Li Xin, Wang Xuan-Kang, Zhu Zhi-Jie, Liang Zhuo-Wen, Li Peng-Hui, Ma Yang-Guang, Ding Tan, Li Kun, Zuo Xiao-Shuang, Ju Cheng, Zhang Zhi-Hao, Song Zhi-Wen, Quan Hui-Lin, Zhang Jia-Wei, Luo Liang, Wang Zhe, Hu Xue-Yu
Department of Orthopedics, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province; 967 Hospital of People's Liberation Army Joint Logistic Support Force, Dalian, Liaoning Province, China.
Department of Orthopedics, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, China.
Neural Regen Res. 2023 Sep;18(9):2005-2010. doi: 10.4103/1673-5374.366491.
Increasing evidence indicates that mitochondrial fission imbalance plays an important role in delayed neuronal cell death. Our previous study found that photobiomodulation improved the motor function of rats with spinal cord injury. However, the precise mechanism remains unclear. To investigate the effect of photobiomodulation on mitochondrial fission imbalance after spinal cord injury, in this study, we treated rat models of spinal cord injury with 60-minute photobiomodulation (810 nm, 150 mW) every day for 14 consecutive days. Transmission electron microscopy results confirmed the swollen and fragmented alterations of mitochondrial morphology in neurons in acute (1 day) and subacute (7 and 14 days) phases. Photobiomodulation alleviated mitochondrial fission imbalance in spinal cord tissue in the subacute phase, reduced neuronal cell death, and improved rat posterior limb motor function in a time-dependent manner. These findings suggest that photobiomodulation targets neuronal mitochondria, alleviates mitochondrial fission imbalance-induced neuronal apoptosis, and thereby promotes the motor function recovery of rats with spinal cord injury.
越来越多的证据表明,线粒体裂变失衡在神经元延迟性细胞死亡中起重要作用。我们之前的研究发现,光生物调节可改善脊髓损伤大鼠的运动功能。然而,确切机制仍不清楚。为了研究光生物调节对脊髓损伤后线粒体裂变失衡的影响,在本研究中,我们对脊髓损伤大鼠模型连续14天每天进行60分钟的光生物调节(810纳米,150毫瓦)。透射电子显微镜结果证实,在急性(1天)和亚急性(7天和14天)阶段,神经元中线粒体形态出现肿胀和碎片化改变。光生物调节在亚急性期减轻了脊髓组织中的线粒体裂变失衡,减少了神经元细胞死亡,并以时间依赖性方式改善了大鼠后肢运动功能。这些发现表明,光生物调节作用于神经元线粒体,减轻线粒体裂变失衡诱导的神经元凋亡,从而促进脊髓损伤大鼠的运动功能恢复。