【摘要】 目的:探讨血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)在缺氧诱导的人肺成纤维细胞(human lung fibroblast,HLF)表型转化及胶原合成中的作用。方法:在缺氧条件下培养HLF-1细胞株,将细胞分为AngⅡ组、AngⅡ+替米沙坦(TST)组和对照组。采用免疫荧光法检测HLF-1细胞α-平滑肌肌动蛋白(α-smooth muscle actin,α-SMA)的表达水平;采用Western blot法检测HLF-1细胞Ⅰ型胶原(collagen typeⅠ,Col-Ⅰ)蛋白的表达水平。结果:AngⅡ组HLF-1细胞α-SMA和Col-Ⅰ蛋白的表达水平较对照组明显上调,AngⅡ+TST组α-SMA和Col-Ⅰ蛋白的表达水平较AngⅡ组明显下降。结论:AngⅡ/血管紧张素Ⅱ1型受体信号通路可诱导缺氧性HLF表型转化以及胶原合成。更多还原

【Abstract】 Objective:To explore the effect of angiotensin Ⅱ(AngⅡ)on hypoxia-induced phenotype switch and collagen synthesis of human lung fibroblasts(HLF). Methods:The HLF-1 cell line was cultured in hypoxic condition,and randomly divided into three groups:control group,AngⅡgroup,and AngⅡ+telmisartan(TST)group.Theα-smooth muscle actin(α-SMA)protein expression levels were measured by immunofluorescence localization analysis.The collagen typeⅠ(Col-Ⅰ)protein expression levels were detected by Western blot. Results:The expression levels ofα-SMA and Col-Ⅰin hypoxic HLF-1 cells were significantly increased after AngⅡ treatment and the effect was significantly inhibited by telmisartan,an angiotensinⅡtype 1 receptor inhibitor. Conclusion:AngⅡ/angiotensinⅡtype 1 receptor can induce phenotype switch and collagen synthesis in hypoxic HLF.更多还原