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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10μg/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(1μg/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(P<0.05),细胞核内NF-κBp65蛋白表达增多(P<0.05),MAPK通路相关蛋白ERK1/2磷酸化和p38MAPK磷酸化水平明显增强(P<0.05),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(10μg/ml)作用时该作用明显(P<0.05)。替米沙坦干预后,p-ERK1/2和p-p38MAPK蛋白表达也受到明显抑制(P<0.05),大剂量(10μg/ml)时作用明显(P<0.05)。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。
Objective To investigate the effect of telmisartan on the inflammatory pathway induced by lipopolysaccharide in 3T1-L1 adipocytes and to explore the anti-inflammatory mechanism of telmisartan. Methods 3T3-L1 adipocytes were induced to 90% maturation and divided into 6 groups according to random number table: control group, LPS group, LPS + telmisartan group (n = 18 ), Adding different concentrations of telmisartan to DMSO, LPS + telmisartan group cells, LPS group and LPS + telmisartan group were added with lipopolysaccharide (1μg / ml) The expression of nuclear protein NF-κBp65, total proteins p-IκBα, IκBα, p-ERK1 / 2, ERK1 / 2, p-p38MAPK and p38MAPK were detected by Western blotting. Results The expression of phosphorylated IκBα protein increased (P <0.05), the expression of NF-κBp65 protein increased (P <0.05) and the phosphorylation of ERK1 / 2 and phosphorylated p38 MAPK in LPS increased significantly (P < 0.05). Telmisartan inhibited the phosphorylation of IκBα and the nuclear translocation of NF-κBp65, the expression of p-IκBα protein and NF-κBp65 protein decreased. The effect of high dose telmisartan (10μg / ml) Obviously (P <0.05). The expression of p-ERK1 / 2 and p-p38MAPK protein was also significantly inhibited after the intervention of telmisartan (P <0.05), and the effect was significant at high dose (10μg / ml) (P <0.05). Conclusion Telmisartan can inhibit IκBα phosphorylation, nuclear translocation of NF-κBp65 and phosphorylation of ERK1 / 2 and p38MAPK in MAPK pathway in 3T3-L1 adipocytes Inflammation.