Modulatory effect of ursolic acid on neurodegenerative activities in oxidative brain injury: An ex vivo study

Natural products-based antioxidants have been well reported for their therapeutic benefits in the treatment and management of neurodegenerative diseases. The neuroprotective effect of ursolic acid (UA) against oxidative injury was investigated in isolated rat brain. Induction of oxidative injury in isolated rat brains with 0.1 mM FeSO₄ led to depleted levels of glutathione, superoxide dismutase, catalase, and ENTPDase activities, with concomitant exacerbation of malondialdehyde and nitric oxide levels, α-chymotrypsin, ATPase, and acetylcholinesterase activities. These levels and activities were significantly reversed following treatment of the brain tissues with UA. Molecular docking studies revealed strong molecular interactions between UA, catalase, and ATPase. Overall, these results indicate the neuroprotective effect of UA against oxidative injury in isolated rat brains as depicted by their ability to mitigate oxidative stress, purinergic, and cholinergic dysfunctions, with concomitant suppression of proteolytic activity. Practical applications: Neurodegenerative diseases are among the common diseases associated with aging and has been implicated as oxidative mediated. Natural products have received increasing recognition in their use as treatment remedy for various oxidative-mediated diseases including neurodegeneration. These natural products include plant secondary metabolites commonly known as phytochemicals. Ursolic acid is a phytochemical usually present in leafy vegetables and fruits. The present study describes the possible therapeutic mechanism of ursolic acid in the amelioration of complications linked to neurodegeneration in oxidative-mediated brain injury. These findings thus give insights into the use of natural products of plant origin in treating and managing neurodegenerative diseases, which may have little or no side effects.