面神经功能障碍是一种常见的临床状况,会导致受影响个体的毁容和情绪困扰。本研究旨在评估光生物调节是否可以促进破碎的面神经的再生,并试图探讨神经保护功能的潜在机制和治疗靶点。在大鼠压碎损伤期间,光生物调节的各种参数分别分配给面神经和雪旺氏细胞(SC)。轴突再生,功能结果,和SC细胞凋亡,扩散,和潜在的作用机制通过形态学评估,组织病理学,和功能评估,流式细胞术,西方印迹,实时PCR,和IncuCyte。结果表明,光生物调节促进轴突再生和功能恢复,还促进了扩散,抑制细胞凋亡,这两个都被认为是250mW组最有效的参数。此外,光生物调节(500mW)的神经保护作用可能与氧化应激通过激活PI3K/Akt信号通路诱导的SC凋亡有关。我们的结果表明,光生物调节显着促进轴突再生,功能恢复,和面部核的再生,其机制与PI3K/Akt信号通路的上调有关。这些发现为光生物调节作为周围神经损伤的替代治疗策略提供了明确的实验证据。
Facial nerve dysfunction is a common clinical condition that leads to disfigurement and emotional distress in the affected individuals. This study aimed to evaluate whether photobiomodulation can enhance regeneration of crushed facial nerves and attempt to investigate the possible underlying mechanism of neuroprotective function and therapeutic target. Various parameters of photobiomodulation were assigned to the facial nerves and Schwann cells (SCs) separately during crushed injury in rats. Axonal regeneration, functional outcomes, and SC apoptosis, proliferation, and underlying mechanisms of action were evaluated by morphological, histopathological, and functional assessments, flow cytometry, western blotting, real-time PCR, and IncuCyte. The results showed that photobiomodulation improved axonal regeneration and functional recovery, and also promoted proliferation, and inhibited apoptosis of SCs, both of these were considered as the most effective parameters in 250mW group. In addition, the neuroprotective effects of photobiomodulation (500mW) were likely associated with oxidative stress-induced SC apoptosis via activation of the PI3K/Akt signaling pathway. Our results revealed that photobiomodulation significantly promoted axonal regeneration, functional recovery, and regeneration of the facial nucleus, and its mechanism was related to the up-regulation of the PI3K/Akt signaling pathway. These findings provide clear experimental evidence of photobiomodulation as an alternative therapeutic strategy for peripheral nerve damage.