Neuro-protective and redox potential of troxerutin against cypermethrin-induced neurotoxicity and oxidative stress in mice.

The present study was designed to evaluate the protective efficacy of troxerutin against cypermethrin-induced behavioral defects, motor function abnormalities, and oxidative stress in mice. Twenty-four adult female albino mice were randomly divided into four equal groups. The first group served as control, the second group was treated with cypermethrin (20 mg/kg b.w) intraperitoneally at day 21, and the remaining two groups were orally supplemented with TRX (150, 300 mg/kg b.w) for 20 days and with cypermethrin (20 mg/kg b.w) intraperitoneally at day 21. Behavior activities recorded after cypermethrin exposure showed significantly impaired motor function (p≤0.05) as evidenced by the beam balance and pole test. The cypermethrin was also found to cause significant memory dysfunction. Moreover, the oxidative stress in terms of increased tissue malondialdehyde level (p≤0.05) was recorded in the cypermethrin group. The antioxidant activities of catalase and glutathione peroxidase were decreased (p≤0.05) after cypermethrin exposure. Troxerutin supplementation significantly improved the cypermethrin-induced motor impairment and memory dysfunction. The supplementation of troxerutin significantly restored the redox status. Troxerutin attenuates the neurotoxic and behavioral deficits caused by cypermethrin. Furthermore, troxerutin also provides significant protection against cypermethrin-induced oxidative stress by improving the oxidative stress markers.