刘阳,王瑞元,康红哲.不同时程下[Ca2+]i介导骨骼肌微细损伤与修复的机制及针刺的干预作用[J].北京体育大学学报,2015,38(2):54-60.
不同时程下[Ca2+]i介导骨骼肌微细损伤与修复的机制及针刺的干预作用
Mechanism of [Ca2+]i Inducing Skeletal Muscle Micro-Damage and Repair in Different Time Periods and the Effect of Acupuncture
投稿时间:2014-09-30  
DOI:10.19582/j.cnki.11-3785/g8.2015.02.010
中文关键词:  关键词:肌细胞  离心运动  钙离子  针刺  RyR
英文关键词:Key words: muscle cells  eccentric exercise  Ca2+  acupuncture  RyR
基金项目:基金项目:国家自然科学基金项目(项目批准号:31271277)资助。通信作者:王瑞元。
作者单位
刘阳 北京体育大学北京 100084河北师范大学体育学院河北师范大学人体运动生物信息省级重点实验室河北 石家庄 050024 
王瑞元 北京体育大学北京 100084 
康红哲 河北师范大学体育学院河北师范大学人体运动生物信息省级重点实验室河北 石家庄 050024 
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中文摘要:
      摘要:目的:观察离心运动介导骨骼肌微损伤与修复过程,肌细胞不同微区钙离子浓度变化所起的作用,以及肌浆网钙释放通道兰尼定受体(RyR)的调控信号。方法:114只雄性SD大鼠,分为离心运动(E组,36只)、离心运动+针刺(EA组,36只)、单纯针刺(A组,36只)和安静对照(C组,6只)。E、EA和A组在运动后即刻、6、12、24、48和72h取材,电镜观察结构,能谱分析Z线和H区钙元素,WB观察磷酸二酯酶-4-D3(PDE4D3)和FK506绑定蛋白12(FKBP12)表达。结果:E与EA组Z线附近的钙离子浓度在运动后即刻和恢复期的12-72h呈两次上升趋势,其中EA组第2次上升更早且明显。 1次离心运动不能破坏RyR的稳定性。结论:运动后即刻的[Ca2+]i升高介导导了损伤,而运动后12-72h内的第2次[Ca2+]i升高与组织修复有关,此升高非RyR不稳产生“钙漏”而导致的破坏性“钙超载”。研究价值:本研究发现离心运动过后72h内不同时间段内,钙离子升高具有截然不同的效应,为肌肉损伤和恢复的钙机制研究提供新的方向。
英文摘要:
      Abstract: Objective: This study observed the effect of eccentric exercise on skeletal muscle micro-damage and repair, the effect of Ca2+ concentration in different areas of muscle cells and the regulatory signals of calcium release channel Ryanodine Receptor (RyR) in sarcoplasmic reticulum. Methods: One hundred and fourteen male SD rats were divided into eccentric exercise (E group, n=36), eccentric exercise combined acupuncture (EA group, n=36), simple acupuncture (A, n=36) and control (C group, n=6) groups. Muscle samples of E, EA and A groups were isolated at 0h, 6h, 12h, 24h, 48h, 72h after exercise. Cells microstructure was observed by electron microscope. Ca2+ concentration of Z-line and H-band was analyzed by Energy Dispersive X-ray Spectroscopy (EDS). Expressions of hosphodiestera-4-D3 (PDE4D3) and FK506 binding protein 12 (FKBP12) were tested by Western blotting. Results: Ca2+ concentration in Z-line of E and EA groups rose both at 0h and 12-72 h after exercise, it of EA group rose earlierly and more obviously during12-72h. An acute eccentric exercise could not damage the stability of RyR. Conclusion: The increase of Ca2+ concentration at 0h after exercise induces cell damage, and the increase during 12-72h after exercise is related to cell damage repair, but not induced by “calcium leak” of RyR. Value: This study found that Ca2+ concentration changes differently in different time periods of 0-72h after exercise, which provides a new research direction for calcium mechanism of muscle damage and repair.
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