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肌纤维内肌质网钙漏可能诱发肌钙蛋白抑制亚基降解

李全, 王云英, 李辉, 焦博, 余志斌^*

第四军医大学航空航天医学教育部重点实验室，航空航天生理教研室，西安 710032

摘要

本文以肌钙蛋白抑制亚基(troponin I subunit, TnI)作为肌节蛋白降解的分子标记，探讨舒张期肌纤维内Ca2+ 浓度升 高与肌原纤维降解的关系。采用在收缩期增加肌质网(sarcoplasmic reticulum, SR)钙离子释放通道开放机率的caffeine，以及 在舒张期引起SR 钙离子释放通道钙漏的H2O2，灌流大鼠离体比目鱼肌，以Western blot 技术检测TnI 表达水平，并比较 其降解程度。结果显示，离体比目鱼肌肌条在40 min 无钙Krebs 液灌流期间，静息张力未见明显改变，发展张力缓慢降 低，TnI 未发生降解。用低浓度caffeine (1 与5 mmol/L)灌流肌条，静息张力仅在疲劳收缩期间短暂升高，对肌条疲劳程 度与疲劳后的恢复速率均无显著性影响，灌流后肌条的TnI 未发生降解；高浓度caffeine (10 mmol/L)灌流使静息张力持续 升高，肌条易发生疲劳，且疲劳收缩后肌条的发展张力不能恢复，TnI 发生明显降解。H2O2 灌流对肌条疲劳程度没有明 显影响，疲劳收缩后发展张力呈迅速恢复后较快下降，静息张力持续增加，且呈浓度依赖性。用1 mmol/L H2O2 灌流肌 条，TnI 未发生降解，用5 与10 mmol/L H2O2 灌流肌条时，TnI 降解程度随浓度增大而增加。由于肌条静息张力与舒张 期间肌纤维内Ca2+ 浓度密切相关，以上结果提示，舒张期SR 钙离子释放通道钙漏增加，可能引起肌纤维TnI 降解。

关键词： 肌钙蛋白抑制亚基; 静息张力; 发展张力; 降解

分类号：R337.2

[Calcium leak of sarcoplasmic reticulum induces degradation of troponin I in skeletal muscle fibers.] [Ariticle in Chinese]

LI Quan, WANG Yun-Ying, LI Hui, JIAO Bo, YU Zhi-Bin

Key Laboratory of Aerospace Medicine, Ministry of Education； Department of Aerospace Physiology, the Fourth Military Medical University, Xi'an 710032, China

Abstract

The troponin I subunit (TnI) was used as a molecular marker to explore the relationship between the resting intracellular Ca2+ concentration and myofibril degradation in muscle fibers. The isolated soleus muscle strips of rats were treated by caffeine and H2O2. Caffeine is an opener to increase the calcium release channel open probability of sarcoplasmic reticulum (SR) in contraction phase. H2O2 induces a calcium leak of SR calcium release channel in relaxation phase. The expression and degradation of TnI were detected by Western blot. The resting tension of tetanic contraction and expression of TnI were not changed, but the developed tension was lowered in isolated soleus muscle strips during 40 min of calcium-free Krebs perfusion. Low concentrations of caffeine (1 and 5 mmol/L) perfusion induced a transient increase in resting tension during fatigue period, but did not alter the extent of fatigue, recovery rate after fatigue and expression of TnI in muscle strips. High concentration of caffeine (10 mmol/L) perfusion induced a progressive increase in resting tension, a higher rate of fatigue and a decrease in recovery rate after fatigue in muscle strips. There was a detectable degradation of TnI in soleus after 10 mmol/L caffeine treatment. H2O2 perfusion facilitated a progressive increase in resting tension in a dosedependent manner, but did not influence the fatigue rate of tetanic contraction. The recovery rate after fatigue showed a quick resumption before decline during H2O2 perfusion. Degradation of TnI occurred in 5 and 10 mmol/L H2O2-treated soleus muscles. Since resting tension is dependent on intracellular Ca2+ concentration, the above-mentioned results suggest that SR Ca2+ leakage in relaxation phase may induce a degradation of TnI in skeletal muscle fibers.

Key words: troponin I; resting tension; developed tension; degradation

收稿日期：2008-12-01　　录用日期：2009-03-31

通讯作者：余志斌　　E-mail: yuzhib@fmmu.edu.cn

引用本文：

李全, 王云英, 李辉, 焦博, 余志斌. 肌纤维内肌质网钙漏可能诱发肌钙蛋白抑制亚基降解[J]. 生理学报 2009; 61 (3): 223-229.

LI Quan, WANG Yun-Ying, LI Hui, JIAO Bo, YU Zhi-Bin. [Calcium leak of sarcoplasmic reticulum induces degradation of troponin I in skeletal muscle fibers.] [Ariticle in Chinese] . Acta Physiol Sin 2009; 61 (3): 223-229 (in Chinese with English abstract).