Telmisartan modulates phlogistic pathways in LPS-induced 3T3-L1 adipocytes

赵珏; 窦京涛; 臧丽; 李晓瑾; 薛冰; 汪保安; 马芳玲

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Telmisartan modulates phlogistic pathways in LPS-induced 3T3-L1 adipocytes

更新时间：2026-01-09

- Telmisartan modulates phlogistic pathways in LPS-induced 3T3-L1 adipocytes
- Journal of Army Medical University Vol. 33, Issue 15, Pages: 1572-1575(2011)
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  CLC： R587.1;R392.32;R972.6
- Published：2011
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赵珏,窦京涛,臧丽,李晓瑾,薛冰,汪保安,马芳玲.替米沙坦对脂多糖诱导3T3-L1脂肪细胞炎症通路的影响[J].陆军军医大学学报(原第三军医大学学报),2011,33(15):1572-1575.

　Zhao Jue,Dou Jingtao,Zang Li,Li Xiaojin,Xue Bing,Wang Baoan,Ma Fangling.Telmisartan modulates phlogistic pathways in LPS-induced 3T3-L1 adipocytes[J].J Amry Med Univ (J Third Mil Med Univ),2011,33(15):1572-1575.
赵珏,窦京涛,臧丽,李晓瑾,薛冰,汪保安,马芳玲.替米沙坦对脂多糖诱导3T3-L1脂肪细胞炎症通路的影响[J].陆军军医大学学报(原第三军医大学学报),2011,33(15):1572-1575. DOI：

　Zhao Jue,Dou Jingtao,Zang Li,Li Xiaojin,Xue Bing,Wang Baoan,Ma Fangling.Telmisartan modulates phlogistic pathways in LPS-induced 3T3-L1 adipocytes[J].J Amry Med Univ (J Third Mil Med Univ),2011,33(15):1572-1575. DOI：

摘要

目的研究替米沙坦对脂多糖诱导3T1-L1脂肪细胞炎症通路的影响，探讨替米沙坦的抗炎机制。方法将3T3-L1脂肪细胞诱导至90%成熟，按随机数字表法分为6组：对照组、LPS组、LPS+替米沙坦（0.01、0.1、1和10 μg/ml）组（n=18），向对照组细胞中加DMSO，LPS+替米沙坦组细胞中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1 h，Western免疫印记法比较各组核蛋白NF-κBp65、总蛋白p-IκBα、IκBα、p-ERK1/2、ERK1/2、p-p38MAPK、p38MAPK的表达水平。结果脂多糖刺激后IκBα磷酸化蛋白表达增强（P0.05），细胞核内NF-κBp65 蛋白表达增多（P0.05），MAPK通路相关蛋白ERK1/2磷酸化和p38MAPK磷酸化水平明显增强（P0.05），替米沙坦可抑制IκBα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（10 μg/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（10 μg/ml）时作用明显（P0.05）。结论在3T3-L1脂肪细胞中，替米沙坦可以抑制NF-κB通路中IκBα蛋白磷酸化、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。

Abstract

Objective To investigate the anti-inflammatory role of angiotensin Ⅱ AT1 receptor antagonist

telmisartan

in LPS-induced 3T3-L1 adipocytes. Methods After differentiated 3T3-L1 adipocytes were exposed to telmisartan (0

0.01

0.1

1 and 10 μg/ml) respectively for 2 h

they were treated with LPS (1 μg/ml) for another 1 h. The cells treated with DMSO served as control. The expression of NF-κBp65

IκBα

p-IκBα

p38MAPK

p-p38MAPK

ERK1/2 and p-ERK1/2 was detected by Western blotting. Results Compared with control group

LPS significantly increased the translocation of NF-κBp65 from the cytoplasm to the nucleus and phosphorylation of IκBα

ERK1/2 and p38MAPK (P0.05)

but telmisartan

especially when at high dose (10 μg/ml) inhibited the above mentioned process significantly(P0.05). Conclusion In 3T3-L1 adipocytes

telmisartan can inhibit the translocation of NF-κBp65 from cytoplasm to the nucleus and phosphorylation of IκBα

ERK1/2 and p38MAPK

which may explain the anti-inflammation effect of telmisartan.

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