Okamoto T, Kubota N, Takahata K, Takahashi T, Goshima K, Kishi T
Department of Biochemistry, Faculty of Pharmaceutical Sciences, Kobe Gakuin University, Japan.
Biochem Biophys Res Commun. 1995 Nov 22;216(3):1006-12. doi: 10.1006/bbrc.1995.2720.
The protective effect of coenzyme Q10 (CoQ10) on continuous electric field stimulation-induced muscular injury was investigated in cultured cells established from neonatal rat femoral muscles. After cultivation for 9 days, skeletal muscle cells contracted and relaxed rhythmically for 4 hr in response to continuous electric field stimulation (power, 5 V; duration, 5 msec; amplitude, 3 Hz). After the onset of the stimulation, lactate and lactate dehydrogenase (LDH) release and intracellular Ca2+ contents ([Ca2+]i) at relaxation increased gradually. In contrast, the intracellular ATP contents decreased. The addition of 5 microM CoQ10, but not alpha-tocopherol and radical scavengers, to the culture medium protected the cells against these biochemical changes after the stimulation. Verapamil, an inhibitor of Ca2+ channels, also attenuated the increase in [Ca2+]i at relaxation and LDH. These results suggested that one of the causal mechanisms of muscular injury is an increase in [Ca2+]i due to the excess entry of extracellular Ca2+, and that CoQ10 can protect skeletal muscle cells against such undesirable biochemical changes.
在新生大鼠股四头肌来源的培养细胞中，研究了辅酶Q10（CoQ10）对连续电场刺激诱导的肌肉损伤的保护作用。培养9天后，骨骼肌细胞在连续电场刺激（功率5V；持续时间5毫秒；幅度3Hz）下有节奏地收缩和舒张4小时。刺激开始后，舒张期乳酸和乳酸脱氢酶（LDH）释放以及细胞内Ca2+含量（[Ca2+]i）逐渐增加。相反，细胞内ATP含量降低。向培养基中添加5μM CoQ10可保护细胞免受刺激后的这些生化变化影响，而α-生育酚和自由基清除剂则无此作用。钙通道抑制剂维拉帕米也可减弱舒张期[Ca2+]i和LDH的增加。这些结果表明，肌肉损伤的一个因果机制是细胞外Ca2+过度内流导致[Ca2+]i增加，并且CoQ10可保护骨骼肌细胞免受此类不良生化变化的影响。
