AT2对成年压力超负荷性肥大心肌细胞TNFα、IL-1β及IL-6分泌的调控  

Regulation of AT2 on TNFα,IL-1β and IL-6 synthesis of adult hypertrophic cardiomyocytes induced by pressure overload

作　　者：周娟[1] 徐心[2] 刘进军[1] 林元喜[1] 高广道[1] 

机构地区：[1]西安交通大学医学院生理学与病理生理学系,陕西西安710061 [2]西安交通大学医学院第二附属医院普外科,陕西西安710004

出　　处：《西安交通大学学报（医学版）》2008年第1期25-28,32,共5页Journal of Xi’an Jiaotong University（Medical Sciences）

基　　金：国家自然科学基金资助项目(No.30271435)

摘　　要：目的观察AT2对肥大心肌细胞炎症因子合成的调控作用及AT1和AT2间的相互关系。方法采用腹主动脉缩窄法构建SD大鼠压力超负荷性心肌肥大模型。选用术后8周肥大的心肌细胞,将其分为AngⅡ组、AngⅡ+losartan组、AngⅡ+PD123319及AngⅡ+losartan+PD123319组。待实验结束,RT-PCR法检测细胞TNFα、IL-1β及IL-6的mRNA表达水平,放免法检测TNFα、IL-1β及IL-6的蛋白表达。结果与AngⅡ组相比,AT1拮抗剂losartan不影响TNFα和IL-1β的mRNA及蛋白表达。单独应用AT2拮抗剂PD123319及联合应用losartan和PD123319均可使TNFα和IL-1β的mRNA及蛋白表达水平下调。联合应用二者TNFα和IL-1βmRNA的表达水平介于单独应用losartan和PD123319组之间。与AngⅡ单独联用losartan或PD123319相比,同时联用二者可使IL-6mRNA的表达水平上调。结论AT2参与了肥大心肌细胞炎症因子的表达调控。AT1与AT2之间并非简单的拮抗关系。Objective To investigate the role of AT2 in inflammatory factor synthesis of adult hypertrophic cardiomyocytes induced by pressure overload and the relationship between AT1 and AT2. Methods The left ventricular hypertrophy induced by pressure overload was achieved by placing a band around the abdominal aorta. We isolated and purified hypertrophic cardiomyocytes at 8 weeks after operation. The cardiomyocytes were randomly divided into 4 groups： Ang Ⅱ , Ang Ⅱ ＋ losartan, Ang Ⅱ ＋ PD123319 and Ang Ⅱ ＋losartan＋ PD123319 groups. The mRNA levels of TNFα , IL- 1β and IL-6 were detected by RT-PCR and the protein expression of TNFα, IL- 1β and IL-6 in medium were detected by radioimmunoassay. Results Compared with that of the Ang Ⅱ group, losartan could not influence the mRNA and protein expression of TNFα and IL- 1β, but PD123319 decreased them severely. The mRNA and protein expression of TNFα and IL-1β also decreased with losartan and PD123319 treatment, but they were higher than in PD123319 alone treatment group. Compared with the Ang Ⅱ , Ang Ⅱ ＋ losartan and Ang Ⅱ ＋ PD123319 groups, the IL-6 mRNA increased when cells were treated with losartan and PD123319 simultaneously. Conclusion AT2 can regulate the expression of inflammatory factors of hypertrophic cardiomyocytes. The relationship between AT1 and AT2 is not only antagonistic.

关 键 词：心肌细胞 血管紧张素Ⅱ二型受体 肿瘤坏死因子α 白介素-1Β 白介素-6 

分 类 号：R363.2[医药卫生—病理学]