Department of Structural and Functional Biology, Institute of Biology, University of Campinas (Unicamp), Campinas, São Paulo, Brazil.
Department of Structural and Functional Biology, Institute of Biology, University of Campinas (Unicamp), Campinas, São Paulo, Brazil.
J Manipulative Physiol Ther. 2022 Feb;45(2):97-103. doi: 10.1016/j.jmpt.2022.03.011. Epub 2022 Jun 24.
The purpose of this study was to investigate whether photobiomodulation (PBM) can protect against and attenuate muscle atrophy owing to complete peripheral nerve lesion in mice by acting on autophagy.
C57BL/10 mice underwent right sciatic nerve transection to induce tibialis anterior muscle atrophy. After 6 hours of denervation, the mice received PBM (wavelength, 830 nm) daily, transcutaneously over the tibialis anterior muscle region for 5 or 14 days. Some mice with sciatic nerve lesion did not receive PBM. Mice that did not have sciatic nerve lesion and PBM were used as controls. After 5 and 14 days, the right tibialis anterior muscle was examined using histomorphometric (cross-sectional area of muscle fibers), Western blot (levels of the autophagy marker LC3), and immunofluorescence analyses (number of LC3 puncta in the muscle fibers).
The cross-sectional area of the tibialis anterior muscle fibers decreased after 5 and 14 days of denervation. PBM protected against muscle fiber atrophy after 5 days of denervation and attenuated muscle fiber atrophy after 14 days of denervation. After 5 days of muscle denervation, autophagy did not change, as demonstrated by the comparable levels of LC3-I/II ratio and LC3 puncta between the controls and the mice with atrophic muscle; PBM did not change this profile. After 14 days of denervation, an increased LC3-I/II ratio suggested an ongoing autophagy, which was not affected by PBM.
PBM attenuated the tibialis anterior muscle atrophy induced by sciatic nerve transection in the mice after at least 5 and 14 days of muscle denervation, without affecting autophagy. The transient protective effect of PBM was observed as early as 5 days after the of complete nerve lesion.
本研究旨在探讨光生物调节(PBM)是否可以通过作用于自噬来预防和减轻小鼠完全周围神经损伤引起的肌肉萎缩。
C57BL/10 小鼠接受右侧坐骨神经横断术以诱导胫骨前肌萎缩。在去神经 6 小时后,小鼠接受 PBM(波长 830nm),每天经皮照射胫骨前肌区域 5 或 14 天。一些坐骨神经损伤的小鼠未接受 PBM。未接受坐骨神经损伤和 PBM 的小鼠作为对照组。在 5 和 14 天后,使用组织形态计量学(肌纤维横截面积)、Western blot(自噬标志物 LC3 水平)和免疫荧光分析(肌纤维中 LC3 斑点数量)检查右侧胫骨前肌。
去神经后 5 和 14 天,胫骨前肌纤维的横截面积减小。PBM 可预防去神经后 5 天的肌肉纤维萎缩,并减轻去神经后 14 天的肌肉纤维萎缩。在肌肉去神经后 5 天,自噬没有变化,对照组和萎缩肌肉的 LC3-I/II 比值和 LC3 斑点数量相当表明了这一点;PBM 没有改变这种情况。在去神经后 14 天,LC3-I/II 比值增加表明持续的自噬,而 PBM 对其没有影响。
PBM 减轻了至少 5 和 14 天肌肉去神经后小鼠坐骨神经横断引起的胫骨前肌萎缩,而不影响自噬。PBM 的短暂保护作用在完全神经损伤后 5 天即可观察到。