ATTENUATION OF HESPERIDIN ON VANCOMYCIN-INDUCED NEUROTOXICITY IN RATS

Vancomycin, a bactericidal antibiotic used for selective clinical infections confers its antibacterial activity via the inhibition of bacterial cell wall biosynthesis. This process thus results in oxidative stress. Hesperidin, a flavonoid found in citrus fruits has been reported to possess antioxidant activity. This study investigated the ameliorative effect of hesperidin on vancomycin-induced neurotoxicity. Male Wistar rats (n=24, 130-300 g) were divided into four groups of six rats each. Group 1 (Control) received distilled water, Group 2 received Hesperidin (50 mg/kg/day) orally, Group 3 received Vancomycin (10 mg/kg/day)intraperitoneally and Group 4 received Vancomycin (10mg/kg/day)
and Hesperidin (50mg/kg/day). The administration was done for seven days. Data were analyzed using ANOVA at P 0.05. Administration of Vancomycin significantly reduced the levels of Reduced Glutathione (GSH) and Ascorbic Acid (AA) in the brain sections of the rats relative to control. The activities of Glutathione Peroxidase (GPx), Catalase (CAT), Glutathione-S-Transferase (GST), and Superoxide Dismutase (SOD) were down-regulated relative to control. Furthermore, an increased level of Nitric Oxide (NO), Malondialdehyde (MDA), and activity of Myeloperoxidase (MPO) was observed relative to control (P 0.05). However, co-treatment with Hesperidin significantly attenuated levels of GSH, AA, NO, MDA, and activities of MPO, GST, SOD, CAT, and GPx when compared with Vancomycin treated groups. Histopathological examination of the brain sections of Vancomycin-treated rats showed the presence of lesions. Administration of Hesperidin alongside Vancomycin reversed these lesions. Data obtained from this study showed that Hesperidin attenuated oxidative stress induced by Vancomycin in the brain of rats via antioxidant mechanisms.