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Article Publish Status: FREE
Abstract Title:

Pinocembrin attenuates gentamicin-induced nephrotoxicity in rats.

Abstract Source:

Can J Physiol Pharmacol. 2016 Aug ;94(8):808-18. Epub 2016 Mar 29. PMID: 27245556

Abstract Author(s):

Sasivimon Promsan, Krit Jaikumkao, Anchalee Pongchaidecha, Nipon Chattipakorn, Varanuj Chatsudthipong, Phatchawan Arjinajarn, Wilart Pompimon, Anusorn Lungkaphin

Article Affiliation:

Sasivimon Promsan

Abstract:

Oxidative stress mediated apoptosis of renal tubular cells is a major pathology of gentamicin-induced nephrotoxicity, which is one of the prevailing causes of acute renal failure. Pinocembrin is a major flavonoid found in rhizomes of fingerroot (Boesenbergia pandurata). It has pharmacological and biological activities including antimicrobial, anti-inflammatory, and antioxidant effects. Preclinical studies have suggested that pinocembrin protects rat brain and heart against oxidation and apoptosis induced by ischemia-reperfusion. The aim of the current study was to investigate the mechanisms of renoprotection elicited by pinocembrin in gentamicin-induced nephrotoxicity. Nephrotoxicity was induced in rats by intraperitoneal injection (i.p.) of gentamicin, and pinocembrin was administered via i.p. 30 min before gentamicin treatment for 10 days. Gentamicin-induced nephrotoxicity was indicated by the reduced renal function and renal Oat3 function and expression. Gentamicin treatment also stimulated Nrf2, HO-1, and NQO1, as well as the pro-apoptotic proteins Bax and caspase-3, concomitant with the attenuation of Bcl-XL expression in the renal cortical tissues. Pinocembrin pretreatment improved renal function and renal Oat3 function and reduced oxidative stress and apoptotic conditions. These findings indicate that pinocembrin has a protective effect against gentamicin-induced nephrotoxicity, which may be due in part to its antioxidant and anti-apoptotic effects, subsequently leading to improved renal function.

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