Edaravone Dexborneol facilitates peripheral nerve regeneration through suppressing oxidative damage and autophagy flow
CHEN Jinghao, LOU Chenghao, WEI Shengzhe, LU Yingfeng, YU Fangzheng, WANG Jian.
1.Department of Wound Repair, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, China; 2.Department of Hand Surgery and Peripheral Neurosurgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, China; 3.School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou 325035, China
Abstract：Objective: To investigate the role of Edaravone Dexborneol (C-EDA) in regulating oxidative stress and autophagy flow in peripheral nerve injury (PNI). Methods: PNI model was established by moderate crush injury to the sciatic nerve with a vascular clamp. The rats were randomly divided into Sham group, PNI group, C-EDA group (C-EDA+PNI), and 3MA group [PNI+C-EDA+3MA (3-methyladenine)]. At the 4th week after operation, gait imprinting, neuroelectrophysiological detection, wet weight measurement of gastnemius muscle, HE staining of muscle tissue and NF-200+MBP immunofluorescence staining of nerve tissue were performed in all rats. The levels of oxidative stress-related proteins Nrf2 and HO-1, autophagy related proteins LC3 II/LC3 I and p62 (autophagy substrate protein, reflecting whether autophagy flow was unobstructed), apoptosisrelated proteins Bcl-2 and Bax were detected by Western blot. Results: Compared with the PNI group, C-EDA+ PNI improved the posterior foot deformity, improved nerve conduction function and reduced gastrocnemius atrophy. 3MA reversed the effect of C-EDA on improving neurological function after injury. Compared with PNI group, C-EDA up-regulated the expressions of oxidative stress-related proteins Nrf2, HO-1 and anti-apoptotic protein Bcl-2, and down-regulated the expressions of autophagy substrate protein p62 and pro-apoptotic protein Bax (P<0.05). Conclusion: Our study confirms that C-EDA can unobstruct autophagy flow, playing a role in improving neural structure repair and functional recovery after PNI. Therefore, it is a potentially effective method for the treatment of PNI.
