【摘要】 运动人体科学界、运动医学界普遍认为炎症诱导肌卫星细胞激活的机制是运动性骨骼肌适应的最重要机制。运动肌会因机械损伤、缺血/再灌注、钙离子升高尤其牵拉激活型Ca2+通道激活导致的Ca2+升高,产生肿瘤坏死因子-α(tumor necrosis factor,TNF-α)、白细胞介素-1β(interleukin-1β,IL-1β)、白细胞介素-8(interleukin-8,IL-8)等各种促炎症因子。这些细胞因子以内皮细胞为媒介将白细胞尤其是中性粒细胞由血液引向骨骼肌组织导致炎症发生。一定范围内或一定程度的炎症反应过程中,炎症造成的缺氧及炎症募集的ED2+巨噬细胞产生的成纤生长因子、胰岛素样生长因子-1会激活卫星,随着卫星细胞内各种肌源性调节因子的程序性合成,卫星细胞并从G0期重返细胞周期,进行细胞的增殖,既实现卫星细胞的自我更新、维持,又有序地进行细胞分化、同损伤肌细胞融合,最终完成骨骼肌的正常生长、损伤肌肉的修复及再生。更多还原

【Abstract】 It is acknowledged in the fields of Sports Medicine and Human Movement Science that the mechanism through which inflammation in skeletal muscles activates satellite cells is the most important one. Contracting muscles,because of mechanic injury,ischemia and reperfusion,Ca2 +going up associated with the stretch-activated calcium channels,produce some kinds of cytokines such as tumor necrosis factor- α,interleukin- 1β,interleukin- 8 and other pro-inflammatory ones. These cytokines,with the endothelia cells as media,lead white blood cells out of the blood and to the damaged tissues,which can give rise to inflammation. Within some extent of inflammation,lack of oxygen and all kinds of cytokines produced by ED2 +macrophages can stimulate the satellite cells,making it leave G0 phase for mitosis,with MRFs production step by step,fulfilling the self-renewal,selfmaintenance,skeletal normal growth,repair and regeneration of injured skeletal muscles.更多还原