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目的观察血管紧张素(1-7)[Ang(1-7)]及AngⅡ对THP-1巨噬细胞高密度脂蛋白受体I(SR-BI)表达的影响。方法将THP-1巨噬细胞根据AngⅡ和Ang(1-7)对SR-B1表达的影响分别分为:空白对照组及不同浓度AngⅡ组(10～10~4 nmol/L组);空白对照组及不同浓度Ang(1-7)组(10～10~4 nmol/L组);空白对照组、AngⅡ10~2nmol/L组、AngⅡ10~2 nmol/L+Ang(1-7)组(10~2～10~4 nmol/L组)、AngⅡ+Ang(1-7)+A-779组。运用RT-PCR和Western blot法检测各组SR-BI mRNA及SR-BI蛋白表达的变化。结果与空白对照组比较,AngⅡ10～10~4nmol/L组SR-BI mRNA及蛋白表达明显下调,呈浓度依赖性(P<0.05);而Ang(1-7)10～10~4 nmol/L组SR-BImRNA及蛋白表达明显上调,呈浓度依赖性(P<0.05);与空白对照组和AngⅡ组比较,AngⅡ10~2 nmol/L+Ang(1-7)组(10~2～10~4 nmol/L组)SR-BI表达明显上调,呈浓度依赖性(P<0.05)。与空白对照组比较,AngⅡ+Ang(1-7)10~2 nmol/L+A-779组SR-BI mRNA及蛋白表达明显下调(P<0.05)。结论 Ang(1-7)通过其特异性MAS受体浓度依赖性地拮抗AngⅡ抑制SR-BI的表达,促进胆固醇外流,提高了胆固醇逆转运的效率。
Objective To investigate the effects of angiotensin (1-7) [Ang (1-7)] and AngⅡ on the expression of high density lipoprotein receptor I (SR-BI) in THP-1 macrophages. Methods The effects of Ang Ⅱ and Ang (1-7) on the expression of SR-B1 in THP-1 macrophages were divided into blank control group and Ang Ⅱ group (10 ~ 10 ~ 4 nmol / L group) (10 ~ 10 ~ 4 nmol / L), Ang Ⅱ 10 ~ 2 nmol / L, Ang Ⅱ 10 ~ 2 nmol / L + Ang (1-7) ~ 2 ~ 10 ~ 4 nmol / L group), AngⅡ + Ang (1-7) + A-779 group. The expression of SR-BI mRNA and SR-BI protein in each group were detected by RT-PCR and Western blot. Results Compared with the blank control group, the expression of SR-BI mRNA and protein in AngⅡ10 ~ 10 ~ 4nmol / L group was significantly down-regulated (P <0.05) The expression of SR-BI mRNA and protein was significantly up-regulated in a concentration-dependent manner (P <0.05). Compared with the blank control group and the AngⅡ group, AngⅡ10 ~ 2 nmol / L + 4 nmol / L group) SR-BI expression was significantly increased in a concentration-dependent manner (P <0.05). Compared with the blank control group, the expression of SR-BI mRNA and protein in AngⅡ + Ang (1-7) 10 ~ 2 nmol / L + A-779 group was significantly decreased (P <0.05). Conclusions Ang (1-7) can inhibit the expression of SR-BI in a concentration-dependent manner by its specific MAS receptor in a concentration-dependent manner, promote cholesterol efflux and increase the efficiency of reverse cholesterol transport.