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目的:探讨阿托伐他汀(Ato)干预下,醛固酮(Ald)诱导新生大鼠心脏成纤维细胞内皮素A型受体(ET-AR)mRNA表达的变化及其机制。方法:采用胰酶消化法和差速贴壁分离法获取新生大鼠心脏成纤维细胞,应用RT-PCR测定不同条件下心脏成纤维细胞中的ET-AR mRNA的表达。结果:Ald(0.1μmol/L)可促进心脏成纤维细胞ET-AR mRNA的表达,提前给予Ato(1,10,100μmol/L)能剂量依赖性地抑制Ald的上述作用,同时Ato的这种抑制作用可被甲羟戊酸逆转。结论:Ato可抑制Ald诱导的心脏成纤维细胞ET-AR mRNA表达,发挥其抗心肌纤维化作用,其机制可能与甲羟戊酸代谢途径有关。
AIM: To investigate the alteration of aldosterone (Ald) induced endothelin A receptor (ET-AR) mRNA expression in neonatal rat cardiac fibroblasts induced by atorvastatin (Ato) and its mechanism. Methods: Newborn rat cardiac fibroblasts were obtained by trypsin digestion and differential adherent separation. The expression of ET-AR mRNA in cardiac fibroblasts was determined by RT-PCR. Results: Ald (0.1μmol / L) promoted the expression of ET-AR mRNA in cardiac fibroblasts. Ato (1,10,100μmol / L) pretreatment inhibited the above effects of Ald in a dose-dependent manner The role of mevalonate can be reversed. CONCLUSION: Ato can inhibit the expression of ET-AR mRNA induced by Ald in cardiac fibroblasts and exert its anti-myocardial fibrosis effect, which may be related to the metabolic pathway of mevalonate.