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SIRT1对肺癌A549细胞增殖和迁移的影响于娜;陈建明;李晓才;张海涛;汪亚君;伍俊;张佳喜【期刊名称】《广东医学》【年(卷),期】2017(038)001【摘要】目的通过调节肺癌A549细胞中沉默信息调节因子1(SIRT1)的表达,探讨SIRT1对肺癌细胞增殖和转移的影响及其分子机制.方法培养肺癌A549细胞,用重组腺病毒感染A549细胞上调/下调SIRT1的表达;通过MTT实验、克隆形成实验、划痕实验和Transwell迁移实验检测上调/下调SIRT1表达对肺癌A549细胞增殖和转移的影响;干扰SIRT1表达后用Western blot检测SIRT1对肺癌A549细胞中上皮细胞向间质细胞转化(EMT)相关蛋白标记物ZO-1、β-连环蛋白(β-catenin)、Snail和ZEB1表达的影响.结果上调/下调SIRT1表达对肺癌A549细胞增殖无明显影响,但是可以促进/抑制肺癌A549细胞迁移;下调SIRT1表达后EMT相关上皮性标记蛋白ZO-1表达增多,间质性标记蛋白β-catenin、Snail和ZEB1表达减少.结论 SIRT1可能通过影响EMT相关标记蛋白的表达促进肺癌A549细胞迁移.%Objective To investigate the influence of SIRT1 on cell proliferationand migration in A549 cells. Methods lung cancer A549 cells wereculture .The recombinant adenovirus was applied to up -regulate/down-regu-late the expression of SIRT1.MTT assay, colony formation, wound-healing assay and trans -well migration assay were performed to measure multiplication capacity and migration ability .Western Blot assay was performed to detect the influ-ence of down -regulating SIRT1 on the expression of EMT related proteins , including ZO -1, β-catenin, Snail andZEB1.Results After up -regulating/down -regulating the expression of SIRT1, the proliferation rate of A549 cell showed no obvious change , but healing rate and migration ability of A 549 cells wereenhanced/weakened .The level of EMT related epithelial markers ZO -1 was increased, while the level of interstitial markers β-catenin, Snail and ZEB1 were decreased after down -regulating the expression of SIRT1.Conclusion SIRT1 promotes lung cancer cell A549 mi-gration through influencing EMT related proteins .【总页数】7页(P65-71)【作者】于娜;陈建明;李晓才;张海涛;汪亚君;伍俊;张佳喜【作者单位】广东医科大学呼吸疾病研究所广东湛江524001;广东医科大学呼吸疾病研究所广东湛江524001;广东医科大学呼吸疾病研究所广东湛江524001;广东医科大学生物化学与分子生物学教研室广东湛江524023;广东医科大学呼吸疾病研究所广东湛江524001;广东医科大学呼吸疾病研究所广东湛江524001;广东医科大学呼吸疾病研究所广东湛江524001【正文语种】中文【相关文献】1.大黄酸对非小细胞肺癌A549细胞增殖、迁移和侵袭能力的影响及其机制 [J], 和莹莹; 薛金慧; 赵娜2.雌激素受体β拮抗剂对非小细胞肺癌A549细胞增殖、迁移及侵袭能力的影响[J], 信波;张开亮;宋晓鹏;李海波;贾丽;庞海林3.苏芬太尼通过PI3K/Akt信号通路对肺癌A549细胞增殖、凋亡、迁移和侵袭的影响 [J], 杜淑芳;苏智霞;樊肖冲;夏金;王峰4.LncRNA-p21调控Notch信号通路对非小细胞肺癌A549细胞增殖、迁移及侵袭的影响 [J], 张冠磊;马苗苗;兰文静;王琳5.姜黄素联合KLF8-siRNA干扰对肺癌A549细胞增殖、迁移和凋亡的影响及其机制 [J], 谷见法;刘松格;潘琼;闫巧辉因版权原因，仅展示原文概要，查看原文内容请购买。
D-siRNAs抑制A549细胞COX-2表达罗红;胡冬煦;陈平【期刊名称】《基础医学与临床》【年(卷),期】2008(028)007【摘要】目的长片段双链COX-2 RNA(dsRNAs)在体外经Dicer酶消化获得小RNA(D-siRNAs)抑制A549细胞COX-2的表达.方法 (1)IL-1β5 g/L干预A549细胞,Western blot法观察其COX-2蛋白表达的时间依赖性.(2)Trizol法抽提A549细胞总RNA,RT-PGR扩增COX-2基因.(3)设计两端带T7 promoter,SP6 promoter的COX-2 cDNA的PCR引物,通过PCR方法,获得两端带,T7及SP6 promoter的COX-2 DNA.(4)用RiboMAX Large Scale RNA Produc-tion Systems-SP6 and T7试剂盒体外将COX-2 DNA转录为RNA.(5)长片段COX-2 RNA经Dicer酶消化为小RNA(D-siRNAs).(6)用TransMessenger Transfection Reagent将D-siRNAs转染A549细胞.(7)COX-2 mRNA表达用RT-PCR检测,细胞培养上清液中PGE2含量用ELISA测定.结果 (1)IL-1β干预A549细胞9 haCOX-2表达到高峰.(2)在体外,长片段COX-2 dsRNAs经Dicer酶消化获得D-siRNAs.(3)D-siRNAs可有效抑制A549细胞COX-2的表达并降低PGE2的分泌.结论长片段双链COX-2 RNA(dsRNAs)在体外经Dicer酶消化获得小RNA可有效抑制A549细胞COX-2的表达.【总页数】6页(P707-712)【作者】罗红;胡冬煦;陈平【作者单位】中南大学,湘雅二医院呼吸科,湖南,长沙,410011;中南大学,湘雅二医院胸心外科,湖南,长沙,410011;中南大学,湘雅二医院呼吸科,湖南,长沙,410011【正文语种】中文【中图分类】Q256.2【相关文献】1.抑制A549细胞COX-2表达的D-siRNAs的合成 [J], 罗红;胡冬煦;陈平2.COX-2抑制剂对人舌鳞状细胞癌Tca-8113细胞COX-2和Ang-1基因表达的影响 [J], 王晓彦;武云霞3.COX-2选择性抑制剂西乐葆对IL-1β诱导下A549细胞COX-2表达的影响 [J], 罗红;胡冬煦;陈平4.乌索酸通过抑制A549细胞中ERK的激活而抑制COX-2的表达(英文) [J], 王劲松;沈晶;张婷;唐聪;任天年;奚涛5.Cox-2抑制剂对人肺腺癌A549细胞VEGF和Angs基因表达的影响 [J], 邢丽华;张珍祥;徐永健;张惠兰;刘剑波因版权原因，仅展示原文概要，查看原文内容请购买。
SiRNA沉默CDK2和CyclinE对人肺腺A549细胞周期的影响曹银芳;王文灏【期刊名称】《内蒙古医学杂志》【年(卷),期】2017(049)001【摘要】目的探讨小干扰RNA沉默CDK2(cyclin-dependent-kinase2)、CyclinE基因表达对人肺癌细胞株A549细胞增殖、及细胞周期的影响.方法以脂质体Lipofectamine2000将化学合成的CDK2、Cy-clinE siRNA转染人肺癌A549细胞,转染48 h后流式细胞术检测各组细胞凋亡及细胞周期的变化.结果SiRNA基因沉默后CDK2、CyclinE蛋白表达明显下降,与对照组相比,G1期细胞增加,G2/M及S期细胞减少,A549细胞增殖明显受到抑制,凋亡细胞比例增加.结论SiRNA沉默CDK2、CyclinE基因表达能抑制肺癌A549细胞的增殖;并激活细胞凋亡通路,诱导人肺腺癌细胞A549的凋亡.【总页数】3页(P1-3)【作者】曹银芳;王文灏【作者单位】内蒙古自治区人民医院检验科,内蒙古呼和浩特010017;内蒙古自治区人民医院检验科,内蒙古呼和浩特010017【正文语种】中文【中图分类】R734.2【相关文献】1.靶向CDK2、cyclinE的siRNA对HepG2细胞周期及凋亡的影响 [J], 曹银芳;关泽红;刘新风2.siRNA 靶向沉默 Lipocalin-2基因下调 MMP-9表达对降低人肺癌 A549细胞的侵袭、迁移能力的影响 [J], 马小刚;杨晓光;任敬;赵峥3.siRNA靶向沉默人多梳基因2对鼻咽癌细胞增殖及细胞周期的影响 [J], 吴梅;杨丽;再努拉·艾未肉拉;唐亮4.CDK1、CDK2 siRNA干扰对肿瘤细胞凋亡和细胞周期的影响(英文) [J], Hui Xiao Wanjun Gong Jingpeng Cao Xiaolan Li Deding Tao Junbo Hu Jianping Gong5.狗舌草提取物对多发性骨髓瘤U266细胞株细胞周期调控通路蛋白cyclinE和cdk2,p27的影响 [J], 范小莉;马智刚;张晓录;王天;范会兵因版权原因，仅展示原文概要，查看原文内容请购买。
siRNA靶向沉默HIF-1α基因对肺癌A549细胞转移和侵袭的影响冯潇;杨成梁;郑晓丽;翟冲亚;赵慧云;葛红【摘要】目的:探讨质粒介导RNA干扰抑制HIF-1α基因对肺癌A549细胞转移和侵袭能力的影响.方法:利用基因工程方法构建HIF-1α的干扰表达载体,并将其转染至肺腺癌A549细胞;分别用RT-PCR方法、Western blot方法检测细胞转染前后HIF-1d以及MMP-2的mRNA及蛋白表达的变化.细胞划痕试验和Tran-swell实验检测转染前后肺腺癌A549细胞迁移及侵袭能力的改变.结果:转染后脯腺癌A549细胞中HIF-1α和MMP-2的mRNA表达分别下降86％和64％ (P ＜0.05).转染后细胞蛋白表达明显下降.转染前后穿膜细胞数分别为(135.2±13.2)、(63.7±10.5),差异具有统计学意义(P＜0.05).转染前后划痕宽度分别为(0.48±0.14)、(1.04±0.15)mm,差异具有统计学意义(P＜0.05).结论:RNAi可有效抑制HIF-1α的表达,同时可结合MMP-2启动子下调MMP-2基因和蛋白的表达,降低肺癌A549细胞的转移和侵袭能力.【期刊名称】《河南医学研究》【年(卷),期】2014(023)011【总页数】5页(P1-5)【关键词】RNA干扰;乏氧诱导因子;基质金属蛋白酶-2【作者】冯潇;杨成梁;郑晓丽;翟冲亚;赵慧云;葛红【作者单位】郑州大学附属肿瘤医院放疗科河南郑州 450008;郑州大学附属肿瘤医院放疗科河南郑州 450008;郑州大学附属肿瘤医院放疗科河南郑州 450008;郑州大学附属肿瘤医院放疗科河南郑州 450008;郑州大学附属肿瘤医院放疗科河南郑州 450008;郑州大学附属肿瘤医院放疗科河南郑州 450008【正文语种】中文【中图分类】R734.2低氧诱导因子-1α（hypoxia inducible factor-1α，HIF-1α）是调节肿瘤细胞适应低氧的核心转录因子，参与多种基因的转录调控，在肿瘤的血管形成、能量代谢、侵袭转移等方面扮演重要角色，是在低氧环境中起到中枢纽带的重要转录因子［1］，也是参与多种肿瘤转移和侵袭相关的调节通路。
HDAC1 siRNA转染对肺腺癌A549细胞增殖及凋亡的影响顾红军;董宇超;李强【期刊名称】《中国癌症杂志》【年(卷),期】2010(020)008【摘要】背景与目的:多项研究表明组蛋白去乙酰化酶(histone deacetylases,HDACs)抑制剂对人非小细胞肺癌细胞株有抑制增殖和诱导凋亡作用.而HDAC抑制剂对HDAC Ⅰ型和Ⅱ型均有抑制作用,在非小细胞肺癌细胞株中尚未明确HDACs中哪一类受抑制能影响肿瘤生长.本研究通过HDAC1 siRNA转染肺腺癌细胞株A549,观察HDACs中HDAC1对肺腺癌细胞增殖、周期和凋亡的影响,明确HDAC1在肺腺癌细胞生长中的作用.方法:MTT法检测不同时间点HDAC1 si RNA转染对A549细胞体外增殖的影响,流式细胞术检测RNA干扰后细胞周期及凋亡率的变化;Western blot法检测细胞内组蛋白H4乙酰化水平的变化.结果:HDAC1 siRNA转染A549细胞后,HDAC1在转录和表达水平均下降,组蛋白H4乙酰化表达增高.siRNA干扰后A549细胞的体外生长抑制呈时间依赖性,流式细胞术检测结果显示细胞阻滞于G2/M期,细胞凋亡增加.结论:HDAC1 siRNA转染能有效地抑制HDAC1在A549细胞中的表达,增加A549细胞中组蛋白的乙酰化,并影响A549细胞相关生物学行为,抑制肺腺癌细胞的生长,为HDAC1基因治疗应用于肺腺癌奠定了基础.【总页数】5页(P578-582)【作者】顾红军;董宇超;李强【作者单位】解放军第一00医院急诊科,江苏,苏州,215007;第二军医大学附属长海医院呼吸内科,上海,200433;第二军医大学附属长海医院呼吸内科,上海,200433【正文语种】中文【中图分类】R73-362+2【相关文献】1.HDAC1 siRNA转染对肺腺癌NCI-H1299细胞增殖及凋亡的影响 [J], 顾红军;董宇超;袁东;李强2.HDAC1在肺腺癌细胞株A549中的表达及TSA对细胞增殖、凋亡的影响 [J], 黄宏;张珍祥;徐永健;邵静芳3.ECT2-siRNA转染对肺腺癌A549细胞周期分布和凋亡的影响 [J], 吴昊;林庆;徐全;柳阳春;陈立如;尹随4.脂质体转染survivin siRNA对A549细胞增殖及凋亡的影响 [J], 刘永全;江涛;冯燕梅5.消岩汤含药血清介导下Survivin siRNA对人肺腺癌A549细胞增殖及凋亡的影响 [J], 张欣;贾英杰;杨佩颖;张蕴超因版权原因，仅展示原文概要，查看原文内容请购买。
A549细胞来源外泌体对肺上皮BEAS-2B细胞紧密连接蛋白及骨架重塑的影响邓仕华;吴东明;韩蓉;刘腾;张婷;谢洪祥;许颖【期刊名称】《医学研究生学报》【年(卷),期】2017(030)010【摘要】Objective A large number of studies have shown that the exosome is closely related to the occurrence and devel -opment of tumor cells , but the specific mechanism is still unknown .The study was to investigate the effects of A 549-derived exosome on tight junction protein and cytoskeleton remodeling in normal lung epithelial BEAS-2B cells. Methods A549-derived exosome were isolated by ultracentrifugation , the morphology of which was observed by transmission electron microscope .Western blot analysis was used to examine the surface markers of CD 9 and CD63.Immunofluorescence assay, western blot assay and qPCR assay were applied to detect the effects of exosome on tight junction protein ZO-1 and occludin mRNA expression in BEAS-2Bcell.Phalloidin-FITC staining experiment was used to detect the effects of exosome on the cytoskeleton remodeling of BEAS-2B cells.The invasiveness of A549 to BEAS-2B was detected by Transwell invasion test . Results Typical vesicles were observed under electron microscope and exosome markers CD 9 and CD63 expression were detected.The expression levels of ZO-1, occludin pro-tain (P<0.05) and mRNA (P<0.01) weredecreased in exosome-treated BEAS-2B cells, and the cytoskeleton remodelled .Transwell invasion test showed that the number of A 549 cells passing through the microporous membrane (22±4) after exosome treatment BEAS-2B was significantly higher than that of the control group (10.6±4.5) (P<0.05). Conclusion A549-derived exosome can promote the cytoskeleton remodeling of BEAS-2B cells by down-regulating the expression of ZO-1 and occludin in BEAS-2B cells, aiming to de-stroy the barrier of BEAS-2B cell to tumor cell A549.%目的外泌体与肿瘤细胞的发生发展密切相关,但具体机制不详.文中旨在探讨非小细胞肺癌A549细胞来源外泌体对正常肺上皮BEAS-2B细胞紧密连接蛋白及骨架重塑的影响.方法超速离心法提取A549细胞exosome,透射电镜进行形态学观察,Western blot鉴定表面标志物CD9、CD63.实验分实验组和对照组,实验组为BEAS-2B细胞中加入终浓度为50μg/mL的exosome,对照组为BEAS-2B细胞中加入等量的PBS液,通过免疫荧光实验、Western blot实验、qPCR实验检测exosome对BEAS-2B细胞紧密连接蛋白ZO-1和Occludin蛋白及mRNA表达的影响,phalloidin-FITC荧光染色实验检测exosome对BEAS-2B细胞骨架重塑的影响,Transwell侵袭实验检测exosome处理BEAS-2B后对A549细胞侵袭BEAS-2B细胞能力的影响.结果免疫荧光实验表明,与对照组相比,实验组的ZO-1及Occuldin的表达明显减少;Western blot实验也表明exosome处理BEAS-2B后可显著减少ZO-1和Occuldin蛋白的表达(P<0.05).qPCR实验表明,与对照组相比,外泌体处理BEAS-2B后可明显下调紧密连接蛋白ZO-1(1.00±0.00 vs 0.45±0.04)和Occuldin mRNA(1.00±0.00 vs 0.52±0.08)水平,差异有统计学意义(P<0.01).phalloidin-FITC检测结果表明,与对照组相比exosome直接处理后BEAS-2B细胞后F-actin 重聚明显增多.Exosome处理BEAS-2B后A549穿过微孔膜的细胞数量[(22.0±4.0)个]明显高于对照组[(10.6±4.5)个],差异有统计学意义(P<0.05).结论A549细胞来源exosome可通过下调BEAS-2B细胞紧密连接蛋白ZO-1、Occludin的表达,促进BEAS-2B细胞骨架重塑,最终破坏BEAS-2B细胞对肿瘤细胞A549的屏障作用.【总页数】6页(P1035-1040)【作者】邓仕华;吴东明;韩蓉;刘腾;张婷;谢洪祥;许颖【作者单位】610500 成都,成都医学院第一附属医院检验科;610500 成都,成都医学院第一附属医院检验科;610500 成都,成都医学院第一附属医院检验科;610500 成都,成都医学院第一附属医院检验科;610500 成都,成都医学院第一附属医院检验科;610500 成都,成都医学院第一附属医院检验科;610500 成都,成都医学院第一附属医院检验科【正文语种】中文【中图分类】R734.2【相关文献】1.人Müller细胞来源的外泌体对脂多糖刺激视网膜色素上皮细胞产生炎症因子的影响 [J], 章淑杰;张荣;张雪瑾;吴继红2.脂多糖联合三磷酸腺苷对肺上皮细胞来源A549细胞IL-1β分泌的影响及其机制研究 [J], 王美菊;王长征;刘双林;谢姿;胡明冬;李琦;徐瑜3.海藻多糖对仔猪小肠上皮细胞紧密连接蛋白及核转录因子-κB信号通路相关基因表达的影响 [J], 郭晓波;邹田德;杨晋;曾永娣;王自蕊;游金明4.低氧或/和糖皮质激素诱导大鼠肺和A549细胞中脂筏蛋白stomatin的表达及其对细胞骨架的影响 [J], 卢建;陈继承;蔡浩昱;马媛媛;王燕5.呼吸道合胞病毒感染对气道上皮细胞表皮生长因子受体、紧密连接相关蛋白及黏蛋白表达的影响 [J], 刘娟娟;张婷;米芋枚因版权原因，仅展示原文概要，查看原文内容请购买。
新型靶向药物对A549细胞体外抑制作用及其能谱CT成像初步研究詹爽;赵小英;汪琛玮;吴兴旺【期刊名称】《安徽医科大学学报》【年(卷),期】2018(053)006【摘要】目的探讨新型靶向药物对人非小细胞肺癌A549细胞的体外抑制作用及其能谱CT成像能力.方法合成具有靶向A549细胞毒性的靶向药物,使用2.5、5、10、20、40 μmol/L靶向药物及吉非替尼分别体外培养A549细胞,应用四甲基偶氮唑蓝( MTT)比色法检测细胞抑制率.对 0、1.87、3.75、7.5、15、30 mmol/L 靶向药物及吉非替尼进行能谱CT GSI模式扫描,分析两种药物细胞增殖抑制率与CT值差别及靶向药物碘浓度测量值与真实值之间关系.结果靶向药物及吉非替尼可随时间及剂量依赖性地抑制 A549细胞增殖,浓度超过10 μmol/L时,靶向药物抑制率高于吉非替尼(P＜0.05);能谱CT GSI模式扫描,靶向药物CT值及碘浓度值明显高于吉非替尼(P＜0.05);靶向药物碘浓度测量值与真实值之间具有明显相关性( r=0.998).结论新型靶向药物在很好的抑制A549细胞的同时,又具有良好的CT 成像性能;利用能谱CT基物质成像能够准确反映不同浓度溶液的碘含量.%Objective To explore the effects of targeting drug on human non-small cell lung cancer A549 cells in vitro and quantification of iodine with gemstone spectral imaging(GSI). Methods In the first part, synthesis of small iodine-containing drugs with cytotoxicity targeting A549 cells. A549 cells were treated in vitro with targeting drugs and gefitinib at a concentration gradient of 2.5,5,10,20,40 μmol/L. Their proliferation effectswere ana-lyzed by the thiazolyl blue ( MTT) assay. In the second part, targeting drugs and gefitinib at a concentration gradi-ent of0,1.87,3.75,7.5,15,30 mmol/L underwent GE HD750 CT with GSI mode. Analyzing the inhibition rate of two kinds of drug cellproliferation ,comparing the relation and discrepancy between measured iodine concentrations and real iodine concentrations. Results In the first part, Targeting drugs and gefitinib induced a dose-and time-independent growth inhibition by MTT. When the concentration was more than 10μmol/L, the inhibitory r ate of targeting drugs was higher than that of gefitinib (P＜0.05). In the second part, in a certain range of concentration, the CT value and iodine concentration of targeting drugs were significantly higher than that of gefitinib(P＜0.05). The measured concentrations of targeting drugs were obviously correlated to the real concentrations ( r=0.998 ) without significant difference between these two values(P＞0.05). Conclusion The targeting drug has good in-hibitory effect on A549 cells in vitro. The high CT value of targeting drugs is good for CT shows. GSI of spectral CT is a reliable method to quantify iodine of the targeting drugs.【总页数】4页(P943-946)【作者】詹爽;赵小英;汪琛玮;吴兴旺【作者单位】安徽医科大学第一附属医院放射科,合肥 230022;安徽医科大学第一附属医院放射科,合肥 230022;中国科学技术大学生命科学学院,合肥 230026;安徽医科大学第一附属医院放射科,合肥 230022【正文语种】中文【中图分类】R445.3【相关文献】1.雷公藤内酯醇对肺腺癌细胞系A549的体外抑制作用的研究 [J], 吕秀红;郭瑞珍;刁路明;刘铭球2.载紫杉醇PLGA多孔微球的可控制备及其对A549人肺癌细胞体外抑制作用的研究 [J], 张婉莹;左杨;奚菊群3.芦荟大黄素对人肺癌A549细胞的体外抑制作用研究 [J], 曹奇峰4.双氢青蒿素对人肺腺癌A549细胞的体外抑制作用研究 [J], 陈卫强;戚好文;吴昌归5.黄芪多糖在人血γδT细胞体外抑制人肺癌A549细胞增殖作用的研究 [J], 席雪琴; 何愉胜因版权原因，仅展示原文概要，查看原文内容请购买。
紫草素通过上调 Nrf2途径及干预胞内氧化还原平衡稳态诱导A549细胞凋亡谢晨;陈韩英;钟晶;王晓琴;张波【期刊名称】《中国药理学通报》【年(卷),期】2014(000)010【摘要】Aim To investigate the roles of intracellu-lar reactive oxygen species ( ROS ) and Nrf2 pathway in shikonin-induced A549 cell apoptosis. Methods The cytotoxicity was analyzed by MTT assay. The ap-optosis of A549 cells was analyzed by both cellular morphological and biochemical methods. The relative changes of the redox marks ( ROS/GSH) were studied by fluorescence assay in the shikonin-treated A549 cells in accompany with the changes of the intracellular redox homeostasis by GSH/GSSG ratio. ROS inhibitor was also employed in the treatment to find the role of ROS in shikonin-induced A549 cell apoptosis. Real-time PCR analysis and ELISA assay were performed as well to determine the role of Nrf2 pathway in the shiko-nin-induced A549 cell apoptosis. Results The IC50 of shikonin on A549 cells was 3. 2 mg·L-1 . The cellu-lar redox homeostasis shifted toward oxidation signifi-cantly in shikonin treatment in a time-dependent man-ner. The expression of the Nrf2 pathway related genes was up-regulated by shikonin ( 3 . 2 mg · L-1 , 8 h ) . The expression of the anti-apoptotic genes was down-regulated , and proapoptotic genes were up-regulated by shikonin (3. 2 mg·L-1, 24h). Futhermore, the inhi-bition of intracellular ROS alleviated the cytotoxicity of shikonin in A549 cells. Conclusion The critical role of shikonin-induced redox imblance inA549 cell, coped with the secondary produced ROS and Nrf2 path-way antioxidants, result in A549 cell apoptosis.%目的：探讨活性氧和Nrf2途径在紫草素诱导A549细胞凋亡过程中的作用。
硫氧还蛋白在凋亡途径中的作用机制徐涛;于涛【摘要】Thioredoxins are a family of small redox proteins which widely express in many organisms . Mammalian thioredoxin family members include thioredoxin 4 (Trxl), mitochondrial thioredoxin-2 (Trx2 ), containing a conserved -Cys-Gly-Pro-Cys-redox catalytic site. Because of its role in stimulating cancer cell growth and as an inhibitor of apoptosis , thioredoxin offers a target for the development of drugs to prevent cancer .%硫氧还蛋白(Trx)是体内广泛存在的氧化还原蛋白,其家族中两种重要的硫氧还蛋白:硫氧还蛋白1(thioredoxin1,Trx1)和硫氧还蛋白2(thioredoxin2,Trx2)都含有保守的-Cys-Gly-Pro-Cys-还原序列.由于Trx具有调节细胞生长增殖和抗凋亡的作用,因此Trx在凋亡途径中的作用机制就成为了对抗肿瘤的研究热点.【期刊名称】《中国比较医学杂志》【年(卷),期】2012(022)011【总页数】6页(P73-78)【关键词】硫氧还蛋白1;硫氧还蛋白2;凋亡途径【作者】徐涛;于涛【作者单位】东北林业大学盐碱地生物资源环境研究中心/东北油田盐碱植被恢复与重建教育部重点实验室,哈尔滨,150040;东北林业大学盐碱地生物资源环境研究中心/东北油田盐碱植被恢复与重建教育部重点实验室,哈尔滨,150040【正文语种】中文【中图分类】R562.2+5;R332硫氧还蛋白（Trx）是一种小分子蛋白质，它广泛存在于原核和真核生物中。
NOX1 siRNA 对 TNF-α诱导的 A549细胞凋亡的影响夏艳秋;王娜;阙菡雅;徐小艳;薛腾;燕贞;姚武;刘莹;周舫【摘要】目的：探讨NOX1对TNF-α诱导的A549细胞凋亡的影响。
方法：将A549细胞分为3组，空白组、TNF-α组和TNF-α＋NOX1 siRNA组。
TNF-α＋NOX1 siRNA组细胞采用瞬时转染技术转染特异性NOX1 siRNA，转染12 h后用含TNF-α（10μg／L）的培养基继续培养；空白组和TNF-α组细胞分别用培养基和含TNF-α的培养基培养。
48 h后，采用Annexin V-FITC和PI双染法检测细胞凋亡率，DCFH荧光标记法检测细胞中ROS的表达量，Western blot法检测NOX1及p-JNK蛋白的表达水平。
结果：与空白组相比， TNF-α组细胞凋亡率和ROS表达量升高（ P＜0．05），NOX1和p-JNK蛋白表达水平升高（ P＜0．05）；与TNF-α组比较，TNF-α＋NOX1 siRNA组细胞凋亡率和ROS表达量降低（P＜0．05），细胞中NOX1和p-JNK蛋白表达水平也降低（P＜0．05）。
结论：NOX1可能通过增加ROS的表达，进而激活JNK／MAPK信号通路，引起A549细胞的凋亡。
%Aim:To investigate the effect of NOX1 on apoptosis of A549 cells induced by TNF-α.Methods: A549 cells were allocated into 3 groups:blank control group,TNF-αgroup and TNF-α+NOX1 siRNA group.Cells in TNF-α+NOX1 siRNA group wer e transfected with NOX1 siRNA through the transient transfection technology for 12 h,then cultured with TNF-α(10 μg/L) for 48 h.Cells in blank control group and TNF-αgroup were only cultured with medium and TNF-α(10 μg/L) for 48 h,respectively.After culture, the apoptosis rate was detected by Annexin V-FITC and PI staining,the ROS level in cells was detected by DCFH fluorescent probe method, and the expressions of NOX1 and p-JNKprotein were detected through Western blot.Results:Compared with blank control group,the apoptosis rate,ROS level and the expres-sions of NOX1 and p-JNK were increased in TNF-αgroup( P<0.05); while compared with TNF-αgroup, the apoptosis rate,ROS level and the expressions of NOX1 and p-JNK were decreased in TNF-α+NOX1 siRNA group(P<0.05).Con-clusion:NOX1 could increase ROS level, then active JNK/MAPK signal pathway, and induce A549 cell apoptosis.【期刊名称】《郑州大学学报（医学版）》【年(卷),期】2016(051)005【总页数】4页(P591-594)【关键词】A549细胞;NOX1;TNF-α;凋亡【作者】夏艳秋;王娜;阙菡雅;徐小艳;薛腾;燕贞;姚武;刘莹;周舫【作者单位】郑州大学公共卫生学院劳动卫生学教研室郑州450001;郑州大学公共卫生学院劳动卫生学教研室郑州450001;郑州市疾病预防控制中心公共卫生科郑州450000;郑州大学公共卫生学院劳动卫生学教研室郑州450001;郑州大学公共卫生学院劳动卫生学教研室郑州450001;郑州大学公共卫生学院劳动卫生学教研室郑州450001;郑州大学公共卫生学院劳动卫生学教研室郑州450001;郑州大学第一附属医院呼吸内科郑州450052;郑州大学公共卫生学院劳动卫生学教研室郑州450001【正文语种】中文【中图分类】R734.2肺癌是目前中国发病率和死亡率最高的恶性肿瘤[1]。
