- Clinical and Experimental Health Sciences
- Vol: 11 Issue: 2
- Naringenin Reduces Hepatic Inflammation and Apoptosis Induced by Vancomycin in Rats
Naringenin Reduces Hepatic Inflammation and Apoptosis Induced by Vancomycin in Rats
Authors : Zuhal Uçkun Şahinoğullari, Sevda Güzel, Necmiye Canacankatan, Cem Yalaza, Deniz Kibar, Gulsen Bayrak
Pages : 191-198
Doi:10.33808/clinexphealthsci.741916
View : 24 | Download : 9
Publication Date : 2021-06-30
Article Type : Research
Abstract :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.Keywords : Vancomycin, Naringenin, Liver, Apoptosis, Inflammation