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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