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.

中文翻译：

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光生物调节通过调节脊髓损伤亚急性期的线粒体裂变失衡来提供神经保护。

越来越多的证据表明，线粒体分裂失衡在延迟神经元细胞死亡中起着重要作用。我们之前的研究发现，光生物调节改善了脊髓损伤大鼠的运动功能。然而，确切的机制仍不清楚。为了研究光生物调节对脊髓损伤后线粒体分裂失衡的影响，在这项研究中，我们连续 14 天每天用 60 分钟光生物调节（810 nm，150 mW）治疗脊髓损伤大鼠模型。透射电子显微镜结果证实了急性（1 天）和亚急性（7 和 14 天）阶段神经元线粒体形态的肿胀和碎片化改变。光生物调节减轻了亚急性期脊髓组织中的线粒体裂变失衡，减少了神经元细胞死亡，并以时间依赖的方式改善大鼠后肢运动功能。这些发现表明，光生物调节以神经元线粒体为靶点，减轻线粒体分裂失衡引起的神经元凋亡，从而促进脊髓损伤大鼠运动功能的恢复。