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作 者:屈朝法[1] 马礼坤[1] 徐少东[1] 吴学平[2]
机构地区:[1]安徽省立医院心内科安徽省心血管病研究所,安徽合肥230001 [2]安徽医科大学形态学中心实验室,安徽合肥230032
出 处:《中国病理生理杂志》2007年第4期656-659,共4页Chinese Journal of Pathophysiology
基 金:安徽省自然科学基金资助项目(No.03043710);安徽省优秀青年基金资助项目(No.04043054)
摘 要:目的:探讨犬急性心肌梗死后晚期再灌注对梗死周边缺血区心肌细胞凋亡及凋亡相关蛋白Bcl-2、Bax表达的影响。方法:健康成年杂交犬28只,全麻下常规开胸暴露冠状动脉后随机分为3组:假手术组(n=8),急性心肌梗死组(n=10)、晚期再灌注组(n=10)。假手术组仅行左冠状动脉前降支下穿过丝线而不结扎冠状动脉,急性心肌梗死组行左冠状动脉前降支高位永久结扎,晚期再灌注组在高位结扎左冠状动脉前降支6 h后松解结扎线予以再灌注6 h。共有23只犬模型制作成功。各组犬均于术后12 h处死,采集心肌标本。使用TUNEL法检测心肌细胞凋亡,免疫组化染色和Western blotting蛋白印迹分析Bcl-2、Bax在心肌细胞中表达情况。结果:晚期再灌注组心肌细胞凋亡数较急性心肌梗死组明显减少(P<0.05),但两组心肌细胞凋亡数均高于假手术组(P<0.01)。与假手术组相比,急性心肌梗死组和晚期再灌注组Bcl-2蛋白的表达均升高(P<0.01),其中在晚期再灌注组的表达略多于急性心肌梗死组,但无显著差异(P>0.05)。Bax蛋白在晚期再灌注组的表达高于假手术组(P<0.01),但低于急性心肌梗死组(P<0.05)。结论:急性心肌梗死后晚期再灌注可以减少梗死周边缺血区心肌细胞凋亡,其机制可能与心肌细胞表达Bax蛋白减少有关。AIM: To study the effect of late reperfusion on apoptotic cardiomyocytes in the risk area of acute myocardial infarctin in dogs. METHODS: The experiment was divided into three groups: sham operation group, acute myocardial infarction (AMI) group, and late reperfusion (LR) group. Apart from sham operation group, the other two groups were subjected to left anterior descending branch of coronary artery ligation. The acute myocardial infarction group was only subjected to ligation for 12 hours, late reperfusion group was subjected to ligation for 6 hours following by 6 hours of reperfusion. The cardiomyocyte apoptosis was measured by TUNEL assay. Immunohistochemistry and Western blotting analysis were used to detect the expression of Bcl - 2 and Bax protein. RESULTS. The number of apoptotic cardiomyocytes in late reperfusion group was much less than acute myocardial infarction group ( P 〈 0. 05 ), and increased significantily as compared with sham operation group ( P 〈 0. 01 ). The expression of Bcl - 2 protein was enhanced gently in late reperfusion group in contrast to acute myocardial infarction group, but no significant difference in the two groups ( P 〉 0. 05 ) was observed, although it was much more in the two groups than that in sham operation group ( P 〈 0. 01 ). The expression of Bax protein in late reperfusion group was much higher than that in sham operation group (P 〈 0.01 ), and was lower than that in acute myocardial infarction group (P 〈 0.05 ). CONCLUSION: Late reperfusion reduces cardiomyocyte apoptosis in the risk area of acute myocardial infarction. The mechanism may be that late reperfusion can decrease the expression of Bax protein.
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