Hesperidin Alleviates Gentamicin Ototoxicity in Rats by Inhibiting Oxidative Stress, Inflammation and Apoptosis

Rajab A. Alzahrani and Amr A. Fouad

Background and Objective: Ototoxicity induced by gentamicin (GTN) mediated mainly by oxidative stress, inflammation and apoptosis. Hesperidin (HPN) possesses antioxidant, anti-inflammatory and antiapoptotic activities. This study investigated the possible protective effect of HPN against GTN-induced ototoxicity in rats. Materials and Methods: Rats received GTN (100 mg/kg/day, i.p.) for 14 days. The HPN treatment (200 mg/kg/day, p.o.) started on the same day of GTN administration and continued for 14 days. Malondialdehyde, total antioxidant capacity, nitric oxide, calcium ion, tumor necrosis factor-α, interleukin-6, inducible nitric oxide synthase, nitric oxide, nuclear factor-κB p65, Bax/Bcl-2 ratio and cleaved caspase-3 measured in cochlear homogenates. Data analysed by one-way ANOVA test using GraphPad Prism Software Program (version 6.01). Results: The HPN significantly decreased malondialdehyde, inducible nitric oxide synthase, nitric oxide and calcium ion and significantly increased total antioxidant capacity in the ear cochleae of GTN-challenged rats. In addition, HPN significantly reduced cochlear tumor necrosis factor-α, interleukin-6, nuclear factor-κB p65, Bax/Bcl-2 ratio and cleaved caspase-3 in rats received GTN. Conclusion: The HPN protected against GTN-induced ototoxicity in rats by inhibiting oxidative/nitrative stress, inflammation and apoptosis.

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