吡格列酮对缺氧复氧心肌细胞损伤的保护作用及对蛋白激酶C表达的影响  

Effect of pioglitazone on hypoxia/reoxygenation injury and protein kinase C expression in neonatal rat cardiomyocytes

作　　者：朱启伟[1] 王浩[1] 张今尧[1] 叶平[1] 骆雷鸣[1] 

机构地区：[1]解放军总医院南楼心血管内二科,北京100853

出　　处：《南方医科大学学报》2011年第11期1819-1823,共5页Journal of Southern Medical University

基　　金：国家自然科学基金(30872713);北京市自然科学基金(7082083)~~

摘　　要：目的观察吡格列酮对缺氧复氧后新生大鼠心肌细胞的保护作用及对蛋白激酶C(PKC)表达的影响。方法原代培养新生SD大鼠心肌细胞,予吡格列酮、GW9662等预处理24 h后建立缺氧复氧模型。Hoechst33258染色法检测心肌细胞凋亡,免疫印迹方法检测PKC表达。结果缺氧复氧后心肌细胞早期凋亡率升高(由溶媒对照组的(0.20±0.03)%增加至(12.22±1.45)%,P<0.05);吡格列酮减少心肌细胞凋亡(8.32±0.89)%,而吡格列酮抗心肌细胞凋亡的作用可以被GW9662阻断(12.46±1.62)%,P<0.05;与单纯缺氧复氧组相比,吡格列酮不增加PKC(1.033±0.026,P>0.05)表达。结论吡格列酮预处理减轻心肌细胞缺氧复氧后损伤,这种作用部分通过激活PPARγ途径实现;吡格列酮预处理不增加PKC表达。Objective To observe the effect of pioglitazone on hypoxia/reoxygenation injury and the expression of protein kinase C（PKC） in neonatal rat cardiomyocytes.Methods Neonatal Sprague-Dawley rat cardiomyocytes in primary culture were treated with pioglitazone or GW9662 for 24 h prior to hypoxia/reoxygenation injury.Cardiomyocyte apoptosis was evaluated with Hoechst33258 staining and the expression of PKC was detected using Western blotting.Results In the early stage of hypoxia/reoxygenation injury,the apoptosis rates of the cardiomyocytes increased significantly from（0.20±0.03）% of the control level to（12.22±1.45）%（P0.05）.Pretreatment with pioglitazone significantly lowered the apoptosis rate of the cardiomyocytes with hypoxia/reoxygenation injury to（8.32±0.89）%,and this effect was antagonized by GW9662,a specific blocker of peroxisome proliferators activated receptors γ（PPARγ）.Pioglitazone did not cause increased expression of PKC in the cardiomyocytes.Conclusion Pioglitazone can ameliorate neonatal rat cardiomyocyte injury induced by hypoxia/reoxygenation partially by activating PPARγ and does not increase the expression of PKC in the cells.

关 键 词：过氧化物酶体增殖物激活型受体Γ 缺血再灌注损伤 缺血预适应 

分 类 号：R965[医药卫生—药理学]