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机构地区:[1]辽宁医学院附属第一医院心血管内科,辽宁锦州121000
出 处:《辽宁医学院学报》2010年第3期206-208,共3页Journal of Liaoning Medical University (LNMU) Bimonthly
摘 要:目的观察苯那普利对大鼠心肌缺血再灌注损伤的保护作用,并初步探讨其可能的作用机制。方法32只SD大鼠随机分为3组:假手术组、缺血再灌注组、苯那普利预处理组。大鼠在体结扎冠状动脉前降支30 min后,松开结扎线再灌注120 min制备心肌缺血再灌注损伤模型,测定血清肌酸激酶(CK)的含量,TTC染色后计算心肌梗死范围(MIS),TUNEL法检测心肌细胞凋亡并用免疫组化方法测定抑凋亡基因(Bcl-2)和促凋亡基因(Bax)的表达。结果缺血再灌注损伤组较假手术组的CK明显增高,其凋亡指数增多,Bcl-2的蛋白表达减少而Bax的蛋白表达增加。苯那普利预处理组的CK较缺血再灌注组明显降低,其凋亡指数减少,Bcl-2蛋白表达增加而Bax的蛋白表达降低;心肌梗死面积明显减小。结论苯那普利预处理通过抑制心肌细胞的凋亡而对缺血再灌注的心肌起保护作用。Objective To observe the protective effects of benazepril preconditioning during ischemia reperfusion in rats hearts,and investigate the possible mechanism.Methods Thirty-two SD rats were randomized into three groups,sham group(n=8),ischemia reperfusion injury group(IRI n=12) and benazepril preconditioning group(n=12).The level of Creatine kianse isoenzyme and the infarction size were measured.The apoptotic index(AI) was measured by TUNEL staining.The protein expression of Bcl-2 and Bax was studied by immunohistochemical staining.Results Compared with IRI group,the activity of CK in serum was markedly decreased in benazepril preconditioning group(P〈0.01) AI was significantly decreased in benazepril preconditioning group(P〈0.01).The expression of Bax protein was decreased significantly and bcl-2 protein was increased significantly in benazepril preconditioning group(P〈0.01).Conclusions These data suggest that benazepril pretreatment could protect against myocardial ischemia-reperfusion injury in rats by inhibiting apoptosis.
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