Neuroprotective effect of asiatic acid against spinal cord injury in rats

  • Life Sci. 2016 Jul 15:157:45-51. doi: 10.1016/j.lfs.2016.05.004.
Wu Jiang  1 ,  Maoqiang Li  1 ,  Fan He  1 ,  Zhenyu Bian  1 ,  Qifang He  2 ,  Xuepeng Wang  1 ,  Wangxiang Yao  1 ,  Liulong Zhu  3
Affiliations
  • 1. Department of Orthopedics, Hangzhou First People's Hospital, Nanjing Medical University, No. 261 Huansha Road, Shangcheng District, Hangzhou 310006, China.
  • 2. Department of Orthopedics, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, No. 600 Yi Shan Road, Shanghai 200233, China.
  • 3. Department of Orthopedics, Hangzhou First People's Hospital, Nanjing Medical University, No. 261 Huansha Road, Shangcheng District, Hangzhou 310006, China. Electronic address: [email protected].
PMID: 27153777 DOI: 10.1016/j.lfs.2016.05.004
Abstract

Aims: The present study investigated the therapeutic efficacy of asiatic acid (AA) on spinal cord injury (SCI) as well as the underlying mechanisms.

Main methods: Sprague-Dawley rats (n=150) were randomly assigned to five groups: sham, SCI, SCI+methylprednisolone (30mg/kg), SCI+AA (30mg/kg), and SCI+AA (75mg/kg). Motor function, histological changes, neutrophil infiltration, proinflammatory cytokine production, and oxidative stress as well as nuclear factor erythroid 2-related factor (Nrf)2, heme oxygenase (HO)-1, and nucleotide-binding domain-like receptor protein (NLRP)3 levels were evaluated.

Key findings: AA treatment increased Basso, Beattie and Bresnahan scores and inclined plane test scores that were reduced by SCI. In addition, AA suppressed myeloperoxidase activity and reduced the levels of interleukin-1β, -18, and -6 and tumor necrosis factor-α as well as Reactive Oxygen Species (ROS), H2O2, and malondialdehyde levels while increasing superoxide dismutase activity and glutathione production. AA treatment results in the upregulation in Nrf2/HO-1 levels and downregulation of NLRP3 inflammasome protein expression in SC tissue.

Significance: AA protects against SCI via suppression of inflammation and oxidative stress. The underlying mechanism likely involves activation of Nrf2 and HO-1 and inhibition of ROS and the NLRP3 inflammasome pathway. AA has therapeutic potential for SCI treatment.

Keywords
Asiatic acid; Inflammation; NLRP3 inflammasome; Nrf2; Oxidative stress; Spinal cord injury.
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