4-OL causes allergic reactions,even though some studies have indicated that the activation of TLR4can reduce allergic reactions.A previous study found that Tlr4?/?mice have re-duced proportions of CD4+Foxp3+Tregs in the colonic lamina propria and exhibit increased susceptibility to food-induced allergic responses.Moreover,it has also been reported that dermal expo-sure to the TLR4ligand lipopolysaccharide (LPS)or TLR2ligand
Pam(3)Cys suppresses asthmatic responses by reducing airway hy-perreactivity,mucus production,Th2-type in ?ammation in the lungs,and IgE antibodies in the serum in a dose-dependent manner.In addition,LBPF4-OL contains no protein,as was con ?rmed by the Bradford method in our previous research.In consequence,as a po-tent immunity-enhancing agent,LBPF4-OL may not cause an aller-gic reaction;on the contrary,it may attenuate an allergic reaction.Thus,the observation of the anti-allergic effect of LBPF4-OL may be a valuable future research direction.
LPS is currently the most widely studied TLR4ligand,but the biolog-ical activity of LPS may require the participation of more than one pro-tein.These proteins are called a receptor cluster [32,36–38].Through its interaction with the receptor cluster,LPS activates intracellular sig-naling by binding with TLR4.In addition,it has been reported that some polysaccharide activities are closely associated with TLR4.The Japanese scholar Izuru Ando ?rst reported that saf ?ower polysaccha-rides activate the transcription factor NF-kB via Toll-like receptor 4and induce cytokine production [16].Later,South Korean and Chinese scholars began to report that the Toll-like receptor-mediated activation of B cells and macrophages by the polysaccharides isolated from the cell culture of A.senticosus and the polysaccharides from D.batatas induce tumor necrosis factor-alpha secretion via Toll-like receptor 4-mediated protein kinase signaling pathways [17,18].Anti-TLR4/MD2monoclonal antibody blocking and the use of cells from TLR4-defective mice are two mainstream methods used to reveal the mechanisms of active poly-saccharides,but these methods do not directly indicate whether the polysaccharide of interest is a ligand of TLR4.Therefore,in this study,in addition to these two methods,bio-layer interferometry technology (BLI)was also used to observe the binding of LBPF4-OL to TLR4.The ex-perimental results show that LBPF4-OL does not directly bind to TLR4in vitro .Based on the results,we speculated that LBPF4-OL may act sim-ilarly to LPS,which requires a variety of receptor clusters to participate in the activation of TLR4.In addition,the results also indicate that more data are required to determine whether the reported polysaccha-rides,such as saf ?ower polysaccharide,the activity of which is associat-ed with TLR4,can interact directly with TLR4in vitro .
Dziarski ?rst reported that LPS induces tyrosine phosphorylation and the activation of MAPKs,such as ERK1/2,p38,and SAPK/JNK,in macrophages [39].Because the MAPK signal itself has not yet been fully elucidated,particularly the core signaling pathways of the JNK MAPK molecular mechanism [27],it is presently dif ?cult to reveal the intrinsic link between the biological activity of a polysaccharide and the MAPK signaling pathway.The ERK,JNK,and P38MAPK core pathways and their targets are activated by stresses,such as radia-tion injury,fatigue,oxidative stress,and in ?ammatory mediators [40,41].L.barbarum polysaccharides have signi ?cant resistance to radiation damage and alleviate physical fatigue and all types of oxi-dative stress [42–44].However,the effect of L.barbarum polysaccha-rides on the MAPK signal has not been reported.This study found that the L.barbarum polysaccharide LBPF4-OL signi ?cantly induces the phosphorylation of p38-MAPK and also signi ?cantly inhibits the phosphorylation of ERK and JNK.Many polysaccharides,such as the Ganoderma lucidum (Reishi or Ling-Zhi)polysaccharide EORP [45],the Paecilomyces polysaccharide PCP [46],the acetyl fucoidan from Cladosiphon okamuranus [47],and the polysaccha-rides from Angelica dahurica ,can increase the phosphorylation of P38,JNK,and ERK1/2MAPK [48].In contrast,previous studies have reported that P38a leads to feedback control loops that suppress the activities of upstream MAP kinase kinase kinases (MAP3Ks),such as TAK1and MLKs [49,50],which are associated with the acti-vation of other pro-in ?ammatory pathways,including those that lead to the activation of JNK.It is possible that this mechanism may explain why the phosphorylation of P38-MAPK was increased and the phosphorylation of JNK was inhibited by LBPF4-OL.
Previous studies have found that the activation of P38and JNK sig-naling can directly or indirectly promote diabetes [51].Strong
evidence
Fig.7.LBPF4-OL increases p-38and inhibits ERK1/2and JNK phosphorylation of the MAPK signaling pathway in peritoneal macrophages.Peritoneal macrophages were treated with LBPF4-OL (100μg/mL)or LPS (100μg/mL)for 15–60min.The cell lysates were prepared,and western immunoblotting was performed against p-p38MAP kinase or p38,p-ERK1/2or ERK1/2,and p-SAPK/JNK or SAPK/JNK.*P b 0.05and **P b 0.01compared with the p-p38control;#P b 0.05and ##P b 0.01compared with p-ERK control;$P b 0.05and $$P b 0.01compared with p-JNK control.The experiment was repeated three times,and representa-tive results are shown.
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has emerged that JNK,especially JNK1,possibly in conjunction with other MAPK groups,can directly contribute to insulin resistance[52]. These?ndings are consistent with the antidiabetic effect and the inhib-itory effect of LBPF4-OL on JNK phosphorylation.However,further stud-ies are required to determine whether the antidiabetic effect of L.barbarum polysaccharide is directly linked to JNK.
In conclusion,we found that L.barbarum polysaccharide LBPF4-OL promotes TNF-αand IL-1βsecretion and lymphocyte proliferation in a TLR4/MD2-dependent manner.We also found that LBPF4-OL is stronger than LPS in inducing TLR4expression in macrophages.In addition, LBPF4-OL can signi?cantly enhance the phosphorylation of P38and in-hibit JNK and ERK1/2MAPK phosphorylation,whereas LPS can induce P38,JNK,and ERK1/2MAPK phosphorylation.These results indicate that L.barbarum polysaccharide LBPF4-OL is a new Toll-like receptor 4/MD2-MAPK signaling activator and inducer.
Acknowledgments
This work was supported by the National Natural Science Founda-tion of China(no.81102451).
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所有茶的功效都全了,您喝对了不? 1、铁观音:除具有一般茶叶的保健功能外,还具有抗衰老、抗癌症、抗动脉硬化、防治糖尿病、减肥健美、降火,敌烟醒酒。 2、普洱茶:同时具有清热、消暑、解毒、消食、去肥腻、利水、通便、祛痰、祛风解表、止咳生津、益力气、延年益寿等功效。又由于普洱茶经历了生茶到熟茶的转变过程,其生茶具有祛风解表、清头目等功效,而熟茶又有下气、利水通便等功效。 3、武夷岩茶:含有多种化学元素与咖啡碱、茶多酚、脂多糖等、其药理性能特别显着.不但能醒心、明目、健神、消愁、止渴、杀菌、去垢、利尿、解暑、醒酒等,还有降压、减肥、抗辐射、防癌、延缓衰老等延年益寿效。 4、龙井茶:可以净化血管,预防中风与心脏病 5、碧螺春:属于绿茶具有抗衰老,抗菌,防癌降血脂,瘦身减脂,防龋齿,清口臭,防癌,美白及防紫外用。 ６、黄山毛峰:对出尽血液循环、降低胆固醇、增加毛细血管单行,增强血液抗凝性都有一定好处:同事,黄山毛峰对防癌、抗癌还能起到一定的作用。 7、庐山云雾茶:具有六大功效,即降脂、减肥、降压、抗动脉硬化;抑制肿瘤细胞产生;养胃、护胃;健牙护齿;消炎、杀菌、治痢;抗衰老等这样的一些功效。 ８、六安瓜片:有利于预防与抑制癌症;有利于心血管疾病的保健治疗;有利于减肥与清理肠道脂肪;有利于清热除燥、排毒养颜。 9、君山银针:具有一般茶类索有的保健功效:兴奋解倦,益思少睡,消食祛痰,解毒止渴,利尿明目,增加营养。还有杀菌、抗氧化、抗衰老、预防癌症的功效。 1０、信阳毛尖:不但营养成分含量较高,而且不清心明目、散热解渴、去烦提神、助消化、健脾。 11、太平猴魁:防辐射,降血压,防龋齿,清口臭。 1２、祁门红茶:可以匡助胃肠消化、促近食欲,可利尿、消除水肿,并强壮心肌功能。 13、菊花茶: 降火,利尿。 1４、玫瑰花茶: 美化皮肤,舒解神经。玫瑰花:滋润养颜,护肤美容,活血,保护肝脏,消除疲劳,促进血液循环之功能。可治慢性胃炎及肝炎。适女性,小孩饮用。 15、桂桂香:滋阴补肾,调整机能,调节内分泌,保肝养胃,排毒养颜。 １6、薰衣草茶: 去疤美容,舒解神经,适女性,小孩饮用。 17、铃典: 减肥,健身,适女性,小孩饮用。 18、卡蒙米罗:预防感冒,适女性,小孩饮用。 19、洛神花茶:降血压。 ２0、莎波力: 味道重,调整消化系统,醒酒醒脑,适男性饮用。 21、波芦媚那: 味道重,调整消化系统,醒酒醒脑, 2２、泰姆茶: 抑制气喘,适小孩饮用。 23、姜母茶: 去风发汗,开脾胃。 24、决明茶: 明目,清血,味淡。
富硒荞子茶功效有哪些 众所周知，喝富硒荞子茶对人体很多好处，所以受到了很多喝茶人的喜爱。富硒荞子茶功效有哪些呢？如：它可以清肝明目；保护人体的血管防止硬化；可以降低人体血压、血糖和血脂；调节人体营养平衡，疏通肠胃，治疗便秘；通过抗氧化作用，减慢皮肤的衰老等等。一般不适合身体虚弱的的人群长期饮用。 富硒荞子茶和大麦茶比较类似，因为它们都是用五谷杂粮加工制作的茶，和我们通常喝的绿茶、红茶有着很大的区别。大麦茶功效我们比较熟悉，富硒荞子茶的功效比大麦茶还要更丰富一些，所以富硒荞子茶也更受一些特殊人群（三高人群）的喜爱，让我们一起看看富硒荞子茶该怎么喝，喝荞子茶有什么好处呢？ 富硒荞子茶怎么喝？ 1、对于荞子茶的的喝法我们一般就是，用开水冲泡4-5分钟，放置稍凉的时候即可饮用。使用皿器的时候，最好是玻璃杯，这样的话，可以看到浸泡时候的颜色。还有就是苦荞和其它不太一样，因为一般的茶叶是用紫砂壶浸泡比较好，而苦荞则不需要。 2、在浸泡的时候，饮用第一杯的时候，我们会觉得它的味道有点不太浓，最好的是第二杯，因为在第二杯的时候，苦荞的效果发挥到最佳。这个时候，有股饼干味还有一些咖啡的味道。 3、冲泡几次后，不想再继续饮用的话，还可以把杯中的变软的苦荞吃了，这样的话，可以充分发挥苦荞的营养价值。 富硒荞子茶与什么搭配喝起来效果更好？
荞子茶+黄芪：适用于气虚者。 荞子茶+枸杞：有益于肾虚者。 荞子茶+绿茶：有提神醒脑之功效，也是白领女性的时尚饮品。 荞子茶+腊梅花：有益于慢性咽炎、声音嘶哑者。 荞子茶+灵芝：能更有效的提高免疫力。 荞子茶+红花：更有助于血液循环。 喝富硒荞子茶有什么好处？ 1、喝荞子茶的好处有很多，饮用荞子茶可以降低血压，降低血糖，还有就是降低血脂，这是现在白领以及中老年人最为烦恼的“三高”，是三高人士最安全的绿色饮品。 2、饮用荞子茶的时候，还可以改善心脑微循环，让患有心脑疾病的人得到舒服。还有就是可以清楚体内的垃圾，消除劳累时候的疲劳，恢复身体的能量。 3、荞子茶和红茶一样，有抗氧化，抗辐射等的作用，可以增强人体的免疫力。让人体变得更加的健康，变得更加舒服。 4、饮用荞子茶，还可以治疗糖尿病了，对那些没有糖尿病的人有很好的预防作用。此外还有就是荞子茶中含有大量的纤维，对身体的便秘有很好的疗效。因此那些喜欢饮茶的朋友，最好选用饮用荞子茶。
各类花茶的功效大全
花茶功效分类 花茶都有理气、疏肝、开胃的作用,下面为大家介绍一些花草茶搭配大全，不同的花茶功效各异。像月季花、红花茶有活血的作用，怀孕的妇女就不能喝。而海棠花、野菊花茶比较寒凉，脾胃虚弱的人也不宜饮用。因此，大家在挑选花茶时不能只重外观，一定要了解清楚花茶的功效。另外还要提醒的是，在家喝花茶，合适的器皿也很重要。最适宜的是用透明精致的玻璃壶和玻璃小杯，用沸水冲泡。花茶宜现泡现饮，不能喝隔夜花茶。 一、祛痘花茶搭配大全: 玫瑰花茶 + 玫瑰茄 + 桃花 = 祛斑除痘补水 桃花茶 + 柠檬片 + 百合花 = 除痘清火 红巧梅 + 美容花 + 贡菊 = 美容消斑茶 玫瑰花 + 苹果花 = 调经补血粉刺美白 雪中情：抗衰老祛皱纹增白皮肤 二、祛斑花茶搭配大全: 紫罗兰 + 薰衣草+ 洋甘菊 = 滋润皮肤除皱祛斑、对喉咙、支气管炎便密、消除口腔气味. 薰衣草 + 柠檬片 + 玫瑰花 + 玉美人 = 减少皱纹祛斑 迷迭香 + 玉美人+牡丹花 = 对雀斑有明显消除功能 玫瑰 + 茉莉花茶 = 治青春痘、黑斑，让皮肤变得光滑 三、美白、瘦身花茶搭配大全：
苦丁茶 + 决明子 = 可治疗肝炎 野菊花＋百合花＝清肝火润肺 莲子心 + 金莲花 + 甘草 = 清热下火 玫瑰 + 柠檬草 = 排除宿便 玫瑰＋菩提叶＋迷迭香＋甜叶菊= 帮助睡眠 洋甘菊 + 熏衣草 + 培提叶 + 玫瑰 = 安眠、治头痛 洋甘菊 + 迷迭香+ 熏衣草 + 玫瑰 = 治头痛： 紫罗兰 + 薄荷 + 麦冬 + 胖大海 = 咳嗽 薄荷＋熏衣草＋金盏花＋甜叶菊 = 提神醒脑、解除宿醉 玫瑰+ 桂花 + 茉莉 = 强肝消除疲劳 七、治头痛、失眠、减轻压力、恢复脑部疲劳 1、黄金菊--降血压、对头痛眩晕、神经性头痛有疗效 2、薰衣草--头痛，失眠，预防感冒，舒缓焦虑紧张的心情 3、野菊花--平肝，明目，用于风热感冒，头昏目眩，目赤肿痛 4、合欢花--宁神作用，主要是治郁结胸闷,失眠,健忘,眼疾，神经衰弱等 5、迷迭香--有助于恢复脑部疲劳，并能增强记忆力，对宿醉、头昏晕眩及紧张性头痛也有良效。兼具有美容功效，可减少皱纹的产生，去除斑纹。 6、柠檬草--具有化痰止咳、理气开胃、治咳喘、腹胀、止泻、祛暑、安胎、滋阴养血、治高血压、头晕等的功效 八、明目去火花草茶搭配大全：
六堡茶营销策划书 院校：广西师范学院师园学院 专业班级：11级国际经济与贸易1班 策划人：朱柳清黄春妮农凯婷 学号：110210211021271102134 任课教师：官锡强教授 二〇一三年十二月十九日
目录 一、什么是六堡茶………………………………………（一）六堡茶的概念………………………………………（二）六堡茶的作用……………………………………… 二、六堡茶的发展历程……………………………………（一）六堡名茶历史悠久………………………………（二）茶排古道西江船帮……………………………… 三、茶叶环境分析—同行业内竞争环境……………… 四、六堡茶的SWOT分析…………………………………（一）优势…………………………………………………（二）劣势…………………………………………………（三）机会…………………………………………………（四）威胁………………………………………………… 五、六堡茶的营销策略……………………………………（一）分销…………………………………………………（二）促销………………………………………………… 六、六堡茶的营销行动方案及风险控制措施……………（一）营销行动方案…………………………………………（二）营销风险控制措施…………………………………… 七、六堡茶的营销预算费用……………………………… 八、发展方向……………………………………………… 九、总结……………………………………………………
参考文献…………………………………………………… 梧州六堡茶营销策划方案 【摘要】随着人们生活水平的提高以及市委市政府近几年的大力扶持与宣传，六堡茶已成为了梧州一张崭新的名片，得到了众多人的喜爱和认可。但与云南普洱茶相比，六堡茶的知名度及销售状况仍存在着不少问题，这也制约了六堡茶产业的发展。因此，根据其存在的问题并提出相对合理的营销策略建议成为本文的主要目标。本文简单介绍六堡茶，然后概括总结六堡茶的销售现状，其次分析总结制约六堡茶产业发展的主要问题，接着对所存在问题提出相应的解决对策，最后总结六堡茶产业的发展方向。 关键词：六堡茶销售现状问题营销策略 一、六堡茶的概念及作用 （一）六堡茶的概念 六堡茶是中国历史名茶，远在唐代已有生产，因其原产于梧州市苍梧县六堡镇而得名，至今已有1500多年历史。六堡茶属黑茶类发酵茶，其外形色泽黑褐光润，叶底红褐色，间有金黄花，汤色红浓，香气陈醇，滋味甘醇爽滑，具有独特的类槟榔香，素以“红、浓、陈、醇“四绝著称。 （二）六堡茶的作用
黑茶的功效与作用 黑茶有很多种，黑茶的功效与作用与作用也各有不同。湖南黑茶著名的是安化黑茶，但是，近些年，随着安化黑茶的兴起，一说黑茶，通常情况下指的就是湖南安化黑茶。 黑茶的功效与作用与作用主要表现在以下四个方面： ①清脂肪，减肥胖：安化黑茶中的多酚类及其氧化产物能溶解脂肪，促进脂类物质排出；还可活化蛋白质激酶，加速脂肪分解，降低体内脂肪的含量。因此安化黑茶被韩国人称为“瘦身茶”；日本人称为“美容茶”；台湾人称为“消食茶”。 ②清肠胃，助消化：安化黑茶富含膳食纤维，具有调理肠胃的功能，清肠胃；且有益生菌参与，能改善肠道微生物环境，助消化。我国民间有利用老黑茶治疗腹胀、痢疾、消化不良的传统。 ③清血管，降三高：安化黑茶中富含茶黄素，能软化血管，有效清除血管壁内的粥样物质，被称为“心血管的清道夫”；茶氨酸有效抑制血压升高，类黄酮物质能使血管壁松弛，增加血管的有效直径，降低血压；茶多糖具有类似胰岛素的作用，降低血糖含量；多酚类及其氧化产物能溶解脂肪，促进血管内脂类物质排出，降低血液中胆固醇的含量。 ④清毒素，护肝肾：安化黑茶中独特的益生菌的功能因子和多酚类氧化物、儿茶素等多种化合物成分，参与人体内新陈代谢，对人体内脏具有特殊的净化功能，吸附体内的有毒物质（酒精、重金属、体内垃圾）排出体外，能深层排毒；又对病菌有抑制作用，保护肝肾。 为什么说黑茶有降“三高”的功效与作用？ 我国著名茶叶专家，湖南农业大学博士生导师、湖南怡清源茶业科研中心专家组教授刘仲华研究发现黑茶对人体健康有利，其主要作用表现为控制血压、血糖、血脂和体重。刘教授还通过模型评价发现，千两茶和茯砖茶对除压、降脂、降血糖有明显效果，对控制人体脂肪和体重非常有帮助，这早已被人们实践所证明；此外，千两茶的提取物对胃癌细胞、肝癌细胞的扩散有抑制作用。刘仲华说：湖南安化黑茶：人类健康的新希望。 粥样物质，被称为心血管的“清道夫”。
甘草大麦茶的功效 可能我们很多中年男性朋友经常过度饮酒使我们自身容易 出现酒精中毒的情况，这时候喝一些甘草大麦茶可以帮助们达到很好的解酒的效果，可以有效的降低酒精对于我们自身带来的伤害，还可以有效地帮助我们缓解容易出现咽喉肿痛的症状，简述一下甘草大麦茶的功效吧。 1.甘草的主要功效有，补脾益气，清热解毒，祛痰止咳，缓急止痛，调和诸药。用于脾胃虚弱，倦怠乏力，心悸气短，咳嗽痰多，脘腹、四肢挛急疼痛，痈肿疮毒，缓解药物毒性、烈性。用于心气虚，心悸怔忡，脉结代，以及脾胃气虚，倦怠乏力等。前者，常与桂枝配伍，如桂枝甘草汤、炙甘草汤。后者，常与党参、白术等同用，如四君子汤、理中丸等。 2.肾上腺皮质激素样作用：甘草浸膏、甘草甜素及甘草次酸对健康人及动物都有促进钠，水潴留的作用;小剂量甘草甜素(每只100ug)能使大鼠胸腺萎缩及肾上腺重量增加，产生糖皮质激 素可的松样作用。大剂量时则糖皮质激素样作用不明显，只呈现盐皮质激素样作用。 3.解毒作用甘草浸膏及甘草甜素对某些药物中毒、食物中毒、
体内代谢产物中毒都有一定的解毒能力。解毒作用的有效成份为甘草甜素，解毒机制为甘草甜素对毒物有吸附作用，甘草甜素水解产物葡萄糖醛酸能与毒物结合，以及甘草甜素有肾上腺皮质激素样作用，增强肝脏的解毒能力等方面因素综合作用的结果。 4.止咳平喘作用甘草次酸有明显的中枢性镇咳作用，大剂量的甘草次酸可使小鼠呼吸抑制。此外甘草甜素、甘草次酸盐尚有抗炎症及抗过敏、抗肝损伤、抗促癌、抗菌、抗艾滋病毒(甘草甜素)作用。 我们可以利用甘草大麦茶的功效为我们自身的生活谋取更大的好处。多喝一些甘草大麦茶还可以有效地帮助我们降低自身容易出现感冒发烧的几率，甘草大麦茶还需有非常不错的活血化瘀，调理肠胃的效果，适合我们日常饮用。
干花饮用说明 花卉的医用，在我国有悠久历史，在药用著作《神农本草经》中记有菊花、辛夷、款冬、旋复花等药用方法。明代医学家李时珍在《本草纲目》中记载了金银花、菊花、红花、合欢花、茉莉花、素馨花等几十种花卉，对各种花的形态、形状、性味、功效、主治等都一一作了说明。花卉为什么是名副其实的“良药”呢？花卉治病的奥秘何在呢？因为花卉能分泌出芳香物质，如柠檬油、百里香油、肉桂油等。这些物质内还有各种醇、醛、酮、酯等物质，具有杀菌和调节中枢神经的作用。近年来国外成立了“香花姻缘”，对患者有神经衰弱、高血压、哮喘和流感的病人进行治疗。 花卉药用的功效按中医理论可以归纳为以下几个方面： 清热利气、活血化瘀、宽中理气、引血止滞、凉血解毒。 1、千日红：清热散风、保肝潜阳、明目止痛、解毒消肿。 2、七彩菊：疏散风热、保肝明目、清热解毒。 3、金银花：清热解毒、凉血止痢、降血降火、消咽利喉。 4、竹叶茶；生津止渴、滋阴清热、消暑解毒、活络利尿无副作用。 5、红花：具有降压、降血脂、改善机体微循环的功能。 6、玉蝴蝶：能清肺热、利咽喉、对慢性支气管炎、咳嗽、咽喉肿痛、 扁桃体炎有很好效果。 7、红雪茶：清心开窍、降低血脂、胆固醇的作用。 8、莲子心：清新定热、活血止血、祛湿清心的功效，对面部色斑、 心火旺盛有良效。 9、百合花：清热、解毒、化痰润肺、清心安神、特别通用阳虚久咳、 痰中带血、虚烦、惊悸、失眠多梦、精神恍惚等效果明显。 10、粉玫瑰：疏肝解郁、健脾降火等功效，还能养颜美容、降脂减肥。 11、牡丹花：调经活血，行经腹痛。 12、杭白菊：生津止渴、清心安神、清热解毒、治一切痛肿恶疮。 13、月季花：活血调经、解毒、消肿、养颜美容 14、茉莉花：理气开郁、辟秽、和中。 15、桂花：化痰散瘀、牙疼、口臭。 16、白雪茶：养肝、疏肝、和胃化痰，调血脂降血压。
一、黑茶产业概况 黑茶作为中国特有的传统茶类，距今已有1700多年的历史。在新疆、西藏、内蒙等边疆地区，素有“宁可三日无食，不可一日无茶”之说，其饮食习惯和地域文化使黑茶成为边疆少数民族的日常必需品。黑茶主要产于湖南、四川、湖北、广西和云南等省（区），产品类型丰富，微生物参与的后发酵过程缔造了其独特的品质风味与保健养生功效。 近年来，黑茶产业转型升级发展迅速，湖南华莱生物、泾渭茯茶、湖北羊楼洞茶业、云南大益、柏联茶业、广西茂圣茶业等企业均建立起现代化茶叶加工生产线，将传统茶叶制作精髓与现代工艺有机结合，突破了黑茶产业的技术发展瓶颈。湖南怡清源茶业推行“化整为零”的产品创新，其“黑玫瑰”、“原叶茯茶”等产品得到了 图1 2009-2013年全国黑茶产量概况
二、六堡茶历史探源 三、六堡茶产业现状 大批消费者的青睐。随着人们对黑茶有益健康的认识与实践不断深入，黑茶产品的收藏价值大幅提高，驱动市场消费。2013年，全国黑茶总产量9.19万吨，占全国茶叶总产量的4.78%，同比增长15.16%，国内销量大幅增长,连同过去年间贮藏的黑茶，其总销量达18.2万吨，涨幅居六大茶类之 六堡茶发源于广西梧州辖区的桂江两岸,其产制历史可追溯到1500多年前，早在清嘉庆年间前后,六堡茶就已作为粤桂等地人祛湿、驱痢和调理肠胃的生活饮品,以其独特的槟榔香味而入选中国名茶之列，并通过六堡茶易锡等贸易方式享誉海内外，涌现出一批六堡茶老字号。清同治版《苍梧县志》记载:“茶产多贤乡六堡,味厚隔宿而不变,茶色香味俱佳”。《广西通志》记载:“六堡茶在苍梧,茶叶出产之盛,以多贤乡之六堡及五堡为最,六堡尤为著名,畅销于穗、佛、港、澳等埠。” 梧州，位于广西东部，与粤、港、澳一水相连，是岭南文化和珠江文化的发祥地，也是近、现代“两广商埠”、“水上门户”，农林资源丰富，多元文化交汇。现今，梧州市的六堡镇及周边地域是六堡茶的最佳种植地区，该区域植被茂盛而水质洁净，气候温暖湿润，酸性红壤，有机 质丰富，生态条件十分优越。特有的地理气候环境所出产的六堡茶外形条索壮重,色泽黑褐油润,内质香气陈纯,具有独特槟榔香味,汤色红浓,滋味醇厚爽口,耐于久藏，素以“红、浓、陈、醇”四绝著称。梧州市作为六堡茶的主要生产、加工和集散地，具有其得天独厚的自然地理优势、人文历史资源优势和品牌优势，生产的六堡茶深受国内外消费者的欢迎，其年产量六堡茶全产区茶叶总产量的95%以上。 首，成为消费热点。 六堡茶产于广西梧州，当地优越的自然环境和丰富的社会资源造就了六堡茶独特的品质特征，在黑茶产业中稳占一席。2013年，六堡茶共生产0.98万吨，占全国黑茶产量的10.7%，发展基础扎实，前景广阔。 1.产销情况 （1）梧州六堡茶生产情况 2013年，国内外黑茶的热销带动了六堡茶产业的发展，梧州市作为六堡茶的主产区，茶园面 积于2013年达6.58万亩，同比增长2600亩，增幅4.11%，此外，在广西自治区内其他地区仍有小量 六堡茶原料种植区域及适制茶叶品种，部分新增
黑茶的功效与作用与作用 黑茶有很多种，黑茶的功效与作用与作用也各有不同。湖南黑茶著名的是安化黑茶，云南黑茶著名的是普洱，四川黑茶著名的是边茶。但是，近些年，随着安化黑茶的兴起，一说黑茶，通常情况下指的就是湖南安化黑茶。 黑茶的功效与作用与作用主要表现在以下四个方面： ①清脂肪，减肥胖：安化黑茶中的多酚类及其氧化产物能溶解脂肪，促进脂类物质排出；还可活化蛋白质激酶，加速脂肪分解，降低体内脂肪的含量。因此安化黑茶被韩国人称为“瘦身茶”；日本人称为“美容茶”；台湾人称为“消食茶”。 ②清肠胃，助消化：安化黑茶富含膳食纤维，具有调理肠胃的功能，清肠胃；且有益生菌参与，能改善肠道微生物环境，助消化。我国民间有利用老黑茶治疗腹胀、痢疾、消化不良的传统。 ③清血管，降三高：安化黑茶中富含茶黄素，能软化血管，有效清除血管壁内的粥样物质，被称为“心血管的清道夫”；茶氨酸有效抑制血压升高，类黄酮物质能使血管壁松弛，增加血管的有效直径，降低血压；茶多糖具有类似胰岛素的作用，降低血糖含量；多酚类及其氧化产物能溶解脂肪，促进血管内脂类物质排出，降低血液中胆固醇的含量。 ④清毒素，护肝肾：安化黑茶中独特的益生菌的功能因子和多酚类氧化物、儿茶素等多种化合物成分，参与人体内新陈代谢，对人体内脏具有特殊的净化功能，吸附体内的有毒物质（酒精、重金属、体内垃圾）排出体外，能深层排毒；又对病菌有抑制作用，保护肝肾。 为什么说黑茶有降“三高”的功效与作用？ 我国著名茶叶专家，湖南农业大学博士生导师、湖南怡清源茶业科研中心专家组教授刘仲华研究发现黑茶对人体健康有利，其主要作用表现为控制血压、血糖、血脂和体重。刘教授还通过模型评价发现，千两茶和茯砖茶对除压、降脂、降血糖有明显效果，对控制人体脂肪和体重非常有帮助，这早已被人们实践所证明；此外，千两茶的提取物对胃癌细胞、肝癌细胞的扩散有抑制作用。刘仲华说：湖南安化黑茶：人类健康的新希望。 为什么黑茶有降血压、降血糖的功效与作用？
喝大麦茶需牢记6个禁忌 大麦茶是中国、日本、韩国等民间广泛流传的传统清凉饮料，把大麦炒制成焦黄，食用前，只需要用热水冲泡就可浸出浓郁的香茶。大麦茶的功效与禁忌有哪些？ 大麦茶的功效 据《本草纲目》记载：“大麦味甘、性平、有去食疗胀、消积进食、平胃止渴、消暑除热、益气调中、宽胸大气、补虚劣、壮血脉、益颜色、实五脏、化谷食之功。治小便淋痛;治麦芒入目;治老人烦渴不止、饮水不定、舌卷干焦;治水气病;夏季清暑热;治急性咽喉炎、扁桃体炎、咽喉部脓肿。大麦面粉可以食用，大麦还可以制成啤酒，帮助消化，疏肝利气，帮助调整肠胃功能的功效。 大麦具有健脾消食、除热止渴、下气利水等功效。大麦茶主要用于消温解毒，健脾减肥，清热解暑，去腥膻，去油腻，助消化，润肤乌发。 大麦茶喝多了拉肚子吗 喝大麦茶是不会腹泻的。大麦茶制作工艺先进，产品优良，不含任何添加剂，具有医疗保健作用。大麦茶属传统饮品，冷饮具有防暑降温之功，热饮具有助消化、解油腻、养胃、暖胃、健胃的作用。长期饮用，能收到养颜、减肥之功效。大麦茶为纯天然、四季皆宜、适宜各种年龄人群的保健饮品。大麦具有健脾消食、除热止渴、下气利水等功效。大麦茶主要用于消温解毒，健脾减肥，清热解暑，去腥膻，去油腻，助消化，润肤乌发。
喝大麦茶需牢记的六点禁忌 禁忌一、胃不好的人不宜饮用 据研究表明，胃不好的人不适合饮用大麦茶，喝了会感觉胃部不适，严重的可能会拉肚子。 禁忌二、空腹不宜喝大麦茶 空腹的时候不能喝茶，这是喝茶的基本常识，大麦茶也一样，空腹的时候不能喝。 禁忌三、孕妇慎饮 怀了宝宝的准妈妈们尽量不要喝大麦茶，因为大麦茶可能会引起孕妇回奶的情况出现。 禁忌四、隔夜的大麦茶不能喝 大麦茶最好是现泡煮现喝，隔夜或者已经过了几天的大麦茶就不要喝了，因为它的茶香和保健功效早已跟随空气远走高飞了。 禁忌五、肝、肾病患者忌喝 习惯性便秘，肝、肾病患者和高血压、心脏病的人都不能饮用大麦茶。 禁忌六、湿热引起的腹胀不能饮用 因湿热或者食积引起的脘闷腹胀患者不能饮用，否者会加重病情。 大麦茶的其他功效 全身美白。家里有浴缸可以把喝过的茶包放进浴缸里，或是直接把茶水倒进浴缸，可以根据个人需要滴入一些精油，例如玫瑰、薰衣
茶叶在传统意义上分为6种：红茶，黄茶，绿茶，白茶，黑茶，青茶。那么不同的茶叶有哪些功效作用呢?一起来了解下。 一、红茶 红茶是在绿茶的基础上经发酵创制而成的。以适宜的茶树新芽叶为原料，经工萎凋、揉捻(切)、发酵、干燥等典型工艺过程精制而成。因其干茶色泽和冲泡的茶汤以红色为主调，故名红茶。 红茶的种类较多，产地较广，按照其加工的方法与出品的茶形，主要可以分为三大类：工夫红茶、小种红茶和红碎茶。 工夫红茶是中国特有的红茶，比如祁门工夫、滇红工夫等等。其工夫两字有双重含义，一是指加工的时候较别种红茶下的工夫更多，二是冲泡的时候要用充裕的时间慢慢品味。 小种红茶是福建省的特产，有正山小种和外山小种之分。正山小种产于1000米以上的高山，如今那里已经实行了原产地保护。正山小种又可分为东方口味和欧洲口味，东方口味讲究的是松烟香，桂圆汤，欧洲口味的松香味则更浓郁，比较适合配薰鱼和薰肉。 红碎茶可是国际茶叶市场的大宗产品，用红碎茶通过机器加工即成国际CTC红茶，这种茶最适合做调味茶、冰红茶和奶茶。 红茶可以帮助胃肠消化、促进食欲，可利尿、消除水肿，并强壮心脏功能。预防疾病方面：红茶的抗菌力强，用红茶漱口可防滤过性病毒引起的感冒，并预防蛀牙与食物中毒，降低血糖值与高血压。美国心脏学会曾经得出红茶是“富含能消除自由基，具有抗酸化作用的黄酮类化合物的饮料之一，能够使心肌梗塞的发病率降低”的结论。 二、黄茶 黄茶是一种与绿茶的加工工艺略有不同的茶，多了一道焖堆渥黄工序。焖堆后，叶已变黄，再经干燥制成，黄茶浸泡后是黄汤黄叶。 黄茶是我国特产。其按鲜叶老嫩又分为黄小茶和黄大茶。如蒙顶黄芽、君山银针、沩山毛尖、平阳黄汤等均属黄小茶;而安徽皖西金寨、霍山、湖北英山所产的一些黄茶则为黄大茶。黄茶的品质特点是“黄叶黄汤”。湖南岳阳为中国黄茶之乡。 黄茶是沤茶，在沤的过程中，会产生大量的消化酶，对脾胃最有好处，消化不良，食欲不振、懒动肥胖、都可饮而化之。而温州黄汤能更好发挥黄茶原茶的功能，温州黄汤更能穿入脂肪细胞，使脂肪细胞在消化酶的作用下恢复代谢功能，将脂肪化除。 黄茶中富含茶多酚、氨基酸、可溶糖、维生素等丰富营养物质，对防治食道癌有明显功效。此外，黄茶鲜叶中天然物质保留有85%以上，而这些物质对防癌、抗癌、杀菌、消炎均有特殊效果，为其他茶叶所不及。 三、绿茶 绿茶，又称不发酵茶。以适宜茶树新梢为原料，经杀青、揉捻、干燥等典型工艺过程制成的茶叶。其干茶色泽和冲泡后的茶汤、叶底以绿色为主调，故名。 绿茶按其干燥和杀青方法的不同，一般分为炒青、烘青、晒青和蒸青绿茶这四种绿茶种类。
六堡茶是广西梧州最具有浓郁地方特色的名茶，喝六堡茶、谈论六堡茶、收藏六堡茶已成为梧州饮茶爱好者追求的新时尚，今天就和大家一起聊聊六堡茶的功效与作用。 六堡茶属于温性茶，除了具有其他茶类所共有的保健作用外，更具有清热润肺、消暑祛湿，明目清心，帮助消化，消滞去积的功效，既可饱食之后助消化，也可空腹饮之清肠胃，六堡茶还具有更强的分解油腻，降低人体类脂肪化合物，胆固醇，三酸甘油脂的功效，长期饮用可以健胃养神，健身减肥。 下面主要简述六堡茶茶叶中主要特质所产生的这些功效与作用。 1、胃兼养胃 六堡茶为碱性食品，它能跟酸发生离子反应，中和胃内过多的胃酸，避免了饥饿时的疼痛。六堡茶中的淀粉可以在胃壁上形成保护膜，它们都具有调和及收敛酸分泌物过多的作用。胃的脾性喜燥恶寒，而六堡茶经过后发酵后，茶性是比较柔和的，因此六堡茶适合胃不太好的人群来喝，对身体无刺激作用。 2、容抗衰老 适量饮茶有化痣润肤健美的功能。茶多酚、维生素C和烟酸能降脂、降血压和改善血管功能，促进血管微循环。茶多酚既能为人清除“氧自由基”，就有效地防止低密度脂蛋白的过氧化，保护了内皮细胞，防止了平
滑肌斑块状增生和动脉粥样硬化，促进新陈代谢，并有维持心脏、血管、肠胃等正常机能的作用。 3、道“清道夫 六堡茶中含有的氨基酸等维生素物质，以及脂多糖和芳香族化合物等都具有调节、促进脂肪代谢的功能，帮助消化肉类食物，并且茶叶中的咖啡碱能兴奋中枢神经，影响全身各器官的生理功能，刺激胃液分泌，消除胃内积食，帮助消化。 4、体防火墙 六堡茶中含有的维生素C、维生素E，特别是茶多酚，具有很强的抗 氧化活性，可以清除人体内的氧自由基，从而起到抗辐射、增强机体免疫力的作用。此外，茶叶中含有胡萝卜素，它在肠壁和肝脏的作用下，可 以转变为维生素A。而维生素A具有滋养眼睛、缓解眼睛疲劳、预防夜盲 症的作用。 5、痢防便秘 茶的止痢作用早就在临床中应用。茶中所含的鞣质有较好的抑菌作用，对痢疾杆菌，葡萄球菌，肺炎球菌都有很好的抑制作用，对皮肤粘膜还有保护作用。越谚有“不喝凉水多喝茶，不拉稀痢不发痧”的说法。茶单宁的收敛作用使得肠管蠕动能力增强，因此具有治疗便秘的效果。 6、湿去瘴气
茶功效—六大茶类主要功效简介 酸性体质容易生病，而弱碱性体质能预防疾病。茶叶是生活中最常见的强碱性食物，与葡萄，海带并称三强碱食物。喝茶有利于调节人体内的酸碱平衡。可是每个人的身体状况都不同，因此需要适量、适度、适合的饮茶。 喝茶一分钟，可以解渴;喝茶一小时，可以身心愉悦;喝茶一个月可以修身养性;喝茶一年，可以健康;喝茶一生，可以长寿。 茶，宜常饮而不宜过量，浓淡要适中。
红茶-----暖胃护心 红茶属于全发酵茶，在发酵工序中，茶多酚被氧化、聚合、缩合，形成红茶色泽和滋味的主要成分茶黄素、茶红索和茶褐素。 茶黄素是红茶中最主要的功能性成分。参考大量医药文献报告，饮用红茶有助调节人体动脉中低密度脂蛋白和高密度脂蛋白的含量，从而降低心血管疾病的发生概率。与其他茶类相比，一般红茶预防心血管疾病的功效较好。从中医的角度来说，红茶性温，有暖胃的作用，虚寒体质者和老年人宜饮性温的红茶。
绿茶----降火防癌 绿茶属于不发酵茶，保留了鲜叶的天然物质，含有的茶多酚、儿茶素、叶绿素、咖啡碱、氨基酸、维生素等营养成分也较多。绿茶中的这些天然营养成份对防衰老、防癌、抗癌、杀菌、消炎等具有特殊效果，而茶素等多酚类化合物被公认为是绿茶中对健康有益。 与其他茶类相比，绿茶的抗癌功效较好。参考多项文献研究，绿茶能降低乳腺、前列腺等多部位肿瘤发生的危险性。从中医的角度来说，绿茶微寒，有助降火，胃寒的人应该少喝，而容易上火、体壮身热的燥热体质者宜饮。
黄茶----人人皆宜 黄茶属于轻发酵茶，按照鲜叶老嫩度通常分为黄芽茶、黄小芽和黄大茶。黄茶的主要品质特点是黄叶黄汤，不仅叶底黄，茶汤黄，干茶也显黄亮，且香气清悦，味厚爽口。 黄茶是沤茶，参考多项文献研究，黄茶在沤的过程中会产生大量的消化酶，对脾胃有好处，消化不良，食欲不振、懒动肥胖、都有益处。与绿茶清凉和红茶温热的性味相比较，黄茶类的性味特征居于两者之间，普通人几乎都适合。
课题：对中国茶文化的初探 课题组：201113107 任务：茶的功效与禁忌 我的内容： 云南普洱茶的功效有如下几点: 1. 防辐射：据广东中山大学何国藩等用普洱茶进行的研究结果表明，饮用2%普洱茶汤可以解除用钴60辐射引起的伤害。 2. 消除肥胖:普洱茶具有强力的消化作用,可以分解和消除脂肪. 3. 冷症:冷症为血液循环不良的结果,同时也是女性常有的症状.普洱茶具有促进血液循环,使身体温暖 的功用,可在茶中放几片干姜,效果更佳 4.便秘:习惯性迟延便秘,因普洱茶内的普洱单宁有收敛作用,可使肠的活动更活泼,普洱茶亦可强力促进胃液分泌,帮助消化及通顺,故在每餐前后都要喝普洱茶,如此便可改善通便,减低便秘所带来的威胁. 5. 清净血液:由于生活品质提升,营养过剩,缺少运动,很容易造成胆固醇在血管壁中积存,引发中风.普洱茶中含有相当于抑制血压升高的安妥明成份,能中和血脂肪.产生净血作用,茶中并含有丰富的叶绿素,根据医学实验报导,叶绿素不但可以阻止体内吸收胆固醇,还能进一步帮助消化胆固醇,若能习惯饮之,能将动物性脂肪排出体外,增加血液良性循环,促进新陈代谢,使人年轻焕发,精力充沛. 6. 解酒:清人赵学敏有云:普洱茶茶香独绝也,醒酒第一,消食化痰,清胃生津,功力尤大也 苦丁茶是什么?苦丁茶(Ilex kudingcha C. J. Tseng)又叫万承茶、一叶青等，顾名思义，“苦”就是指其味甘苦，“丁”就是“一丁点”的意思，苦丁茶的意思就是“有一点苦的茶”。苦丁茶的功效是什么？喝苦丁茶有哪些好处呢？苦丁茶的功效有解酒除腻、清头目，降压降脂等。苦丁茶的功效成有200余种，有苦丁皂甙、氨基酸、维生素C、多酚类、黄酮类、咖啡碱、蛋白质等。苦丁茶怎么喝好?苦丁茶什么时候喝好?苦丁茶具有“药”的特点，单纯以苦丁茶冲泡和将其与其他茶叶(乌龙茶、绿茶、花茶)等混合冲泡均可，冲泡时可与人参、桂元、红栆、枸杞、冰糖等热补药材还可以加强苦丁茶的功效。用开水泡的苦丁茶，茶渣放置3-4天仍然可以冲泡，老叶做成的苦丁茶，其滋味与嫩叶做成的相近，只是耐泡次数稍少些，每次冲泡出的茶味淡些而已。如稍增加茶叶量，饮用口感仍较好。 老年人和婴幼儿
花茶的功效与作用 1，玫瑰花：它清火润喉，具有消斑，除皱，养颜之功效，是花中之王 2：康乃馨：美白皮肤，祛斑除皱 3：红乃梅：消火祛斑，美白润肤，调节内分泌，促进新陈代谢。 4：紫罗兰：清火养颜，滋润皮肤，给皮肤增加水分，增强光泽，防紫外线照射。5：芍药花：养血柔肝，使气血充沛，容颜红润。 6：勿忘我：美容增白，清火明目，特别是对雀斑粉刺有一定的消除作用。 7：杜鹃花：润肤养颜（主治：月经不调等妇科病） 8：熏衣草：祛痘祛斑，去火安神，增白紧肤，修复疤痕 9：玉美人：调养气血，润肤乌发，又能瘦身（贵妃们的专用减肥茶哦！） 10：桃花：女人之花，能美容养颜，又能调节经血，还能减肥瘦身（和玉美人一起减肥效果好！无副作用） 特殊功效花茶 1，玫瑰茄：排毒养颜，开胃健脾，软化血管 2：白雪茶：消除体内垃圾，排除毒素（高血压，高血脂，肥胖者的首选佳品） 3：红雪茶：降血压血脂 4：雪里开花：滋润壮肾 5：胖大海：咽喉肿痛，扁桃体炎，鼻炎都有其独特的功效 6，野生苦丁：口感甘甜，清热解毒，明目肝胆，降血脂血压，是中老年人和男士最喜爱的茶 清香解渴，解暑（消炎解毒），清凉润肺，润咽喉的花茶 1，玉蝴蝶：清肺热利咽喉 2，金莲花：消炎止咳，调理肠胃，帮助消化 3，百合花：去火安神，清凉润肺 上三种搭配，效果更佳 4，玉兰：养颜美白，改善睡眠 5，野菊花：避暑消热，清心明目 上两种搭配，效果更佳 6，人参花：清香解渴，清凉降火，补血补气，健康脑提神 7，绞股兰：是滋补安神，保护肝脏的（是中老年人和男士最喜爱的茶） 8，竹叶青：解渴消暑，解毒利尿（夏日首选） 9，金银花：清火润喉，清热解毒（咽喉肿痛，扁桃体炎） 10，金盏菊：养肝明目，养颜美容，解毒消炎（头晕，胃寒痛等） 11，君白菊：清热解毒，保肝明目（解暑，抗疲劳，软化血管） 12，金黄菊：清热解暑，消肿明目（有效排出毒素，消除体内垃圾） 13，茉莉花：疏肝和胃，理气解郁（月经不调，痢疾，肿毒等） 柠檬－有效分解脂肪，泡茶或柠檬醋对减肥很有帮助 小贴士 1、选购干燥度好的花草茶，水分最好在4%以下，便于保存。 2、自行调配花草茶时，要注意花草的性质，如安眠作用的熏衣草，就不要与可振奋精神的迷迭香一起冲泡。如果不知道各种花的药性，最好单独饮用。 3、若觉得冲泡出来的复方花草茶味道不好，可以放入一两朵干燥的玫瑰花，玫瑰的香气可使整壶茶变得好喝起来，而且玫瑰属于中性，不会跟其他花草茶相冲突。 4、想喝甜甜的花草茶，最好添加蜂蜜，因为蜂蜜同样属于大自然的产物，且与花朵的味道
六大茶各有的养生特长和保健功能 *导读：现如今，人们在注重中药养生方式选择的时候，对于的养生茶，也是在平时最常进行选择的，可见，大家对于养生茶的认可度是很高的。…… 现如今，人们在注重中药养生方式选择的时候，对于的养生茶，也是在平时最常进行选择的，可见，大家对于养生茶的认可度是很高的。中国茶叶形态万千，按照制作方法和茶多酚氧化(发酵)程度的不同，可分为六大类：绿茶(不发酵)、白茶(轻微发酵)、黄茶(轻发酵)、青茶(乌龙茶、半发酵)、黑茶(后发酵)、红茶(全发酵)。 下面为你解读六大茶各有的养生特长和保健功能。 黑茶：御寒降脂 黑茶是我国特有的茶类，种类比较丰富，例如有云南普洱茶、湖南茯砖茶、广西六堡茶、湖北青砖茶以及四川边茶(康砖)等。 现阶段研究表明，普洱茶具有降血糖、降血脂、抗病毒等保健功能;茯砖茶也有很好的消脂去腻作用，降脂减肥功能较强。此外，黑茶有助御寒，适合虚寒体质者引用。 绿茶：降火防癌 我国绿茶生产历史最久，品类最多，如西湖龙井、黄山毛峰、洞庭碧螺春、太平猴魁等。
绿茶具有多种保健功能，包括预防癌症、改善心血管健康、减肥、抵御电离辐射等。此外，绿茶有助降火，胃寒者应少喝，而易上火、体壮身热的燥热体质者宜饮。 青茶：润燥减肥 乌龙茶又名青茶，主要分四类，闽南乌龙(如铁观音)、闽北乌龙(如大红袍)、广东乌龙(如岭头单枞)、台湾乌龙(如冻顶乌龙)。 某些乌龙茶品种中富含甲基化儿茶素成分，具有抗过敏、抗炎、抗氧化、保护肝细胞、降血压等功能。与其他茶类相比，乌龙茶在减肥方面效果较好。此外，乌龙茶能清除体内积热，适合秋天喝。 红茶：暖胃护心 我国红茶产地较广，种类较多，一般分为工夫红茶、小种红茶、红碎茶三大类。 大量医学研究表明，饮用红茶有助调节人体动脉中低密度脂蛋白和高密度脂蛋白的含量，从而降低心血管疾病的发生概率。此外，红茶有暖胃的作用，适合虚寒体质者和老年人饮用。 白茶：抑菌抗辐射 白茶按采摘标准不同可分为白毫银针、白牡丹、贡眉和寿眉。 白茶的化学成分一般与绿茶比较接近。与其他茶类相比，白茶的抗菌效果比较好。此外，白茶也具有较好的抗辐射效果，在美国和欧洲地区白茶提取物被用于脸部护肤品的开发。从中医角
01. 性寒的绿茶。 绿茶（西湖龙井、安吉白茶、洞庭碧螺春、六安瓜片等）性寒，适合体质偏热、胃火旺、精力充沛的人饮用，且汤色透彻，或水清茶绿，或浅黄透绿，天热、心躁之时品饮，给人清凉爽新之感。绿茶有很好的防辐射效果，非常适合常在电脑前工作的人。 禁忌：肝脏病人忌喝，绿茶中咖啡碱经肝脏代谢，饮茶过多影响损害肝功能。孕妇和手术病人不宜喝，绿茶含有一种物质会阻止新生血管生成。胃寒的人不宜喝，以免引起肠胃不适，神经衰弱者和失眠症者临睡前不宜饮茶。 02. 性寒的黄茶。 黄茶（君山银针、蒙顶白芽、霍山黄芽等）性寒，功效也跟绿茶大致相似，不同的是口感，绿茶清爽、黄茶醇厚。 禁忌：黄茶归于轻发酵茶，制造工艺近似绿茶，富含很多的茶碱、茶多酚等成分，能影响胃部的活动，因而胃部不适者不适宜饮用。其次，黄茶中富含鞣酸成分，会影响身体对铁的吸收，因而孕妈妈不适宜饮用黄茶，不然可能形成胎儿缺铁。 03. 性凉的白茶。 白茶（白毫银针、月光白、白牡丹等）性凉，适用人群和绿茶相似，但“绿茶的陈茶是草，白茶的陈茶是宝”，陈放的白茶有去邪扶正的功效。 禁忌：白茶性寒凉，对于胃“热”者可在空腹时适量饮用。胃中性者，随时饮用都无妨，而胃“寒”者则要在饭后饮用。白茶用量，一般每人每天只要5克就足够，老年人更不宜太多。其他茶也是如此，饮多了就会“物极必反”。 04. 性平的青茶。 青茶即乌龙茶（大红袍、武夷水仙、凤凰单从等）性平，适宜人群最广。有不少好的乌龙茶，特别是陈放佳的乌龙茶，会出现令人愉悦的果酸，中医认为酸入肝经，因此有疏肝理气之功，但脾胃有病症者不宜多饮。乌龙茶中的武夷岩茶，更是特点鲜明，味重，“令人释躁平矜，怡情悦性”。凤凰单丛茶香气突出，在通窍理气上尤为明显。 禁忌：忌空腹饮乌龙茶，因为这样很容易出现茶醉的现象，出现类似头晕、心慌、手脚无力等症状。忌睡前饮乌龙茶，这样只会让自己难以入眠。另外，冷了凉掉的乌龙茶最好要加温后饮用，因为冷饮乌龙茶会很容易对胃产生不利。 05. 性温的红茶。 红茶（正山小种、金骏眉、祁门红茶、滇红茶等）性温，适合胃寒、手脚发凉、体弱、年龄偏大者饮用，加牛奶、蜂蜜口味更好。甜入脾经，具有补养气血，补充热能，解除疲劳、调和脾胃有好作用。红茶汤色红艳明亮，情绪低沉之时最宜饮红茶。
茶友们，该收藏的收藏吧 1、铁观音：除具有一般茶叶的保健功能外，还具有抗衰老、抗癌症、抗动脉硬化、防治糖piss病、减肥健美、防治龋齿、清热降火，敌烟醒酒。 2、普洱茶：同时具有清热、消暑、解毒、消食、去肥腻、利水、通便、祛痰、祛风解表、止咳生津、益力气、延年益寿等功效。又由于普洱茶经历了生茶到熟茶的转变过程，其生茶具有祛风解表、清头目等功效，而熟茶又有下气、利水、通便等沉降功效。 3、武夷岩茶：含有多种化学元素和咖啡碱、茶多酚、脂多糖等．其药理性能特别显着．不但能醒心、明目、健神、消愁、止渴、杀菌、去垢、利尿、解暑、醒酒等，还有降压、减肥、抗辐射、防癌、延缓衰老等延年益寿之功效。 4、龙井茶：可以净化血管，预防中风和心脏病 5、碧螺春：属于绿茶具有抗衰老，抗菌，防癌，降血脂，瘦身减脂，防龋齿，清口臭，防癌，美白及防紫外线作用。 6、黄山毛峰：对出尽血液循环、降低胆固醇、增加毛细血管单行，增强血液抗凝性都有一定好处：同事，黄山毛峰对防癌、抗癌还能起到一定的作用。 7、庐山云雾茶：具有六大功效，即降脂、减肥、降压、抗动脉硬化；抑制肿瘤细胞产生；养胃、护胃；健牙护齿；消炎、杀菌、治痢；抗衰老等这样的一些功效。 8、六安瓜片：有利于预防和抑制癌症；有利于心血管疾病的保健治疗；有利于减肥和清理肠道脂肪；有利于清热除燥、排毒养颜。 9、君山银针：具有一般茶类索有的保健功效：兴奋解倦，益思少睡，消食祛痰，解毒止渴，利尿明目，增加营养。还有杀菌、抗氧化、抗衰老、预防癌症的功效。 10、信阳毛尖：不但营养成分含量较高，而且不清心明目、散热解渴、去烦提神、助消化、健脾胃、利尿解毒等功用，作药应用效果较好。11、太平猴魁：防辐射，降血压，防龋齿，清口臭。 12、祁门红茶：可以匡助胃肠消化、促近食欲，可利尿、消除水肿，并强壮心肌功能。 13、菊花茶: 降火,利尿。 14、玫瑰花茶产地: 保加利亚 功效: 美化皮肤,舒解神经。玫瑰花：滋润养颜，护肤美容，活血，保护肝脏，促进血液循环之功能。可治慢性胃炎及肝炎。消除疲劳、有效愈合伤口、分泌失调、腰酸背痛、能调气血。抗病毒，抗衰老，养颜美容，降脂减肥，美白肌肤 适宜搭配: 薄荷、紫罗兰、菩提子、金盏花、迷迭香 冲泡方法: 适量的花茶,用开水冲泡即可.孕妇应避免服用. 15、桂桂香：滋阴补肾，调整机能，调节内分泌，保肝养胃，排毒养颜。 16、熏衣草产地: 南欧、地中海 功效: 净化心绪,舒解压力,松弛神经,帮助入眠，具有镇静、隆压，增强免疫、活化身体技能，香身美体，改善失眠头痛。 适宜搭配: 玫瑰花、金盏花、鼠尾草、洋甘菊、菩提子、紫罗兰、薄荷、茉莉
大麦茶的功效与作用 大麦味甘性平，有平胃止渴，消渴除热，益气调中，宽胸下气，消积进食，补虚劣，壮血脉益颜色，宝五脏化谷食之功；治小便淋痛；治麦芒入目；治老人烦渴不止、饮水不定、舌卷干焦；治水气病；夏季清暑热；治急性咽喉炎、扁桃体炎、咽喉部脓肿。大麦面粉可以食用，大麦还可以制成啤酒，帮助消化，疏肝利气，帮助调整肠胃功能的功效。大麦芽中含有“消化酵素”和维生素等，适用小儿、老人病后胃弱引起的食欲不振。人吃五谷杂粮，粗粮有降血、降血糖的神奇功效。时尚、健康一族都越来越注重自身营养问题，大麦茶含有人体所需的17种微量元素，19种以上氨基酸，富含多种维生素及不饱和脂肪酸、蛋白质和膳食纤维，适应了人们回归自然，追求健康的需求。大麦茶能增进食欲，暖肠胃，许多韩国家庭都以大麦茶代替饮用水。大麦茶在日韩非常流行，韩国家庭大多以大麦茶为主要茶饮，在日本料理店喝大麦茶，用以清除吃生鱼片后口中的异味。中国人冬季讲究进补，饮食往往以鸡鸭鱼肉为主，在大快朵颐后，喝一杯浓浓的大麦茶，不仅可以去油腻，还能促进消化。而且，热腾腾的大麦茶具有养胃、暖胃的作用，适合各种年龄段人群饮用。除此之外，大麦茶还不会弄脏茶具，污染牙齿，长期饮用大麦茶能起到养颜、减肥的效果。散装的大麦茶可以用锅煮着喝，一把大麦茶加上两升水，煮15分钟左右。如果是袋装的大麦茶，用沸水冲泡即可。 大麦茶能增进食欲，暖肠胃，许多韩国家庭都以大麦茶代替饮用水
大麦茶在日本也非常流行，在日本料理店喝大麦茶，用以清除吃生鱼片后口中的异味。 大麦茶被称为：“东方咖啡”。据《本草纲目》记载，大麦味甘性平，有去食消胀、平胃止渴、益气调中、壮血脉、实五脏、化谷食的功效。它不仅能消除排档中大鱼大肉的油腻，其所含的微量元素和膳食纤维，还能很好地促进肠胃功能，起到养胃、护胃的效果。中国人的春节，往往以鸡鸭鱼肉为主，在大快朵颐后，喝一杯浓浓的大麦茶，不仅可以去油腻，还能促进消化。而且，热腾腾的大麦茶具有养胃、暖胃的作用，适合各种年龄段人群饮用。 大麦茶为纯天然。四季皆宜。适宜各种年龄人群的保健饮品。 大麦茶是会回奶的，如果在哺乳期建议不要使用。