中文摘要：

本文旨在观察尾部悬吊模拟失重大鼠心肌钙蛋白酶（calpain）与钙蛋白酶抑素（calpastatin）表达的变化,以探讨心肌肌钙蛋白抑制亚基（cardiac troponin I,cTnI）降解的可能机制。采用尾部悬吊模拟失重大鼠模型,Western blotting技术观测心肌calpain-1、calpain-2与calpastatin的表达;PD150606抑制calpain活性,分析cTnI降解程度的变化。结果显示：与同步对照组相比,悬吊2周与4周组大鼠心肌calpastatin表达呈显著性降低（P〈0.05）,calpain-1表达未改变,calpain-2表达略有降低;但是,心肌calpain-1/calpastatin及calpain-2/calpastatin的比值在悬吊2周与4周组明显增高（P〈0.05,P〈0.01）。悬吊4周组cTnI降解显著高于对照组（P〈0.01）;然而,用calpain非特异性抑制剂PD150606处理后,对照组及悬吊组cTnI的降解均被显著抑制（P〈0.01）。这些结果提示模拟失重大鼠心肌calpain活性增高可能增加cTnI的降解。

英文摘要：

The aim of the present study was to investigate the expressions of calpain and calpastatin in the myocardium of simulated weightlessness rats,and to elucidate the underlying mechanism of cardiac troponin I（cTnI） degradations.Tail-suspended（SUS） rats were used as a simulated weightlessness model on the ground.The myocardium of rats was homogenized,and the expressions of calpain-1,calpain-2,calpastatin and cTnI were analyzed by Western blotting technique.Calpastatin expression was significantly decreased in 2and 4-week SUS groups compared with that in the synchronous controls（P0.05）.Calpain-2 expression was slightly decreased,whereas calpain-1 expression was unaltered in SUS groups.However,calpain-1/calpastatin and calpain-2/calpastatin ratios were increased after tailsuspension,being significantly higher in 2-and 4-week SUS groups than those in the synchronous controls（P0.05,P0.01）.Cardiac TnI degradation was significantly increased after tail-suspension（P0.01）,but cTnI degradation in both SUS and control groups was significantly inhibited by a non-specific inhibitor of calpain,PD150606（P0.01）.These results suggest that an increase in calpain activity may enhance cTnI degradation in the myocardium of tail-suspended rats.