Protective effect of naringenin against gentamicin-induced nephrotoxicity in rats

被引:40
作者
Fouad, Amr A. [1 ]
Albuali, Waleed H. [2 ]
Zahran, Ahmed [3 ]
Gomaa, Wafaey [4 ]
机构
[1] King Faisal Univ, Div Pharmacol, Dept Biomed Sci, Coll Med, Al Hasa 31982, Saudi Arabia
[2] King Faisal Univ, Coll Med, Dept Pediat, Al Hasa 31982, Saudi Arabia
[3] King Faisal Univ, Div Nephrol, Dept Internal Med, Coll Med, Al Hasa 31982, Saudi Arabia
[4] King Abdulaziz Univ, Dept Pathol, Fac Med, Jeddah 21413, Saudi Arabia
关键词
Acute kidney injury; Gentamicin; Naringenin; Rats; ACUTE KIDNEY INJURY; CISPLATIN NEPHROTOXICITY; OXIDATIVE DAMAGE; WISTAR RATS; INFLAMMATION; STRESS; CELLS; AMINOGLYCOSIDES; INTERLEUKIN-8; ACTIVATION;
D O I
10.1016/j.etap.2014.07.015
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
The protective effect of naringenin, a flavonoid compound isolated from citrus fruits, was investigated against nephrotoxicity induced by gentamicin (80 mg kg(-1)/day, i.p., for eight days) in rats. Naringenin treatment (50 mg kg(-1)/day, p.o.) was administered for eight days, starting on the same day of gentamicin administration. Gentamicin caused significant elevations of serum creatinine, and kidney tissue levels of malondialdehyde, nitric oxide, and interleuldn-8, and a significant decrease in renal glutathione peroxidase activity. Naringenin treatment significantly ameliorated the changes in the measured biochemical parameters resulted from gentamicin administration. Also, naringenin markedly attenuated the histopathological renal tissue injury observed with gentamicin. Immunohistochemical examinations showed that naringenin significantly reduced the gentamicin-induced expression of kidney injury molecule-1, vascular endothelial growth factor, inducible nitric oxide synthase, and caspase-9, and increased survivin expression in the kidney tissue. It was concluded that naringenin, through its antioxidant and anti-inflammatory effects, may represent a therapeutic option to protect against gentamicin nephrotoxicity. (C) 2014 Elsevier B.V. All rights reserved.
引用
收藏
页码:420 / 429
页数:10
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