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Mediators of Inflammation
Volume 2014, Article ID 983952, 12 pages
http://dx.doi.org/10.1155/2014/983952
Research Article

Beetroot (Beta vulgaris L.) Extract Ameliorates Gentamicin-Induced Nephrotoxicity Associated Oxidative Stress, Inflammation, and Apoptosis in Rodent Model

1Department of Pharmacognosy and Medicinal, Aromatic & Poisonous Plants Research Center (MAPPRC), College of Pharmacy, P.O. Box 2457, King Saud University, Riyadh 11451, Saudi Arabia
2Department of Pharmacognosy, College of Pharmacy, Mansoura University, El Mansoura 35516, Egypt
3Department of Pharmaceutics, College of Pharmacy, P.O. Box 2457, King Saud University, Riyadh 11451, Saudi Arabia
4Department of Medicine and Pathology, Gastroenterology Unit, Collage of Medicine, King Khalid University Hospital, King Saud University P.O., Box 2925, Riyadh 11461, Saudi Arabia
5Department of Clinical Pharmacy, College of Pharmacy, P.O. Box 2457, King Saud University, Riyadh 11451, Saudi Arabia
6Department of Pharmaceutical Chemistry, College of Pharmacy, P.O. Box 2457, King Saud University, Riyadh 11451, Saudi Arabia

Received 4 June 2014; Revised 11 September 2014; Accepted 29 September 2014; Published 22 October 2014

Academic Editor: Elaine Hatanaka

Copyright © 2014 Ali A. El Gamal et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The present investigation was designed to investigate the protective effect of (Beta vulgaris L.) beat root ethanolic extract (BVEE) on gentamicin-induced nephrotoxicity and to elucidate the potential mechanism. Serum specific kidney function parameters (urea, uric acid, total protein, creatinine, and histopathology of kidney tissue) were evaluated to access gentamicin-induced nephrotoxicity. The oxidative/nitrosative stress (Lipid peroxidation, MDA, NP-SH, Catalase, and nitric oxide levels) was assessed. The inflammatory response (TNF-α, IL-6, MPO, NF-κB (p65), and NF-κB (p65) DNA binding) and apoptotic marker (Caspase-3, Bax, and Bcl-2) were also evaluated. BVEE (250 and 500 mg/kg) treatment along with gentamicin restored/increased the renal endogenous antioxidant status. Gentamicin-induced increased renal inflammatory cytokines (TNF-α and IL-6), nuclear protein expression of NF-κB (p65), NF-κB-DNA binding activity, myeloperoxidase (MPO) activity, and nitric oxide level were significantly down regulated upon BVEE treatment. In addition, BVEE treatment significantly reduced the amount of cleaved caspase 3 and Bax, protein expression and increased the Bcl-2 protein expression. BVEE treatment also ameliorated the extent of histologic injury and reduced inflammatory infiltration in renal tubules. These findings suggest that BVEE treatment attenuates renal dysfunction and structural damage through the reduction of oxidative stress, inflammation, and apoptosis in the kidney.