Abstract

Epicatechin (Epi) is one of the most abundant flavonoids present in different fruits and tea leaves. Emerging research illuminates the promising potential of catechins to serve as a shield against the damaging effects of arsenic (As) exposure in diverse organs.This study sought to discern whether Epi exhibits a therapeutic efficacy against arsenic-induced neurotoxicity in a murine model.The Naval Medical Research Institute (NMRI) mice were randomly partitioned into six distinct groups, which included a control group receiving normal saline, a group receiving a daily oral dose of arsenic (10mg/kg) for 5weeks, groups receiving As (10mg/kg/day) orally for 5weeks along with different doses of Epi (25-100mg/kg) orally for the last 2weeks, and a group receiving Epi (100mg/kg) orally for 2weeks. To assess the potential effects of Epi, neurobehavioral tests, various parameters of oxidative stress, and inflammation were evaluated.The findings of this investigation revealed that As-induced neurobehavioral toxicity was associated with a notable surge in lipid peroxidation and nitric oxide (NO) concentration, accompanied by a reduction in the levels of antioxidant markers. As heightened pro-inflammatory cytokines including tumor necrosis factor-α (TNF-α) levels were observed alongside amplified nuclear factor kappa B (NF-κB) and nuclear factor erythroid 2-related factor 2 (Nrf2) expression. However, treatment with Epi reversed these effects.On the whole, these findings indicate that Epi may hold promise therapeutic efficacy on As-induced neurotoxicity by improving antioxidant status and mitigating oxidative stress and inflammation. Nevertheless, further research is imperative to comprehensively grasp the potential protective effects of Epi in this particular context.

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