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地塞米松片，肾上腺皮质激素药物的适应症。
它主要用于变态反应和自身免疫性炎性疾病，例如结缔组织疾病，严重支气管哮喘，皮炎和其他变态反应性疾病，溃疡性结肠炎，急性白血病，恶性淋巴瘤等。
还用于诊断一些肾上腺皮质疾病-地塞米松抑制试验。
作用：抗炎，免疫抑制，抗过敏，抗休克。
地塞米松是一种激素药物。
它具有抗炎，免疫抑制，抗过敏和抗休克作用。
在临床上，它主要使用一些免疫，自身免疫和过敏性疾病，例如结缔组织病，系统性红斑狼疮，支气管哮喘和器官移植后的抗排斥反应。
因此，地塞米松与其他激素一样，也有一些明显的不良反应。
例如，它可以诱发糖尿病，消化性溃疡，传染病等。
它可以抑制儿童的生长发育，并导致骨质疏松和股骨头坏死。
然后对于孕妇会导致胎儿死亡率上升等。
地塞米松属于糖皮质激素类药物，是一种处方药，长期使用，会引起脸胖，水牛背，向心型肥胖，导致机体抵抗力下降，易被真菌，细菌感染，股骨头坏死等副作用。
泼尼松又叫醋酸泼尼松，又叫醋酸脱氢可的松，又叫醋酸泼尼松，是一种合成激素药物。
指导意见：地塞米松是一种糖皮质激素药物，是消炎和抗过敏药。
它主要用作重大疾病的紧急药物和各种炎症的治疗。
它是最常用的激素药。
强力松片可以抑制儿童的成长，并引起成年人的骨质疏松症。
为了预防由于服用本产品引起的骨质疏松症，可以将钙或钙加维生素D一起服用
总之，这类药物的使用应非常谨慎，特别是因为它具有免疫抑制作用。
因此，绝对不允许某些感染患者，特别是细菌感染，病毒感染或真菌感染的患者使用。
地塞米松的作用与功能主治简介地塞米松（Dexamethasone）是一种合成的肾上腺皮质激素类药物，具有强效的抗炎、抗过敏和免疫抑制作用。
地塞米松可通过改变基因转录和蛋白质合成，调节细胞免疫功能，从而影响多种生理过程。
以下将介绍地塞米松常见的作用与功能主治。
作用与功能主治1.抗炎作用–地塞米松能够抑制炎症反应，降低炎症介质的产生，减少红肿、疼痛和组织损伤。
–适用于各种炎症性疾病，如关节炎、肠炎、过敏性皮炎等。
2.免疫抑制作用–地塞米松可以抑制免疫系统的过度反应，减少自身免疫性疾病的症状。
–适用于多种自身免疫性疾病，如系统性红斑狼疮、类风湿关节炎等。
3.抗过敏作用–地塞米松能够抑制过敏反应，减少过敏介质的释放，缓解过敏症状。
–适用于过敏性鼻炎、过敏性骨关节炎等过敏性疾病。
4.抗肿瘤作用–地塞米松在某些肿瘤治疗中可用作辅助药物，能够抑制肿瘤的生长和扩散。
–可用于多种肿瘤的治疗，如白血病、淋巴瘤等。
5.其他功能主治–地塞米松还可用于一些特殊情况下的治疗，如脑水肿、哮喘等。
注意事项•使用地塞米松应按照医生的建议和处方使用，剂量和使用时间需遵循医嘱。
•长期大量使用地塞米松可能会导致肾上腺功能减退等副作用，应定期监测肾上腺功能。
•使用地塞米松时需注意与其他药物的相互作用，以避免不良反应的发生。
•孕妇、哺乳期妇女和儿童等特殊人群需特别注意使用地塞米松的安全性和剂量。
总结地塞米松作为一种合成的肾上腺皮质激素类药物，具有强效的抗炎、抗过敏和免疫抑制作用。
它在各种炎症性疾病、自身免疫性疾病、过敏疾病和一些特殊情况下的治疗中起到重要作用。
在使用地塞米松时，应根据医生的指导和处方正确使用，遵守注意事项，以确保药物的有效性和安全性。
地塞米松 (Dexamethasone)使用说明书地塞米松 (Dexamethasone)使用说明书地塞米松是一种广泛应用于医学领域的糖皮质激素类药物。
它具有抗炎、抗过敏和免疫抑制等作用，可用于治疗多种疾病，并可根据医生的指示依据具体情况使用。
本说明书将为您提供地塞米松的使用方法、适应症、副作用以及禁忌症等相关信息，以确保您正确、安全地使用该药物。
一、药物名称及成分药物名称：地塞米松药物成分：地塞米松酮（Dexamethasone）二、适应症与用途1. 抗炎用途：地塞米松可用于治疗多种炎症性疾病，如关节炎、过敏性皮炎等。
2. 免疫抑制用途：地塞米松常用于移植手术后预防和治疗排斥反应。
3. 器官疾病治疗：地塞米松可用于治疗某些特定器官的疾病，如眼部炎症等。
4. 肿瘤治疗：地塞米松在化疗方案中常用于减轻治疗引起的副作用。
三、使用方法与剂量请在使用地塞米松前咨询医生并确保了解正确的使用方法和剂量。
四、用药注意事项1. 遵医嘱使用：请在医生指导下使用地塞米松，并按照医生建议的剂量和用法使用。
2. 长期使用的限制：长期使用地塞米松可能导致潜在的副作用和并发症，请定期咨询医生并监测相关指标是否正常。
3. 不宜突然停药：地塞米松使用一段时间后应逐渐停药，突然停药可能引发反跳性反应，请在医生的指导下进行调整。
4. 禁忌症：对地塞米松过敏的患者禁止使用。
在患有真菌感染、结核病等感染性疾病的患者中，地塞米松的使用应特别小心，并遵循医生的指导。
五、副作用地塞米松在使用过程中可能引起以下副作用，请在使用过程中关注：1. 免疫系统：使用地塞米松可能导致免疫系统功能下降，容易感染。
2. 消化系统：地塞米松可能引起胃溃疡、消化道出血等消化系统问题。
3. 内分泌系统：地塞米松长期使用可能导致肾上腺皮质功能受抑制，可能引起激素依赖。
4. 心血管系统：地塞米松可能增加患高血压、心脏病等心血管疾病的风险。
5. 其他常见副作用：还包括体重增加、骨质疏松等。
地塞米松片的作用与功效
概述：
1.地塞米松片是常见的激素类药物，主要用于各种原因导致的过敏，过敏性疾病，比如过敏性皮炎，过敏性鼻炎，自身免疫性疾病，皮肌炎，急性白血病，炎症疾病，应用范围非常广，也可以用于支气管哮喘，肾病综合征等的治疗。
2.地塞米松属于片剂的药物，每片0.75毫克，一般用法是口服。
成人一般开始剂量是0.75-3毫克，一日二到四次，一日0.75毫克。
儿童严格遵医嘱口服。
注意事项：
1.由于地塞米松片能够引起胃肠道的反应，所以有消化道溃疡的病人，比如胃炎，胃溃疡，十二指肠炎，十二指肠溃疡的病人，避免使用。
2.大剂量使用地塞米松，能够引起糖尿病，所以糖尿病病人禁止使用。
3.对地塞米松过敏者，避免使用，过敏体质的人慎用。
4.有心梗的病人，或者换肾手术，心脏搭桥手术的病人，青光眼的病人，精神异常的病人，避免使用地塞米松。
5.有脑血栓，静脉血栓的病人，避免使用，有肺结核，肠结核的病人，或者是急性细菌性痢疾，肠炎的病人避免使用。
常识：
1.地塞米松的口服剂量，服用时间长短，以及减量等，必须在专业医生的指导下，严格遵照医嘱进行。
2.孕妇避免使用，哺乳期妇女，避免使用。
儿童慎用。
3.由于长期服用地塞米松会导致高血压，或者是骨质疏松，所以有高血压的病人，避免使用，更年期女性，避免使用。
功能主治（注：使用过量会快速长胖和出现局部红血丝。
）
与其他糖皮质激素相同。
由于本品的抗炎和抗过敏作用比强的松和强的松龙更强，而理盐作用较弱，作用亦较持久，其磷酸钠盐可静脉注射和点滴，故常用于危重病人的抢救，如严重的休克、过敏、脑水肿等。
地塞米松的功能主治是什么概述地塞米松（Dexamethasone）是一种合成的糖皮质激素类药物，常用于医学领域。
地塞米松具有广泛的功能主治，被广泛应用于多个疾病的治疗过程中。
本文将介绍地塞米松的功能主治以及应用领域。
功能主治地塞米松具有以下常见的功能主治：1.抗炎作用：地塞米松通过抑制炎症反应中的炎症细胞的释放，如抑制白细胞的活性、减少炎症介质的释放等，从而达到抗炎作用。
地塞米松可用于治疗多种炎症性疾病，如过敏性疾病、关节炎等。
2.免疫抑制作用：地塞米松可以抑制免疫系统的反应，抑制多种炎症性细胞的活性，从而减少免疫系统的活性。
地塞米松可以用于治疗自身免疫性疾病，如系统性红斑狼疮等。
3.抗过敏作用：地塞米松具有一定的抗过敏作用，可以减少过敏反应的发生，缓解过敏症状。
地塞米松可用于治疗过敏性鼻炎、过敏性皮炎等过敏疾病。
4.抗肿瘤作用：地塞米松可以抑制肿瘤细胞的生长和扩散，减少白细胞的活性，从而发挥抗肿瘤作用。
地塞米松可以作为辅助治疗药物用于化疗后的恢复期，减轻化疗引起的不良反应。
5.治疗肾上腺皮质功能减退症：地塞米松可替代和补充肾上腺皮质激素，治疗肾上腺皮质功能减退症引起的症状和并发症。
应用领域地塞米松广泛应用于以下几个领域的疾病治疗中：1.皮肤科：地塞米松可用于治疗多种皮肤病，如湿疹、银屑病等。
2.消化科：地塞米松可以用于治疗消化系统炎症性疾病，如克隆氏病、溃疡性结肠炎等。
3.呼吸科：地塞米松可用于治疗哮喘、支气管炎等呼吸系统炎症性疾病。
4.风湿免疫科：地塞米松可用于治疗风湿免疫性疾病，如系统性红斑狼疮、类风湿关节炎等。
5.肿瘤科：地塞米松作为辅助治疗药物，可用于减轻化疗引起的不良反应。
使用注意事项在使用地塞米松时，需要注意以下事项：1.严格按照医生的指导和剂量使用地塞米松。
2.长期使用地塞米松应遵循逐渐减量的原则，避免突然停药引起的反应。
3.长期使用地塞米松可能会引起一系列的副作用，如水肿、血糖升高等，需密切监测。
地塞米松又名氟美松、氟甲强地松龙、德沙美松，是糖皮质类激素。
其衍生物有氢化可地松、泼尼松等，其药理作用主要是抗炎、抗毒、抗过敏、抗风湿，临床使用较广泛。
一、地塞米松的作用1、抗炎作用地塞米松能够抑制嗜中性粒细胞向炎症部位的积聚，稳定溶酶体膜，收缩血管，降低血管的通透性，阻止溶酶体酶及炎症化学中介物质的合成和释放，增强细胞基质对粘多糖酸酶的抵抗力，抑制结缔组织的成纤维细胞增生和纤给细胞合成等达到抗炎作用。
如用地塞米松治疗乳房炎、关节炎、腱鞘炎、粘液囊炎，各种眼炎（结膜炎、角膜炎、虹膜睫状体炎、周期性眼炎），肌肉、关节风湿病的急性期效果较好。
2、抗毒作用地塞米松能够保持细胞膜的完整性和降低细胞膜的通透性从而使细菌内毒素不易透入经胞内，起到保护机体的作用，因而地塞米松治疗严重的败血症、中毒性菌痢、中毒性肺炎、腹膜炎、产后急性子宫炎等，具有良好效果。
3、抗过敏作用地塞米松能够减少血液循环的T淋巴细胞、单核细胞、嗜酸性细胞，抑制巨噬细胞对抗原的摄联和处理，促使蛋白质异化，抑制蛋白质合成，影响抗体合成，达到抗过敏作用。
因而用地塞米松治疗过敏性疾病，如荨麻诊、支气管哮喘、光过敏、急性蹄叶炎、过敏性皮炎、过敏性湿疹等效果较好。
4、抗体克作用地塞米松能够稳定机体的溶酶体膜，阻止溶酶体的释放，降低外周血管阻力，改善微循环阻滞，增加回心血量。
因而用地塞米松治疗过敏性休克、创伤性休克、中毒性休克、心源性休克、低血容量休克等可起到良好作用。
5、对物质的代谢作用地塞米松可增强肝糖源异生作用，同时还能与胰岛素的作用拮抗，抑制葡萄糖氧化，使糖的利用率下降。
因此用地塞米松治疗牛的酮血症和马、驴、羊妊娠毒血症有显著疗效。
二、应用时应注意的问题1、地塞米松对炎症的治疗属非特异性作用，只能减轻或抑制炎症的表现，不能根本治疗，同时地塞米松还能降低机体的抗感染能力。
因此，在治疗危及畜禽生命的感染性疾病时必须与足量有效地与抗菌药物同时配合应用；2、地塞米松不能用于无有效抗菌药物治疗的病毒、霉菌、耐药菌株感染以及外毒素所引起的疾病；3、地塞米松可使机体蛋白质异生和抑制蛋白质合成而影响抗体生成，影响疫苗免疫效价，降低免疫效果或引起免疫失败。
地塞米松的作用与功效地塞米松（Dexamethasone）是一种合成的肾上腺皮质激素，可用于治疗多种炎症、免疫性疾病和其他一些疾病。
它具有很强的抗炎和抗过敏的作用，可用于控制炎症反应，并减轻相关症状。
此外，地塞米松还可以用于抑制免疫系统的功能，以预防移植排斥反应，并治疗某些免疫相关的疾病。
1. 地塞米松的作用机制地塞米松是通过与细胞核内的受体结合来发挥其作用的。
一旦与受体结合，地塞米松能够改变基因的转录和翻译过程，进而影响细胞的功能和代谢。
地塞米松主要通过以下机制发挥作用：- 抑制炎症反应：地塞米松能够抑制炎症介质的合成和释放，如白细胞介素（IL）和肿瘤坏死因子（TNF）。
它通过抑制炎症细胞的活性，减少炎性细胞浸润和炎症反应。
- 抗过敏作用：地塞米松可以通过抑制过敏反应的终末效应来减轻过敏症状。
它能够阻断过敏原诱导的炎症反应，减少过敏介质的释放，如组胺、白细胞介素等。
- 抑制免疫功能：地塞米松还可以抑制免疫系统的功能，减少免疫细胞的活性。
它可以抑制T细胞的增殖和活化，减少巨噬细胞的吞噬功能，抑制免疫球蛋白的合成和释放等。
2. 地塞米松的疾病治疗应用地塞米松可用于多种疾病和症状的治疗。
以下是一些常见的应用领域：2.1 炎症性疾病地塞米松是一种强效的抗炎药物，可用于控制各种炎症反应。
它可以用于治疗类风湿关节炎、系统性红斑狼疮、结节病、类风湿性肺炎等自身免疫性疾病。
通过减少炎症细胞的浸润和活性，地塞米松可以减轻患者的疼痛、肿胀和其他相关症状。
2.2 过敏性疾病地塞米松可用于治疗各种过敏性疾病，如过敏性鼻炎、皮肤过敏等。
它可以减少过敏反应导致的炎症和组织损伤，从而缓解患者的过敏症状，如鼻塞、流涕、瘙痒、皮疹等。
2.3 器官移植术后抗排斥治疗地塞米松可用于术后抗排斥治疗，预防器官移植后的排斥反应。
它通过抑制免疫系统的功能，减少移植器官的免疫排斥，提高移植存活率。
通常与其他免疫抑制剂联合应用，以达到最佳的治疗效果。
药理作用地塞米松又名氟美松、氟甲强的松龙、德沙美松,是糖皮质类激素.其衍生物有氢化可地松、泼尼松等,其药理作用主要是抗炎、抗毒、抗过敏、抗风湿,临床使用较广泛.极易自消化道吸收,其血浆T1/2为190分钟,组织T1/2为3日，肌注地塞米松磷酸钠或地塞米松醋酸酯后分别于1小时和8小时达血药浓度峰值.该品血浆蛋白结合率较其他皮质激素类药物为低.该品0.75mg的抗炎活性相当于5mg泼尼松龙.肾上腺皮质激素类药,抗炎、抗过敏和抗毒作用较泼尼松更强,水钠潴留和促进排钾作用很轻,可肌注或静滴对垂体-肾上腺抑制作用较强.1.抗炎作用：本产品可减轻和预防组织对炎症的反响,从而减轻炎症的表现.激素抑制炎症细胞,包括巨噬细胞和白细胞在炎症部位的集聚,并抑制吞噬作用、溶酶体酶的释放以及炎症化学中介物的合成和释放.2.免疫抑制作用：包括预防或抑制细胞介导的免疫反响，延迟性的过敏反响,减少T淋巴细胞、单核细胞、嗜酸性细胞的数目，降低免疫球蛋白与细胞外表受体的结合水平,并抑制白介素的合成与释放，从而降低T淋巴细胞向淋巴母细胞转化,并减轻原发免疫反响的扩展.可降低免疫复合物通过基底膜,并能减少补体成份及免疫球蛋白的浓度.该品极易自消化道吸收,其血浆T1/2为190分钟,组织T1/2为3日，肌注地塞米松磷酸钠或地塞米松醋酸酯后分别于1小时和8小时达血药浓度峰值.该品血浆蛋白结合率较其他皮质激素类药物低，该品0.75mg的抗炎活性相当于5mg泼尼松龙.药代动力学地塞米松易自消化道吸收,也可经皮吸收,肌内注射地塞米松磷酸磷酸钠或醋酸地塞米地塞米松后分别于Ih和8h后到达血浓度峰值.血浆蛋白结合率低于其他皮质激素类药物,约为77%,易于透过胎盘而几乎未灭活.地塞米松生物半衰期约190min,组织半衰期约为3天,65%以上的药物在24h内从尿液中排出主要为非活性代谢产物⑸??.适应症1.可兴奋腺昔酸环化酶，抑制磷酸二酯酶，增高CAMP水平，从而提升支气管。
地塞米松本词条未列出任何参考资料，内容可能缺乏依据。
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欢迎您协助编辑改善该词条。
科技名词定义中文名称：地塞米松英文名称：dexamethasone定义：肾上腺皮质激素类药。
具有抗炎、抗过敏、抗风湿、免疫抑制作用，主要用于治疗严重细菌感染和严重过敏性疾病、各种血小板减少性紫癜、粒细胞减少症、严重皮肤病、器官移植的免疫排斥反应、肿瘤治疗及对糖皮质激素敏感的眼部炎症等。
应用学科：免疫学（一级学科）；应用免疫（二级学科）；免疫治疗（二级学科）以上内容由全国科学技术名词审定委员会审定公布求助编辑百科名片地塞米松，又叫德沙美松、氟甲强的松龙是抗炎、抗过敏药物。
主要作为危重疾病的急救用药和各类炎症的治疗。
目录基本信息药品简介历史药理作用不良反应：禁忌注意事项药代动力学实验室测定方法药物相互作用适应症剂量及用法不良反应来源及前景使用注意配伍禁忌相关数据制备方法展开基本信息药品简介历史药理作用不良反应：禁忌注意事项药代动力学实验室测定方法药物相互作用适应症剂量及用法不良反应来源及前景使用注意配伍禁忌相关数据制备方法展开编辑本段基本信息药品名称：地塞米松英文名：dexamethasone异名：德沙美松；氟甲强的松龙；氟甲去氢氢化可的松；甲氟烯索，地塞米松，Acidocont,Deronil,Dexacortal,dexametona,Flumeprednisolon等。
化学名：（11β，16α）-9-Fluoro-11,17,21-trihydroxy-16-methylpregna-1,4-diene-3,20-dione制造专利：US pat 3,007,923(1961 to Lab.Franc.Chimiother.),Ger pat 1,113,690(1961 to Merck & Co.),Brit Pat 869,511 (to Upjohn）。
CAS号：50-02-2分子式：C22H29FO5分子量：392.5编辑本段药品简介地塞米松（图2)地塞米松又名氟美松、氟甲强地松龙、德沙美松，是糖皮质类激素。
ORIGINAL ARTICLEPrenatal stress programs lipid metabolism enhancing cardiovascular risk in the female F1,F2,and F3generation in the primate model common marmoset(Callithrix jacchus)Ulrike Buchwald1,2,Daniel Teupser2,3,Friederike Kuehnel1,2,Jana Grohmann1,Nancy Schmieder1, Nicola Beindorff4,Christina Schlumbohm5,Herbert Fuhrmann1&Almuth Einspanier1,21Institute of Physiological Chemistry,Veterinary Faculty,University of Leipzig,Leipzig,Germany2LIFE–Leipzig Research Center for Civilization Diseases,University of Leipzig,Leipzig,Germany3Institute of Laboratory Medicine,Clinical Chemistry and Molecular Diagnostics,University Hospital Leipzig,Leipzig,Germany4Department of Reproductive Biology,German Primate Center,Go¨ttingen,Germany5Clinical Neurobiology Laboratory,German Primate Center,Go¨ttingen,GermanyIntroductionNearly every third death in the world is caused by cardiovascular diseases,atherosclerosis being the main pathological process leading to coronary,cere-bral,and peripheral artery disease[56].Causal factors are manifold,including on the one hand such with a significant genetic component,such as athero-genetic imbalances in lipid metabolism,obesity or elevated blood pressure,and on the other hand sev-eral environmental factors,starting already in fetal development[36].As many other diseases occurring in adult life,car-diovascular ones are strongly supposed to date back to an adverse intrauterine environment.This phenom-enon–called prenatal programming or imprinting–describes alterations of gene expression and epigenetic modifications during fetal development,which lead toKeywordsatherosclerosis–cholesterol–dexamethasone–fatty acid–glucocorticoid –high-density lipoprotein–imprinting–lipoprotein–low-density lipoprotein–triglycerideCorrespondenceUlrike Buchwald and Almuth Einspanier, Institute of Physiological Chemistry, Veterinary Faculty,University of Leipzig,An den Tierkliniken1,04103Leipzig,Germany. Tel.:+493419738102;fax:+493419738119;e-mails:buchwald@vmf.uni-leipzig.de; einspanier@vmf.uni-leipzig.deAccepted May8,2012AbstractBackground Many human diseases are modulated by intrauterine environ-ment,which is called prenatal programming.This study investigated effects of prenatal glucocorticoids on the lipid metabolism of threefilial genera-tions of common marmosets.Methods Pregnant primates were treated with dexamethasone during preg-nancy.Body weight and blood lipid parameters of adult female offspring (F1:n=5,F2:n=6,F3:n=3)were compared with age-related female controls(n=12).Results F1,F2,and F3offspring showed significantly lower percentage of plasma n3fatty acids than controls.F2and F3presented higher cholesterol levels,with significantly more LDL cholesterol,significantly less HDL tri-glycerides and an enhanced cholesterol/HDL cholesterol ratio.Body weight was not significantly affected.Conclusions Prenatal dexamethasone led to higher amounts of cardiovas-cular risk factors and less protective parameters in female F1–F3offspring. The intergenerational consequences suggest prenatal programming through epigenetic effects.J Med Primatol doi:10.1111/j.1600-0684.2012.00551.xan altered phenotype with consequences throughout whole life[23,44]and maybe even heritable effects on further generations[16,17].The different direct and indirect pathways of this process can be ascribed to an overexposure of the fetus to glucocorticoids[23, 43,44].Therefore,the aim of this study was to analyze whether prenatal stress hormones influence the lipid metabolism of the F1offspring and following genera-tions F2and F3during their lifespan.There are various studies investigating the outcome of prenatal influences,mainly in rodents[e.g.,45,55] and sheep[e.g.,14,28].Owing to many physiologic dif-ferences,transmitting research results of these species to humans is problematical[19].Human studies are available,but mostly either confine to natural stressors like anxiety[e.g.,7],or are follow-up observations after glucocorticoid treatment because of different indica-tions during pregnancy[e.g.,13,24,57],so standardiza-tion and comparability are naturally limited[12].This study investigated effects of prenatal stress in a primate model,the common marmoset(Callithrix jac-chus).This New World monkey offers the chance to study a species,closely related to humans,under stan-dardized conditions.Owing to its fast reproduction and rather short generation intervals,long-term studies over several generations can be realized easily[19]. Thus,the common marmoset is widely used as animal model for various human illnesses such as Parkinson’s disease[22],multiple sclerosis[50],stroke[37],osteo-porosis[2],and endometriosis[18].As a model for the analyses of lipid metabolism,it has been described as most suitable already in1979[10]and since has been proving itself[11].Dexamethasone was used as stressor,which is well established for the studies of prenatal programming in different animal models,including primates[15,39].In human pregnancies,it is used as medicine for different reasons[54].Owing to the suggestion,that prenatal programming may have gender-specific effects[29,40,41],female offspring was focussed.Materials and methodsAnimalsHousingThe common marmosets were housed under stan-dardized conditions at the Institute of Physiological Chemistry,University of Leipzig,Germany.Each of the females lived together with a male partner.Their rooms had a temperature of23–25°C,a relative humidity of40–60%,12hours of light and12hours of darkness every day.Each couple lived in a stain-less steel cage,enriched with intermediate levels, sleeping boxes,wood shavings as litter,branches and toys.FeedingThe standardized diet for all monkeys based on ssniffÒMar pellets(ssniffÒSpezialdia ten GmbH,Soest,Ger-many)ad libitum.Additionally,they received a special mash,consisting of ssniffÒMar powder,water,milk, natural yoghurt,banana juice and a probiotic suspen-sion in the morning.For lunch,the couples received a small amount of fresh or boiled food,which varied daily between fruits,vegetables,potatoes,rice,noodles, eggs,and chicken breast meat.Dexamethasone treatmentIn a previous experiment at the German Primate Cen-ter(Go ttingen,Germany),pregnant common marmo-sets have been being treated with dexamethasone (Dexamethason,JenapharmÒ,Jena,Germany)orally at a dosage of5mg/kg once daily for1week during pregnancy,either at the end of thefirst(42nd to48th day,embryonic phase)or second trimester(90th to 96th day,fetal phase)of gestation[4,20].The indi-vidual dosage of tablets was dissolved in0.2ml tap water and mixed with a jelly containing vitamins (Nutri-CalÒ;Albrecht,Aulendorf,Germany).This mixture was taken voluntarily by all the experimental animals.Test groupsSeveral daughters of those mothers treated with dexa-methasone moved to the Institute of Physiological Chemistry(Leipzig,Germany)and became the test group DEX F1(n=5).They produced two further generations without receiving glucocorticoids iatrogeni-cally again.Only the female offspring was chosen for the next two groups:DEX F2(n=6)and DEX F3 (n=3).These test groups were compared with control animals,who themselves and whose ancestors as well never had received dexamethasone.Because of the dif-ferent age of the three generations,two age-related control groups were formed:CONTROL OLD (n=8)and CONTROL YOUNG(n=4).DEX F1 (born in2004)was always compared with CONTROL OLD(born between2002and2005),while DEX F2 (born between2006and2008)and DEX F3(born in 2008)were each compared with CONTROL YOUNG (born in2008).Prenatal stress programs lipid metabolism Buchwald et al.ApprovalAll animals were cared for and used humanely.The experiment as well as the husbandry were approved by the Regional Council Leipzig,Saxony,Germany, according to European and national laws and guide-lines.Data collectionFasting blood collection was carried out in the morning after14hours without any food.Therefore,1ml blood samples of the femoral vein were taken using a heparin-ized syringe and a26-Gauge(0.45mm)wide needle. After centrifugation(4000rounds per minute,4°C, 20minutes),the plasma was investigated immediately. Plasma lipids and lipoproteins were determined either by sequential ultracentrifugation,followed by enzymatic determination of cholesterol and triglyce-rides in the isolated lipoprotein fractions(MU)or by direct assay on a Roche Modular Autoanalyzer(Roche Diagnostics GmbH,Mannheim,Germany)(MD).MU was performed using an ultracentrifuge L80XP Bio-SafeÒ(Beckman Coulter GmbH,Krefeld,Germany) with the rotor type42.2Ti.Enzymatic determination of the isolated lipoproteins was performed with the aid of an absorption plate reader SpectraFlour(Tecan Group Ltd.,Ma nnedorf,Switzerland).Measured parameters and their methods are shown in Table1. Furthermore,the plasma samples were analyzed for fatty acids by gas chromatography as described else-where[26],using a GC Varian CP-3800(Varian Medi-cal Systems Inc.,Palo Alto,USA)with the column Omegawax TM320(Sigma-Aldrich Chemie GmbH, Steinheim,Germany).In total,44fatty acids were determined.The sums each of n3,n6,n7,n9,and satu-rated fatty acid concentrations as well as their mole percentages(mol%)of total fatty acids were calculated.Additionally,the animals were weighed weekly.Statistical analysisThe Mann–Whitney U-test for independent samples was used to detect differences between the groups because of the quite small sample sizes(n).A P value <0.05was considered statistically significant.Median (M)was named as measure of central tendency and 25th as well as75th percentile(P25,P75)as measures of spread.All analyses were conducted using PASW statistics,version18.0(IBM corporation,New York, United States of America).ResultsComparison of MU and MDBoth methods for the analysis of lipid metabolism pro-duced reliable results.In the Tables2and3,the lipopro-tein profiles of cholesterol and triglycerides are shown. Cholesterol,HDL cholesterol,LDL cholesterol,and tri-glycerides were measured by both MU and MD.The comparison of those values led to very similar numbers with only slight aberrations.Results of MD were M=91.11%of MU,P25=86.13%,P75=99.61% (mean92.50%and standard deviation9.28%).There-fore,both MU and MD appeared as suitable for the analysis of the lipid metabolism of common marmosets. In this study,complete lipoprotein profiles were measured by MU,while only certain parameters were ascertained by MD as well.Thus,the following results always show the MU values,unless there is an explicit reference to MD.Effects related to ageStatistical parameters of cholesterol and its lipopro-teins are presented in Table2.An interesting age effect could be observed:CONTROL OLD,whose age at blood collection was M=5.2years(middle adult-hood),showed an amount of cholesterol of M=3.78m m,of which M=1.10m m was bound to HDL,M=2.03m m to LDL and M=0.15m m to VLDL.In contrast,the CONTROL YOUNG with an age at blood collection of M=0.75years(early adult-hood[32])had a cholesterol of M=3.23m m,of which M=1.41m m was carried by HDL, M=1.78m m by LDL and M=0.08m m by VLDL. That means,older common marmosets had more plasma cholesterol than younger ones,significantly more of it was carried by LDL(P=0.02)as well as VLDL(P=0.02)and less of it was bound to HDL. The results of the triglyceride analysis are shown in Table3.There an age effect is visible,too.TheTable1Blood plasma parameters analyzed and methods usedPlasma parameters Abbreviation MU MDTotal Cholesterol CHOL X XHigh-density lipoprotein cholesterol HDL CHOL X XLow-density lipoprotein cholesterol LDL CHOL X XVery low-density lipoprotein cholesterol VLDL CHOL XTotal triglycerides TG X XHigh-density lipoprotein triglycerides HDL TG XLow-density lipoprotein triglycerides LDL TG XVery low-density lipoprotein triglycerides VLDL TG XMD:direct assay;MU:determination after ultracentrifugation.Buchwald et al.Prenatal stress programs lipid metabolismPrenatal stress programs lipid metabolism Buchwald et al.Table2Blood plasma cholesterol and lipoproteins[m M],measured by MD or MUCHOL HDL CHOL LDL CHOL VLDL CHOLMD MU MD MU MD MU MUDEX F1M 3.07 3.03 1.40 1.26 1.63 1.960.11P25 2.75 2.880.840.72 1.22 1.520.05P75 3.35 3.44 1.47 1.36 1.79 2.210.30 CONTROL OLD M 3.64 3.78 1.19 1.10 1.4a 2.03a0.15aP25 2.57 2.450.760.65 1.21 1.620.11P75 3.98 4.30 1.91 1.59 2.31 2.940.23DEX F2M 3.86 3.95 2.00 1.73 1.75b 2.200.07P25 3.27 3.37 1.17 1.10 1.65 1.980.04P75 4.61 4.92 2.31 1.95 2.28 2.740.15DEX F3M 4.25 4.40 1.75 1.59 2.19c 2.74c0.07P25 3.74 3.76 1.61 1.41 1.55 2.070.07P75 4.96 5.10 2.54 2.11 2.29 2.920.28 CONTROL YOUNG M 2.87 3.23 1.49 1.41 1.04abc 1.78ac0.08aP25 2.36 2.75 1.10 1.130.96 1.510.06P75 3.80 4.16 2.45 2.05 1.23 2.010.11Significant differences,P<0.05:a between CONTROL OLD and CONTROL YOUNG.b between DEX F2and CONTROL YOUNG.c between DEX F3and CONTROL YOUNG.CHOL,cholesterol;M,median;P25/P75,25th/75th percentile;HDL/LDL/VLDL,high-density lipoprotein/low-density lipoprotein/very low-density lipoprotein.MD:direct assay;MU:determination after ultracentrifugation.Table3Blood plasma triglycerides and lipoproteins[m M],measured by MD or MUTG HDL TG LDL TG VLDL TGMD MU MU MU MUDEX F1M 1.24 1.480.260.680.51P250.760.800.170.410.18P75 1.58 1.810.280.760.81 CONTROL OLD M 1.28 1.440.28a0.720.47P25 1.11 1.240.200.490.32P75 1.61 1.890.360.930.70 DEX F2M0.810.890.24b0.490.16P250.640.730.230.400.10P75 1.03 1.190.280.610.33 DEX F3M0.96 1.260.29c0.690.32P250.87 1.030.240.580.16P75 1.71 1.910.350.780.78 CONTROL YOUNG M 1.11 1.410.40abc0.680.28P250.94 1.160.360.550.25P75 1.21 1.470.420.740.38 Significant differences,P<0.05:a between CONTROL OLD and CONTROL YOUNG.b between DEX F2and CONTROL YOUNG.c between DEX F3and CONTROL YOUNG.TG,triglycerides;M,median;P25/P75,25th/75th percentile;HDL/LDL/VLDL,high-density lipoprotein/low-density lipoprotein/very low-density lipoprotein.MD:direct assay;MU:determination after ultracentrifugation.triglyceride concentration of both control groups was almost equal(CONTROL OLD:M=1.44m m,CON-TROL YOUNG:M=1.41m m),but in the older one significantly less of it was bound to HDL(CONTROL OLD:M=0.28m m,CONTROL YOUNG:M= 0.40m m,P=0.04)and more of it was bound to LDL(CONTROL OLD:M=0.72m m,CONTROL YOUNG:M=0.68m m)and VLDL(CONTROL OLD:M=0.47m m,CONTROL YOUNG:M= 0.28m m).When the fatty acids were analyzed(Table4),differ-ences between the old and the young control group occurred as well.Older animals had significantly less n3fatty acids(M=2.84mol%)than younger ones (M=3.82mol%,P=0.04).Furthermore,the amount of n9fatty acids was signifi-cantly higher in older animals(CONTROL OLD:M= 26.97mol%,CONTROL YOUNG:M=20.82mol %,P=0.01),so was the rate of n7fatty acids(CON-TROL OLD:M=4.20mol%,CONTROL YOUNG: M=3.12mol%,P=0.01).Blood lipids and lipoproteins of DEX F1,F2,and F3 Concerning the lipoprotein patterns of cholesterol and triglycerides,there were no significant differences between the groups DEX F1and CONTROL OLD.In contrast,DEX F2as well as DEX F3showed higher levels of plasma cholesterol(DEX F2:M= 3.95m m,DEX F3:M=4.40m m)and lower levels of plasma triglycerides(DEX F2:M=0.89m m,DEX F3:M=1.26m m)than CONTROL YOUNG(cho-lesterol:M=3.23m m,triglycerides:M=1.41m m), see Tables2and3.Furthermore,there were significant differences between DEX F2as well as DEX F3and CONTROL YOUNG in terms of HDL triglycerides and LDL cholesterol.The LDL cholesterol concentration measured by MU was higher in DEX F2(M=2.20m m)than in CONTROL YOUNG(M=1.78m m),but narrowly missed the level of significance(P=0.09).However,the results of MD showed a significantly larger amount of LDL cholesterol in DEX F2(M=1.75m m)than in CONTROL YOUNG(M=1.04m m,P=0.01).DEX F3had sig-nificantly more LDL cholesterol(MU:M=2.74m m, MD:M=2.19m m)than CONTROL YOUNG(MU: M=1.78m m,MD:M=1.04m m),independently from the used method(MU:P=0.03,MD:P=0.03). The HDL triglyceride levels of both DEX F2and F3 were significantly lower than in the controls(DEX F2: M=0.24m m,P=0.01;DEX F3:M=0.29m m, P=0.03;CONTROL YOUNG:M=0.40m m).The cholesterol/HDL cholesterol ratio was higher in both, DEX F2(M=2.50)as well as DEX F3(M=2.66) than in CONTROL YOUNG(M=2.29).Fatty acids of DEX F1,F2,and F3Referring to cholesterol,triglycerides and their lipoproteins,dexamethasone influenced the F2and F3Table4Blood plasma fatty acids[mol%of total fatty acids]n3FA n6FA n7FA n9FA Saturated FADEX F1M 2.45b37.64 4.7831.1326.43P25 2.0429.58 3.7226.5225.58P75 2.6439.14 5.6535.0328.31 CONTROL OLD M 2.84b38.12 4.20a26.97a27.07P25 2.4137.37 3.6525.5625.42P75 3.3942.61 4.8827.7927.36DEX F2M 3.10c42.96 3.2021.6127.48P25 3.0137.91 3.0319.6825.91P75 3.3644.93 4.1228.8030.27DEX F3M 3.26d45.96 3.5920.2628.11P25 2.4439.11 3.3216.2227.89P75 3.3348.65 3.7425.3828.25 CONTROL YOUNG M 3.82acd41.85 3.12a20.82a30.27P25 3.7040.13 3.0920.0428.94P75 3.8943.69 3.3121.7231.20Significant differences,P<0.05:a between CONTROL OLD and CONTROL YOUNG.b between DEX F1and CONTROL OLD.c between DEX F2and CONTROL YOUNG.d between DEX F3and CONTROL YOUNG.FA,fatty acids;M,median;P25/P75,25th/75th percentile.Buchwald et al.Prenatal stress programs lipid metabolismgeneration,while the F1seemed to be unaffected.In contrast,the investigation of the fatty acid pattern showed an influence of exogenous stress hormones on the F1as well(Table4).All of the DEX generations presented significantly lower rates of n3fatty acids compared with the control groups(DEX F1:M=2.45mol%vs.CONTROL OLD:M=2.84mol%,P=0.04;DEX F2:M= 3.10mol%,P=0.01and DEX F3:M=3.26mol %,P=0.03compared with CONTROL YOUNG: M=3.82mol%).Body weight of DEX F1,F2,and F3Although there were the variances in their blood lipid metabolism aforementioned,the offspring DEX F1, DEX F2,and DEX F3showed a weight development very similar to that of the controls.There were no sig-nificant differences between the test and control groups at any point of time observed.DiscussionIn the present study,prenatal dexamethasone applica-tion led to higher cholesterol levels,significantly more LDL cholesterol and an enhanced cholesterol/HDL cholesterol ratio in the offspring’s blood,which are all known as cardiovascular risk factors.Additionally, healthy and protective n3fatty acids were lowered,while body weight development was not significantly affected. The study concentrated on prenatal programming, because direct heredity is too slow a process to explain the explosively increased prevalence of cardiovascular diseases and predisposing factors like obesity during the last decades alone,although genetics has been pro-ven to do its stint by many twin studies[46,48].Yet, imprinting by fetal exposure to glucocorticoids is a mechanism working much faster[23,43,44]. Choosing the common marmoset as primate model for investigating human diseases has many advantages compared with studying other mammals or humans and thus is well established[19].Nevertheless,there are only few primate models for prenatal programming [e.g.,15,27,39],and none of them investigated the lipid metabolism of the offspring extensively.A special benefit of the chosen species is that it rates as most suitable model for the analyses of lipid metabolism, because of the similarity of its lipoproteins[10],fatty acid composition[11],and obesity-related alterations [53]to the human situation.Three generations of common marmosets(F1up to F3)were investigated,including only female offspring. The genders should be examined separately,because prenatal programming seems to have sex-specific effects [29,40,41].The mothers of the F1generation received a specific dexamethasone application during pregnancy. This synthetic glucocorticoid is able to mimic effects of maternal stress hormones because of its high affinity to fetal glucocorticoid receptors[54],the ability to pass the placental barrier easily[6,58]and the fact that its inacti-vation by fetal hydroxysteroid(11b)dehydrogenase2is very poor[54].In contrast to anxiety or social stressors, used in other studies[e.g.,7,21],the application of a drug can be standardized easily by a defined dosage.In the previous experiment at the German Primate Center,when the dexamethasone treatment took place, the pregnant mothers and their newborns were investi-gated.There were significant effects of dexamethasone on blood hormones during pregnancy(lowered proges-terone and elevated estradiol),but ultrasound examina-tion as well as weight and size of mothers and newborns showed no differences between monkeys treated with dexamethasone and controls[4,20].Body weight and blood lipid metabolism of adult female offspring F1to F3of those monkeys treated with the glucocorticoid were compared with age-related con-trols in the present study.Similar to thefinding afore-mentioned,that dexamethasone did not alter the newborns’body weight,there were no significant differ-ences in body mass between the test and control groups at any point of time.In contrast,another study follow-ing the previous experiment detected a gender-specific influence of prenatal dexamethasone on body weight in the common marmosets:At the age of20months, females showed a significantly higher body weight,while the males where significantly lighter than the controls [20,41].Studies in humans as well as animal models often associate prenatal stress or glucocorticoids with lower birth weight[5,15,17,24,28]as well as over-weight later in life[35,51,52].Contingently,an imprinting effect on body weight could be masked by individualfluctuations in the pres-ent study.In marmosets,more than10%weight loss frequently occurs in response to several adverse influ-ences[31].In humans,other primates and rodents,pre-natal stress correlates with altered behavior, particularly an increased vulnerability to stressful events[7,25,42].This could have further intensified the individual variations of body weight in the off-spring of mothers treated with dexamethasone,so effects of prenatal programming could not be detected. Referring to the blood parameters,thefirst result was,that the methods MU and MD both were suitable for detection of lipids and lipoprotein pattern and pro-duced reliable,comparable results.Thisfinding could make future analyses much easier.MD provides aPrenatal stress programs lipid metabolism Buchwald et al.cost-effective,direct measurement of the most impor-tant parameters with high availability,optimized for human lipoproteins.Thus,the high similarity of com-mon marmosets’lipoproteins to human ones[10]was confirmed.MU is more complex and thus rarer used, but offers the chance to detect a complete lipoprotein profile.According to the aim of investigation,both methods can be recommended.Age-depending differences in healthy animals were observed.So older marmosets showed higher plasma levels of cholesterol than younger ones,of which par-ticularly significantly more was bound to LDL and VLDL and less was carried by HDL.In addition,the older group showed significantly less HDL triglyce-rides,but more LDL triglycerides and VLDL triglyce-rides.Furthermore,older monkeys had significantly lower amounts of n3,but significantly higher levels of n9and n7fatty acids.Those results go along with the human situation,where reference values of many parameters,including several aforementioned,differ depending on age,too[9].This is a further prove for the suitability of the common marmoset as animal model for lipid metabolism.Additionally,it underlines age as an important covariate,which should be respected in future experiments.With regard to the aims of the present study,the most exciting results were the effects of dexamethasone on blood plasma parameters of lipid metabolism in the F1,F2,and F3offspring generation.For assessing a human’s cardiovascular risk,the following blood parameters are usually measured:cholesterol,LDL cholesterol,HDL cholesterol,and triglycerides[38]. High levels of cholesterol,LDL cholesterol,and trigly-cerides as well as low concentrations of HDL choles-terol are associated with an increased risk of coronary heart disease[36,38].There were higher levels of cholesterol but lower levels of triglycerides in both DEX F2and DEX F3than in the controls.Particularly of relevance where the lipopro-teins:LDL cholesterol,one of the cardiovascular risk factors[36,38],was significantly higher in DEX F2as well as DEX F3than in the control group,while HDL triglycerides were significantly lower.The cholesterol/ HDL cholesterol ratio,whose increase is associated with an enhanced risk of heart failure[30],was higher in both DEX F2and DEX F3than in CONTROL YOUNG.The fatty acid pattern was influenced by prenatal dexamethasone treatment,too.All of the analyzed off-spring generations of mothers treated with dexametha-sone during pregnancy presented significantly lower levels of n3fatty acids than the controls,although their nutrition was standardized.N3fatty acids have antiin-flammatory effects and play a protective role against cardiovascular diseases[1,8,33],so lowered concentra-tions suggest a health risk.There are several studies, which investigated effects of dietary intake of certain fatty acids during pregnancy and/or lactation on the off-spring[e.g.,47],but information about imprinting effects on fatty acid pattern is rare.This phenomenon is new and requires further investigation.In many studies,prenatal stress or glucocorticoid treatment is associated with higher cardiovascular risk in the offspring[e.g.,15,49,55],while only in a few ones it is not[e.g.,13].Thisfinding often occurs together with lower birth weight and/or obesity later on.Furthermore,reduced newborn body mass of any etiology is widely accepted to be inversely related to blood pressure in children and adults[34]and linked to further risk factors,such as diabetes mellitus and hyperlipidemia[3].Thus,it is hard to decide,if the enhanced cardiovascular risk following fetal glucocorti-coid exposure is a direct programming effect or just a result of the uncommon weight development.The results of the present study point out to a pri-mary imprinting effect of prenatal glucocorticoids on blood parameters of lipid metabolism,leading to an enhanced cardiovascular risk.Those effects seem to be passable to further generations up to at least F3,which strongly suggests epigenetic modifications. AcknowledgmentsWe wish to thank Gabriele Dobeleit,Corinna Arnold, Cornelia Schwarz,and Anke Hahn for their support. 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