Gastrodin promotes the regeneration of peripheral nerves by regulating miR-497/BDNF axis

• Published in: BMC complementary and alternative medicine Vol. 22; no. 1; p. 45
• Main Authors: Yongguang, Li, Xiaowei, Wang, Huichao, Yan, Yanxiang, Zhang
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 18.02.2022; BioMed Central; BMC
• Subjects: 3' Untranslated regions; Action potential; Amplitudes; Analysis; Animals; Atrophy; Benzyl Alcohols; Binding sites; Brain research; Brain-derived neurotrophic factor; Brain-Derived Neurotrophic Factor - genetics; Brain-Derived Neurotrophic Factor - metabolism; Brain-Derived Neurotrophic Factor - pharmacology; Catalase; Electrophysiology; Experiments; Fetuses; Gastrodin; Glucosides; Glutathione; Growth factors; Herbal medicine; Hydrogen Peroxide; Laboratory animals; Latency; Malondialdehyde; Medicine, Chinese; MicroRNAs; MicroRNAs - genetics; MicroRNAs - metabolism; miR-497; Muscles; Myelin; Myelin basic protein; Myelin proteins; Nervous system; Oxidative stress; Peripheral nerve injury; Peripheral nerves; Phenolic compounds; Phenols; Phosphorylation; Polymerase chain reaction; Proteins; Rats; Reagents; Refractory period; Regeneration; Reporter gene; Schwann cells; Schwann Cells - metabolism; Sciatic nerve; Superoxide; Superoxide dismutase; Surgery; Western blotting; China; United States > US; Peripheral nerve injury; Brain-derived neurotrophic factor; Gastrodin; miR-497
• ISSN: 2662-7671; 2662-7671; 1472-6882
• DOI: 10.1186/s12906-021-03483-z

Gastrodin (GAS), is a kind of phenolic compound extracted from the traditional Chinese herbal medicine Gastrodia elata Blume (GEB). This study was aimed at probing into the protective effect of GAS on peripheral nerve injury (PNI) and the underlying mechanism. A rat model with PNI was established, followed by intraperitoneal injection of GAS (20 mg/kg/day). Sciatic nerve function index (SFI) was used to analyze the function of sciatic nerve. The amplitude and latency of compound muscle action potential (CMAP) were examined by electrophysiology. Schwann cells (SCs) were isolated from fetal rats and treated with GAS 200 μg/mL, and H O -induced model of oxidative stress injury was established. EdU and Transwell assays were adopted to detect the viability and migration of SCs. Dual-luciferase reporter gene assays were applied to verify the binding site between miR-497 and brain-derived neurotrophic factor (BDNF) 3'UTR. MiR-497 expression was probed by quantitative real-time polymerase chain reaction (qRT-PCR). BDNF, neurofilament-200 (NF-200) and myelin basic protein (MBP) expression levels were detected by Western blotting. Malondialdehyde (MDA) content, superoxide dismutase (SOD) activity, glutathione content (GSH) and catalase (CAT) activity in SCs were also measured. GAS treatment could significantly increase the SFI and amplitude of CMAP, shorten the refractory period, and ameliorate muscle atrophy of the rats with PNI. GAS treatment could markedly restrain miR-497 expression and increase the expression levels of BDNF, NF-200 and MBP in SCs. BDNF was confirmed as the target of miR-497 and BDNF overexpression could reverse the impacts of miR-497 overexpression on the proliferation, migration, and oxidative stress response of SCs. GAS promotes the recovery of PNI via modulating miR-497 / BDNF axis and inhibiting oxidative stress.