β-sitosterol protects against cisplatin-induced nephrotoxicity through amelioration of oxidative stress in rats

Muthanna Medical Journal
Volume 4, Issue 2, December 2017, Pages 60-74
http://dx.doi.org/10.18081/2410-4590/2017-60-74

Research Article

Atheer Abbas Yaseen Al-Fatlawi*¹, Aws Rassul Hussain Al-Salih², Mohammed Abdul Reda Yassen³

*Corresponding Author email: atheer.alfatlawi@jmu.edu.iq
¹Department of Pharmacology, Collage of Medicine, Jabir Ibn Hayyan University
²Department of Pathology and Forensic Medicine, College of Medicine, Al-Qadisiyah University
³Department of Clinical Laboratory Science, College of Pharmacy, Al-Qadisiyah University
Received 30 Auqust 2017, Accepted 11 October 2017, Available online 16 November 2017
This is article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Copyright © 2017 AA

Abstract

Kidney damage is a major concern related with Anti-malignancy drugs. It is well established that overproduction of reactive oxygen species plays vital role in progress of the pathogenesis of nephrotoxicity. The aim of this study is investigated the modulatory effect β-sitosterol (BT) on cisplatin (CP) that induced nephrotoxicity by targeting oxidative stress and biochemical parameters for kidney function markers in rats. Following a single dose of cisplatin (CP) an intraperitoneal (7.5 mg/kg BW) at seventh day group II, III and β-sitosterol (BT) 5 ml/kg was administered for 10 days group I,III, IV, after decapitation of the rats, trunk blood was obtained, and the kidney tissue was removed for the measurement of xanthine oxidase, lipid peroxidation, (H2O2) generation and antioxidant enzymes, like, catalase, glutathione reductase and glutathione peroxidase kidney function markers like serum creatinine and BUN, further examination for histopathological changes.  Cisplatin (CP) administration group was increased the glutathione depletion, xanthine oxidase and lipid peroxidation activity and decrease in (glutathione reductase, catalase and glutathione peroxidase) and phase-II detoxifying (quinone reductase and glutathione-S- transferase) enzymes activities significantly (p<0.05) when compared with the control, histological findings provide same the protective effects of β-sitosterol (BT) against cisplatin (CP) induced acute nephrotoxicity. In conclusions; the current study revealed β-sitosterol (BT), through its antioxidant actions, alleviates cisplatin-induced oxidative damage, which suggests that β-sitosterol (BT) may be of therapeutic benefit when used with cisplatin.

Keywords: β-sitosterol; Kidney; Cisplatin; Oxidative stress

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