Abstract
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.
Highlights
Facial nerve injury combined with the loss of facial expression is a health problem that can significantly deteriorate quality of life (Yasui et al 2016)
The Nrf2 protein levels showed a similar trend. These results indicated that the activation of PI3K/Akt signaling contributed to photobiomodulation-treated facial nerve regeneration (Fig. 7A–F)
The levels of Akt phosphorylation were slightly increased after PNI, and these levels were even higher after PNI rats received photobiomodulation treatment, which was confirmed by the p -Akt/Akt ratio. These results suggest that photobiomodulation in 250mW induces mitochondrial-dependent apoptosis by down-regulation of PI3K/Akt signaling in the rat facial nerve in vivo
Summary
Facial nerve injury combined with the loss of facial expression is a health problem that can significantly deteriorate quality of life (Yasui et al 2016). Such a condition can seriously hinder the verbal communication conveyed by facial expressions that are considered essential to social relationships. Schwann cells (SCs) have an essential role in axon remyelination. SCs can be immediately activated and dedifferentiated during PNS injury to repair the cells, which subsequently stimulates the severed axons to promote axon regeneration (Hou et al 2018; Wang et al 2018; Mao et al 2018; Quintes and Brinkmann 2017)
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