血管紧张素Ⅱ2型受体对AngⅡ诱导成年大鼠心肌成纤维细胞分泌α-TNF和IL-1β的作用

Role of AT2 receptors on angiotensin II-induced tumor necrosis factor α and interleukin 1β secretion in adult rat cardiac fibroblasts

目的探讨血管紧张素Ⅱ2型受体(angiotensinⅡtype2 receptors,AT2)在成年心肌成纤维细胞分泌肿瘤坏死因子α(α-TNF)和白介素1β(IL-1β)中的作用,明确AT2受体和AT1受体作用的差异。方法差速贴壁分离及培养成年SD大鼠心肌成纤维细胞,将细胞分为4组进行药物干预:对照组、血管紧张素Ⅱ(AngⅡ)组、AngⅡ+氯沙坦(losartan)组、AngⅡ+PD123319组,应用放射免疫法检测各组细胞分泌α-TNF和IL-1β的水平。结果AngⅡ诱导使心肌成纤维细胞分泌α-TNF和IL-1β明显增加。与AngⅡ组相比,α-TNF在AT1受体阻断后下调了58.7%(P<0.05),AT2受体阻断后下调了65.9%(P<0.05);IL-1β在AT1受体阻断后下调了69.1%(P<0.05),AT2受体阻断后下调了78.7%(P<0.05)。结论AT2受体参与介导心肌成纤维细胞分泌α-TNF和IL-1β。

Objective To investigate the role of AT2 receptors in the secretion of tumor necrosis factor α （α-TNF） and interleukin 1β （IL1β） in adult rat cardiac fibroblasts. Methods Adult rat cardiac fibroblasts in in vitro culture were divided into control, Ang Ⅱ, AngⅡ ＋ Losartan, and AngⅡ ＋ PD 123319 groups with corresponding treatments. Radioimmunoassay was used to determine α-TNF and IL1β levels in the supematant of the treated cardiac fibroblasts. Results Ang Ⅱ treatment resulted in significantly increased α-TNF and IL1β levels. Compared with Ang Ⅱ group, IL1β level was decreased by 69.1% and 78.7% and α-TNF by 58.7% and 65.9% after blocking AT1 and AT2 receptors, respectively. Conclusion AT2 receptors are involved in α-TNF and IL1β secretions in cardiac fibroblasts.