Low-intensity laser irradiation improves the mitochondrial dysfunction of C2C12 induced by electrical stimulation

被引:66
作者
Xu, Xiaoyang [1 ]
Zhao, Xiufeng [1 ]
Liu, Timon Cheng-Yi [1 ,2 ]
Pan, Hongying [1 ]
机构
[1] S China Normal Univ, Coll Sports Sci, Lab Laser Sports Med, Guangzhou 516031, Guangdong, Peoples R China
[2] S China Normal Univ, Minist Educ, Key Lab Laser Life Sci, Guangzhou 516031, Guangdong, Peoples R China
关键词
D O I
10.1089/pho.2007.2125
中图分类号
R61 [外科手术学];
学科分类号
摘要
Objective: We investigated the effects of electrical stimulation and low-intensity laser (LIL) energy on the mitochondrial function of cultured C2C12 myotubes in order to find a dosage that could be used to improve the function of mitochondria, and then rehabilitate exercise-induced damage and fatigue. Background Data: Many other studies in the past demonstrated that LIL had a cytoprotective effect, and a recent study also found that LIL could reduce muscular fatigue during tetanic contractions in rats. Methods: Cultured C2C12 myotubes were subjected to electrical stimulation or/and LIL irradiation at various intensities. Reactive oxygen species (ROS) were detected with a fluorescent probe (DCFH-DA) and mitochondrial function was assessed with an MTT assay. Results: The results showed that electrical stimulation at 20 ms, 5 Hz, and 45 V for 75 min can induce mitochondrial dysfunction in cultured C2C12 myotubes. Electrical stimulation-induced mitochondrial dysfunction was improved, but degeneration occurred with LIL at doses of 0.33-8.22 and 11.22-14.16 J/cm(2), respectively, and these changes were markedly increased with LIL at 0.33 and 1.34 J/cm(2), respectively. Conclusions: We conclude that treatment of myotubes with the proper dosage of LIL irradiation significantly diminished production of ROS and restored mitochondrial function, and this may provide a foundation for the use of photobiomodulation to treat exercise-induced mitochondrial dysfunction or skeletal muscular fatigue.
引用
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页码:197 / 202
页数:6
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