【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);(4)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。更多还原

【Abstract】 Objective To investigate the effects of μ-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.Western blot was used to detect the expression of μ-Calpain,apoptosis inducing factor(AIF) and Bid in rat heart.Results(1)During the I/R protocol,the 76 kDa size of fragment,which was active fragment of μ-Calpain,significantly increased.At the same time,the expression of both AIF in the nuclear and Bid in the cardiomyocytes also increased.(2)Inhibition of μ-Calpain reduced the apoptosis rate from(36.0±4.9)% to(21.0±5.3) %,(P<0.05 vs.I/R group).(3)Inhibition of μ-Calpain reduced the expression of Bid and adjusted the translocation of AIF from mitochondria to the nucleus.Conclusion The increased μ-Calpain can regulate cardiomyocytes apoptosis via AIF and Bid in rat heart I/R injury.更多还原