替米沙坦对脂多糖诱导3tl1脂肪细胞炎症通路-第三军医大学学报.docVIP

替米沙坦对脂多糖诱导3T3-L1脂肪细胞炎症通路的影响 （100853北京，解放军总医院内分泌科） [摘要]目的 研究替米沙坦对3T1-L1脂肪细胞炎症通路的影响。方法 机分：对照组LPS组LPS+替米沙坦0.01、0.1、1和10 μg/ml对照组加DMSO，LPS+替米沙坦组加入不同浓度替米沙坦，孵育2 h后，LPS组和LPS+替米沙坦组再加入脂多糖（1 μg/ml），孵育1hestern 免疫印记法比较各组核蛋白N -κBp65、p-IκBα、IBα、p-ERK1/2、ERK1/2p-p38MAPK、p38MAPK的表达水平。结果 脂多糖刺激后Bα磷酸化蛋白表达增强，胞核内N -κBp65蛋白表达增多，MAPK通路相关蛋白ERK1/2磷酸化p38MAPK磷酸化水平增强，α磷酸化和NF-κBp65核转位，p-IκBα蛋白表达和核蛋白NF-κBp65表达均降低，大剂量替米沙坦（10ug/ml）作用时该作用明显（p0.05）。替米沙坦干预后，p- ERK1/2和p-p38MAPK蛋白表达也受到明显抑制（p0.05），大剂量（10ug/ml）时作用明显（p0.05）。结论 在脂肪细胞中，α蛋白磷酸化以及NF-κBp65蛋白核转位以及MAPK通路中ERK1/2蛋白和p38MAPK蛋白的磷酸化，从而发挥抗炎作用。 [关键词] 受体，血管紧张素，1型；脂肪细胞 ；炎症Telmisartan modulates phlogistic pathways in LPS-induced 3T3-L1 adipocytes Zhao Jue，Dou Jingtao，Zang Li，Li Xiaojin，Xue Bing，Wang Baoan，Ma FanglingDepartment of Endocrinology，Chinese PLA General Hospital，Beijing，100853 ChinaAbstract] Objective To investigate the anti-inflammatory mechanism of angiotensin II AT1 receptor antagonist- telmisartan in LPS induced 3T3-L1 adipocytes. Methods The differentiated 3T3-L1 adipocytes were randomly divided into 6 groups: normal control,LPS,LPS+telmisartan(0.01，0.1，110μg/ml) .The control cells incubated with DMSO ,other cells with 0，0.01，0.1，1，10μg/ml telmisartan for 2 h，some cells were activated for 1 h with LPS （1 μg/ml） after preincubation of telmisartan the protein was extracted， and the expression of NF-κBp65， IκBα， p-IκBα， p38，p-p38， ERK1/2， p-ERK1/2 was detected by Western Blot. Results ompared with normal control group,LPS significantly increased the translocation of NF-κBp65 from cytosol to the nucleus and phosphorylation of IκBα，ERK1/2 and p38but telmisartan inhibited the expresstion of them in high dose（10ug/ml）(p0.05). Conclusion In 3T3-L1 adipocytes， telmisartan can inhibit the translocation of NF-κBp65 from cytosol to the nucleus and phosphorylation of IκBα，ERK1/2 and p38，which may partly explain the anti-inflammation effect of telmisartan.[Key words] receptor， angiotensin， type 1； adipocytes；inflammation. Supported by the National