Hepatic Inflammation and Apoptosis Induced by Vancomycin in Rats and the Potential Protective Effects of Naringenin

Objective: This investigation aimed to detect the possible protective impacts of naringenin (NAR) on vancomycin (VCM)-induced liver toxicity through measuring caspase-3, -8 and -9 activities as markers of apoptosis and the levels of tumor necrosis factor-alpha, cyclooxygenase-2 and vascular endothelial growth factor as inflammation markers and assessing the histopathological alterations in rats. Methods: The rats were allocated into seven groups as, the control group (saline, intraperitoneally (i.p.)), VCM group (400 mg/kg/day, i.p.), Carboxymethyl cellulose group (0.5% CMC, orally), NAR100 group (100 mg/kg/day, orally), VCM+NAR25 group (25 mg/kg/day, orally), VCM+NAR50 group (50 mg/kg/day, orally), VCM+NAR100 group (100 mg/kg/day, orally). The caspase enzyme activities and inflammation markers were measured using colorimetric methods and ELISA, respectively. Histopathological examinations were performed. Results: The caspase activities and levels of inflammation markers were significantly higher in the VCM group as opposed to the other groups. The caspase activities were significantly ameliorated in the VCM+NAR25 group compared to the VCM+NAR50 and VCM+NAR100 groups, but the levels of inflammation markers were significantly attenuated in VCM+NAR50 group and, especially, VCM+NAR100 group compared to VCM+NAR25 group. Conclusion: NAR has potential protective impact on liver injury caused by VCM, and the protective impacts of NAR at distinct doses may occur via different molecular mechanisms.