摘要
目的:观察血管紧张素Ⅱ受体拮抗剂缬沙坦和醛固酮受体拮抗剂螺内酯对SHR心肌中活化的ERK的影响。方法:将18只雄性SHR随机分为三组,每组6只。其中两组分别用缬沙坦30mg/kg/天、螺内酯20mg/kg/天溶于饮水灌胃,连续治疗13周;对照组给正常饮水,并与Wist-ar-kyoto大鼠(WKY)比较。用Western-blot方法检测大鼠心肌磷酸化ERK的表达。结果:SHR对照组心肌磷酸化ERK/actin值高于其余三组(P<0.01),螺内酯和缬沙坦组高于WKY组(P<0.01),两用药组之间无差异。结论:血管紧张素Ⅱ受体拮抗剂缬沙坦和醛固酮受体拮抗剂均能通过抑制ERK途径而抑制左室肥厚和心肌纤维化。
Objective: To investigate the role of spironolactone and valsartan in the expression of the active form of the extracellular signal-regulated kinaseERK in myocardium of spontaneously hypertensive rats(SHR).Method: Six-week male SHRs were divided into three groups at random: Spironolactone 20mg kg d、 Valsartan 30mg kg d were administered to rats in spironolactone group and valsartan group respectively.SHR control group and Wistar Kyoto(WKY) group were given normal water during the same time.Phosphorylation of ERK were assessed by western blot with phosphospecific antibodies.Results: After thirteen-week treatment,The ratio of phospho-ERK actin in valasrtan group and spironolactone group was lower than that in SHR control group( P<0.01),but higher than that in WKY group(P<0.01). The difference between valasrtan group and spironolactone group was not remarkable(P>0.05).Conclusion: These findings showed that both valsartan and spironolactone can ameliorate left ventricular hypertrophy and myocardial fibrosis in SHR by attenuating phosphorylation of ERK.
出处
《微循环学杂志》
2006年第4期12-14,F0002,共4页
Chinese Journal of Microcirculation
基金
湖北省教育厅自然基金资助项目(301140080)
