Calpain-2活性升高促进模拟失重大鼠恢复期心肌细胞凋亡  

Increased activity of Calpain-2 induces cardiomyocyte apoptosis during recovery period of tail-suspended rats

作　　者：常惠[1] 徐彭涛[1] 李全[1] 圣娟娟[1] 张琳[1] 余志斌[1] 

机构地区：[1]第四军医大学航空航天生理教研室,西安710032

出　　处：《空军总医院学报》2011年第1期33-36,共4页Journal of General Hospital of Air Force,PLA

基　　金：国家自然科学基金(31071044)

摘　　要：目的长期失重/模拟失重恢复初期因心血管功能失调而使循环系统儿茶酚胺浓度代偿性增加,在心肌β-肾上腺素受体敏感性增强的基础上,高浓度儿茶酚胺可能导致心肌细胞凋亡率增加,为保障航天员航天飞行返回地面后的健康,亟待探明心肌细胞凋亡的机制。方法采用尾部悬吊大鼠模型在地面模拟失重。结果本研究发现模拟失重4周大鼠心肌钙蛋白酶Calpain-2活性增加,抑制Calpains活性可防止模拟失重大鼠恢复初期发生心肌细胞凋亡。同时证实β-肾上腺素受体激动剂异丙肾上腺素(ISO)可诱导模拟失重大鼠心肌细胞凋亡,ISO刺激会进一步激活Calpain-2,最终导致心肌细胞凋亡增加。结论这些结果表明:ISO是引起模拟失重大鼠恢复期心肌细胞凋亡的原因之一,Calpain-2参与了模拟失重大鼠恢复初期心肌细胞凋亡过程。Objective The compensatory increase in catecholamine release induced by the dysfunction of cardiovascular system results in the increasing apoptotic rates in the myocardium after returning from a long-term spaceflight or recovering from a simulated weightlessness situation.High β-adrenoreceptor responsiveness in the heart may induce cardiac damage.The mechanism of cardiomyocyte apoptosis has not been elucidated.Methods Weightlessness was simulated by the tail-suspended rat model on the ground.Results Calpain-2 activity of tail-suspended rats in the myocardium showed a marked increase in our study.Cardiomyocyte apoptosis during return from 4 weeks of tail-suspension was blocked by PD150606,an inhibitor of calpains.Also,β-adrenoreceptor agonist isoproterenol（ISO） stimulation induced a higher level of cardiomyocyte apoptosis in the tail-suspended group,activated Calpain-2,and further induced cardiomyocyte apoptosis.Conclusion These results suggest that ISO triggers cardiomyocyte apoptosis during return from 4 weeks of tail-suspension and Calpain-2 plays an important role in this process.

关 键 词：卡配因 细胞凋亡 心肌/细胞学 

分 类 号：R332[医药卫生—人体生理学] R977.3[医药卫生—基础医学]