Abstract
•Cypermethrin caused mitochondrial dysfunction, so it causes neurotoxicity and genotoxicity.•Neuronal diseases are linked to apoptotic markers that are related to mitochondrial dysfunction.•Co-treatment with moringa extract ameliorated the mitochondrial dysfunction and AchE.•The moringa extract acts as a neuroprotective agent.
Cypermethrin (CYP) can cause neurotoxicity and plays a role as an inducer for mitochondrial dysfunction. The defensive capability of Moringa oleifera versus neuronal issues prompted by CYP intoxication in adult male albino rats was investigated. Sixty male rats were divided into six experimental groups; G1: controlled group. G2 and G3 were exposed to CYP at different doses of 26.15 mg/Kg/day (representing 1/10 LD50) and 8.72 mg/kg/day (representing1/30 LD50) respectively. G4 treated with moringa extract at 250 mg/kg/day by gavage. G5 and G6 were given moringa extract by gavage (250 mg/kg/day) and CYP as G2 and G3 respectively. G4, G5, and G6 were given moringa extract by gavage (250 mg/kg/day) for 14 days before starting the experiment and during it (28 days). The results indicated that exposure to CYP resulted in a significant reduction in the NADH dehydrogenase, ATPase in mitochondria, and AchE enzyme activity, while the brain caspase-3 activity and DNA fragmentation were increased significantly compared to the controlled group. The co-treatment of moringa extract alleviated the adverse effect of CYP in the treated groups. Moringa declined mitochondrial dysfunction, apoptotic markers, and enhanced AchE activity. In conclusion, moringa extract has an impact to minimize cypermethrin-induced neurotoxicity and apoptosis in rats’ brains.