丝氨酸蛋白酶抑制物vaspin对缺氧/复氧诱导的心肌细胞凋亡的影响  

Effects of vaspin on the apoptosis of cardiomyocytes induced by hypoxia/reoxygenation injury

作　　者：张宝伟[1] 王好[1] 沈冬丽 陶艾彬[1] 张国辉[1] 芮涛[1] 

机构地区：[1]江苏大学附属人民医院心内科,江苏镇江212002

出　　处：《江苏大学学报（医学版）》2017年第5期408-411,共4页Journal of Jiangsu University：Medicine Edition

基　　金：镇江市社会发展项目(SH2014043)

摘　　要：目的:探索丝氨酸蛋白酶抑制物vaspin对缺氧/复氧诱导的心肌细胞凋亡的作用及可能的机制。方法:体外分离培养新生乳鼠心肌细胞,设立对照组(正常培养组)、缺氧/复氧组和缺氧/复氧+vaspin组(300 ng/m L预处理)。经不同处理后通过TUNEL染色评估细胞凋亡情况,蛋白质印迹法检测心肌细胞PI3K及Akt表达。结果:缺氧/复氧处理后心肌细胞凋亡增加,心肌细胞内PI3K p100γ、Akt1、Akt及p-Akt的表达水平降低;而在复氧前予以外源性vaspin处理可增加心肌细胞内PI3K p100γ、Akt1、Akt及p-Akt的表达水平(均P<0.05),且降低心肌细胞凋亡比例(P<0.05)。结论:外源性vaspin可通过激活心肌细胞内PI3K/Akt信号通路抑制缺氧/复氧诱导的心肌细胞凋亡。Objective： To investigate the effects and the possible underlying mechanisms of vaspin on the apoptosis of cardiomyocytes induced by hypoxia/ reoxygenation （H/R） injury in vitro. Methods： I-solated rat cardiomyocytes were divided into the following groups ： control group, H/R group, and H/R ＋ vaspin group （300 ng/mL）. The apoptosis of cardiomyocytes were detected by TUNEL method, and the expressions of phosphatidylinositol 3 kinase （PI3K） and Akt in the cardiomyocytes were evaluated by Western blotting. Results ： Hypoxia/reoxygenation injury increased apoptosis, but this effect was protec-ted by vaspin. In addition, vaspin also promoted the expression of PI3K p100γy, Akt1, Akt and p-Akt in the cardiomyocytes treated with hypoxia/ reoxygenation. Conclusion ; Exogenous vaspin could activate the PI3K/Akt signaling pathways in cardiomyocytes and protected the apoptosis of cardiomyocytes induced by hypoxia/reoxygenation injury.

关 键 词：丝氨酸蛋白酶抑制物 缺氧/复氧损伤 心肌细胞 凋亡 

分 类 号：R541[医药卫生—心血管疾病]