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目的探讨替米沙坦对血管紧张素II(AngII)诱发的肥大心肌细胞膜AT1和AT2受体表达变化的影响。方法体外培养心肌细胞,分为三组:对照组,AngII处理组,替米沙坦处理组。构建AngII诱发心肌细胞肥大模型,提取各组心肌细胞膜蛋白,免疫印记(Western Blotting)观察肥大心肌细胞中AT1和AT2表达。结果相对于对照组,AngII处理组心房利钠肽(ANP),脑钠肽(BNP)基因表达明显上升(P<0.05),AT1和AT2受体表达也显著上升(P<0.05);相对于AngII组,替米沙坦处理组ANP,BNP基因和AT1受体表达明显下降(P<0.05)。结论替米沙坦可以明显抑制AngII诱发的心肌细胞肥大,其机制与其降低因AngII诱发AT1受体表达升高和维持AngII引起的AT2受体高表达有关。
Objective To investigate the effects of telmisartan on the expression of AT1 and AT2 receptors in hypertrophic cardiomyocytes induced by angiotensin Ⅱ (AngII). Methods Cardiomyocytes were cultured in vitro and divided into three groups: control group, AngII-treated group and telmisartan-treated group. The AngII-induced cardiomyocyte hypertrophy model was constructed and the myocardial membrane proteins of each group were extracted. The expression of AT1 and AT2 in hypertrophic cardiomyocytes was observed by Western Blotting. Results Compared with the control group, the expressions of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in AngII group were significantly increased (P <0.05), and the expressions of AT1 and AT2 receptor were significantly increased (P <0.05) AngII group, telmisartan treatment group ANP, BNP gene and AT1 receptor expression was significantly decreased (P <0.05). Conclusion Telmisartan can significantly inhibit AngII-induced hypertrophy of cardiomyocytes, and its mechanism is related to the decrease of AT1 receptor expression induced by AngII and the high expression of AT2 receptor induced by AngII.