Neuroprotective potential of berberine against acetamiprid induced toxicity in rats: Implication of oxidative stress, mitochondrial alterations, and structural changes in brain regions.

Abstract

Acetamiprid (ACMP) is an extensively used neonicotinoid pesticide to control sucking and chewing insects and is known to cause nontarget toxicity. The present study aimed to evaluate the ameliorative potential of berberine (BBR)-a polyphenolic alkaloid- on ACMP-induced oxidative stress, mitochondrial dysfunctioning, and structural changes in different rat brain regions. The male Wistar rats were divided into four groups, that is, control, BBR-treated (150 mg/kg b.wt), ACMP-exposed (21.7 mg/kg b.wt) and BBR + ACMP co-treated; and were dosed intragastrically for 21 consecutive days. Results of the biochemical analysis showed that BBR significantly ameliorated ACMP-induced oxidative stress by decreasing lipid peroxidation and protein oxidation along with a marked increase in endogenous antioxidants and lowered AChE activity in rat brain regions. Inside mitochondria, BBR significantly attenuated the toxic effects of ACMP by increasing the activity of mitochondrial complexes. Findings of polymerase chain reaction also demonstrated the modulatory effects of BBR against ACMP-mediated downregulation of ND1, ND2, COX1, and COX4 subunits of mitochondrial complexes. The histopathological and ultrastructural examination also validated the biochemical and transcriptional alterations following toxicity of ACMP exposure and the protective potential of BBR against ACMP-induced neurotoxicity. Thus, the present study indicates the promising ameliorative potential of BBR against ACMP-induced neurotoxicity via its antioxidative and modulatory activities.