Neuroprotective effect of asiatic acid against spinal cord injury in rats.

Life Sci

Department of Orthopedics, Hangzhou First People's Hospital, Nanjing Medical University, No. 261 Huansha Road, Shangcheng District, Hangzhou 310006, China. Electronic address:

Published: July 2016

AI Article Synopsis

  • The study explored the effects of asiatic acid (AA) on spinal cord injury (SCI) in rats, focusing on its therapeutic benefits and mechanisms of action.
  • AA treatment improved motor function and reduced inflammation, oxidative stress, and pro-inflammatory cytokine levels in SCI rats.
  • The findings suggest that AA protects against SCI by activating certain protective pathways (Nrf2 and HO-1) and inhibiting harmful processes (ROS and NLRP3 inflammasome), indicating its potential as a treatment option.

Article 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.

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Source
http://dx.doi.org/10.1016/j.lfs.2016.05.004DOI Listing

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