【摘要】 目的 :探讨遗传性高血压及左室肥厚过程中心肌组织凋亡调节蛋白bcl 2、bax表达的变化及AT1受体拮抗剂缬沙坦的影响。方法 :实验动物为 8周龄自发性高血压大鼠 (SHR) ,分为缬沙坦治疗组 (SHR +缬沙坦组 )和非治疗组 (SHR无药组 ) ,以Wistar鼠作为正常血压对照组 ,观察期限为 8w。采用免疫组化、Western印迹等方法检测凋亡调节蛋白bcl 2、bax表达。结果 :SHR心肌中存在bax高表达 ,缬沙坦治疗 8w后 ,SHR心肌组织bax蛋白表达显著降低至接近Wistar组。bcl 2蛋白在SHR +缬沙坦组及Wistar组表达较SHR无药组有增高趋势 (P >0 0 5 )。前两组bcl 2 bax比值较后者显著增高 (P <0 0 5 )。结论 :心肌细胞凋亡是代偿性心肌肥厚发展为心力衰竭的可能机制之一。高血压病早期缬沙坦在降压同时有效抑制心肌细胞凋亡。更多还原

【Abstract】 Objective:To explore the change of the expression of apoptotic regulatory protein bcl 2 and bax in genetic hypertension and heart hypertrophy To evaluate the anti apoptotic effect of Valsartan Methods:Thirty SHRs were divided equally into two groups One group was treated with Valsartan 〔20 mg/(kg·d)〕, the other with placebo, with normal Wistar rats as controls The observation period was from 8 week old to 16 week old Expression of bcl 2 and bax in left ventricular myocytes was studied by the techniques of immunohistochemistry and Western blot Results:The expression of bax in SHR+placebo was markedly higher than that of Wistar or SHR+Valsartan, and so was the ratio of bax/ bcl 2 The expression of bcl 2 was similar in the three groups Conclusion:These data suggest that in response to chronic arterial pressure overload , cardiomyocyte specific apoptosis contributes to the transition from compensatory hypertrophy to decompensation Thus, apoptosis may be involved in the pathogenesis of congestive heart failure And Valsartan may reverse such decompensation by inhibiting the expression of bax更多还原