Ameliorative impacts of Glycyrrhiza glabra root extract against nephrotoxicity induced by gentamicin in mice

光果甘草根提取物对小鼠庆大霉素肾毒性的改善作用

阅读:4
作者:Mohamed A Nassan, Mohamed M Soliman, Adil Aldhahrani, Fayez Althobaiti, Adel Q Alkhedaide

Abstract

Gentamicin is an effective antibiotic that has been used worldwide for many years. While considered an essential medicine by the WHO, gentamicin can also lead to severe kidney damage. This study explored the ameliorative effects of Glycyrrhiza glabra root extract on gentamicin-induced renal injury in mice. Four groups of n = 7 mice were used: (a) control; (b) G. glabra-only; (c) gentamicin-only; and (d) gentamicin plus G. glabra. Kidney samples were tested for: antioxidant enzyme activity (superoxide dismutase [SOD] and glutathione peroxidase [Gpx]); expression of HO-1 and nuclear factor erythroid 2-related factor 2 genes; expression of Cox-2 and Bax; cytokine levels (IL-1β, and IL-6); histopathological anomalies; and standard renal functional component levels (creatinine, urea, and blood urea nitrogen). The effects of gentamicin were generally reversed or normalized following treatment with G. glabra root extract. Gentamicin decreased Gpx and SOD parameters and increased IL-1 β and IL-6 levels, but these returned to normal in the G. glabra-treated group. Gentamicin upregulated tissue levels of Cox-2 and Bax, and downregulated HO-1 and Nrf-2 expression but again, and these levels returned to normal in the group treated with G. glabra. Mice that had received gentamicin exhibited acute renal blood vessel congestion, focal interstitial round cell aggregation, and hydropic degeneration of renal tubular epithelium. However, those that had also received G. glabra showed a normal histopathology. Findings from this study indicate that in mouse models, gentamicin-induced kidney damage can be reversed or ameliorated by administering G. glabra, so it can be considered as an effective complimentary therapy.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。