Curcumin Ameliorates Sodium Valproate Induced Neurotoxicity through Suppressing Oxidative Stress and Preventing Mitochondrial Impairments

Abstract

Background and purpose: Curcumin is a natural polyphenolic compound in turmeric (Curcuma longa). Curcumin has potent free radical scavenger and antioxidant properties that could significantly reduce oxidative damage. Oxidative stress and mitochondrial dysfunction contribute to valproate sodium induced tissue damage. This study investigated the protective effects of curcumin against valproate sodium induced oxidative stress and mitochondrial toxicity in brain of rats. Materials and methods: Male rats were exposed to sodium valproate (500 mg/kg/day, i.p.) alone, or in combination with different doses of curcumin (25, 50, and 100 mg/kg/day, i.p.) and vitamin C (100 mg/kg/day, i.p.) for eight weeks. Then, brain tissues were separated and factors associated with oxidative stress, mitochondrial dysfunction, and histopathological changes were investigated. Results: Sodium valproate induced mitochondrial dysfunction, increased oxidative stress parameters and caused significant histopathological changes in brain tissue. Administration of curcumin attenuated the induction of oxidative damage, mitochondrial dysfunction, and histopathological changes induced by sodium valproate in brain tissue. Conclusion: Curcumin showed protective effect against sodium valproate-induced neurotoxicity which may be attributed to its antioxidant activity. So, it can be considered as an effective supplement against oxidative stress and mitochondrial dysfunction induced by sodium valproate in brain tissue.

Keywords

• sodium valproate
• curcumin
• neurotoxicity
• mitochondria
• oxidative stress