Aging
Navigate
Research Paper|Volume 14, Issue 6|pp 2607—2627

2, 3, 5, 4’-tetrahydroxystilbene-2-O-beta-D-glucoside protects against neuronal cell death and traumatic brain injury-induced pathophysiology

Yu-Hsin Chen1,2, Yen-Chou Chen1, Yu-Tang Chin3, Ching-Chiung Wang4, Ling-Ling Hwang1,2, Liang-Yo Yang5,6, Dah-Yuu Lu7,8
  • 1Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan
  • 2Department of Physiology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan
  • 3School of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei 11031, Taiwan
  • 4School of Pharmacy, College of Pharmacy, Taipei Medical University, Taipei 11031, Taiwan
  • 5Department of Physiology, School of Medicine, College of Medicine, China Medical University, Taichung 404333, Taiwan
  • 6Laboratory of Neural Repair, Department of Medical Research, China Medical University Hospital, Taichung 40447, Taiwan
  • 7Department of Pharmacology, School of Medicine, College of Medicine, China Medical University, Taichung 404333, Taiwan
  • 8Department of Photonics and Communication Engineering, Asia University, Taichung 41354, Taiwan
Received: October 28, 2021Accepted: March 1, 2022Published: March 21, 2022

Copyright: © 2022 Chen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Traumatic brain injury (TBI) is a global health issue that affects at least 10 million people per year. Neuronal cell death and brain injury after TBI, including apoptosis, inflammation, and excitotoxicity, have led to detrimental effects in TBI. 2, 3, 5, 4’-tetrahydroxystilbene-2-O-beta-D-glucoside (THSG), a water-soluble compound extracted from the Chinese herb Polygonum multiflorum, has been shown to exert various biological functions. However, the effects of THSG on TBI is still poorly understood. THSG reduced L-glutamate-induced DNA fragmentation and protected glial and neuronal cell death after L-glutamate stimulation. Our results also showed that TBI caused significant behavioral deficits in the performance of beam walking, mNSS, and Morris water maze tasks in a mouse model. Importantly, daily administration of THSG (60 mg/kg/day) after TBI for 21 days attenuated the injury severity score, promoted motor coordination, and improved cognitive performance post-TBI. Moreover, administration of THSG also dramatically decreased the brain lesion volume. THSG reduced TBI-induced neuronal apoptosis in the brain cortex 24 h after TBI. Furthermore, THSG increased the number of immature neurons in the subgranular zone (SGZ) of the dentate gyrus (DG) of the hippocampus. Our results demonstrate that THSG exerts neuroprotective effects on glutamate-induced excitotoxicity and glial and neuronal cell death. The present study also demonstrated that THSG effectively protects against TBI-associated motor and cognitive impairment, at least in part, by inhibiting TBI-induced apoptosis and promoting neurogenesis.