大鼠心脏缺血再灌注损伤中μ-钙蛋白酶通过凋亡诱导因子和Bid调节心肌细胞凋亡  

μ-Calpain adjust cardiomyocytes apoptosis via apoptosis inducing factor and Bid in rat heart ischemia/reperfusion injury

作　　者：宋兆峰[1] 陈东育[2] 王秀 杜波[1] SONG Zhao-feng;CHEN Dong-yu;WANG Xiu;DU Bo(Department of Cardiology,Tai'an Central Hospital,Tai'an 271000,China;Department of Rheumatic Immunity,Tai'an Central Hospital,Tai'an 271000,China;Department of Cardiology,Tai'an First People's Hospital Affiliated to Shandong First Medical University,Tai'an 271000,China)

机构地区：[1]泰安市中心医院心内科,山东省泰安市271000 [2]泰安市中心医院风湿免疫科,山东省泰安市271000 [3]山东第一医科大学附属泰安第一人民医院心内二科

出　　处：《中国心血管病研究》2020年第11期1015-1018,共4页Chinese Journal of Cardiovascular Research

基　　金：山东省自然科学基金(ZR2014HL008);山东省医药卫生科技发展计划(2015WS0116)。

摘　　要：目的探讨μ-钙蛋白酶(μ-Calpain)在大鼠的心脏缺血/再灌注(ischemia/reperfusion,I/R)损伤中所发挥的作用及其调控机制.方法将48只大鼠随机分为四组:I/R组、I/R+MDL-28170、I/R+二甲基亚砜(DMSO)组和对照组,分别测定在I/R前后大鼠心肌中μ-Calpain、凋亡诱导因子(apoptosis inducing factor,AIF)和Bid的表达以及各组大鼠的心肌细胞凋亡率.结果①相对分子质量76 kDa的μ-Calpain为μ-Calpain的活性片段,在I/R的过程中,其表达明显增加,同时大鼠细胞核中的AIF和心肌细胞中Bid的表达亦明显增加;②抑制μ-Calpain的活性可使心肌细胞凋亡率从(36.0±4.9)%降至(21.0±5.3)%(P<0.05);③应用μ-Calpain的抑制剂MDL-28170抑制μ-Calpain后能够减少AIF从心肌细胞线粒体向细胞核的转移,同时能够减少Bid的表达.结论μ-Calpain能够在大鼠心脏I/R损伤中被激活,被激活后的μ-Calpain能通过调节AIF从线粒体到细胞核的转移和Bid的表达调控心肌细胞的凋亡.Objective To investigate the efects ofμ-Calpain on cardiomyocytes apoptosis in rat heart ischemia/reperfusion(I/R)injury.Methods 48 rats were divided into 4 groups randomly.The apoptosis of the cardiomyocytes was detected in different group of the rats.Westermn blot was used to detect the expression ofμ-Calpain,apoptosis inducing factor(AIF)and Bid in rat hearl.Results(1)During the I/R protocol,the 76 kDa size of fragment,which was active firagment ofμ-Calpain.signifcantly increased.At the same time,the expression of both AIF in the nuclear and Bid in the cardiomyocytes also increased.(2)Inhibition ofμ-Calpain reduced the apoptosis rate from(36.0+4.9)%to(21.0+5.3)%(P<0.05 vs.I/R group).(3)Inhibition ofμ-Calpain reduced the expression of Bid and adjusted the translocation of AIF from mitochondria to the nucleus.Conclusion The increasedμ-Calpain can regulate cardiomyocytes apoptosis via AIF and Bid in rat heart I/R injury.

关 键 词：钙蛋白酶 心脏 缺血/再灌注 细胞凋亡 

分 类 号：Q95-33[生物学—动物学] R542.2[医药卫生—心血管疾病]