Hemin Attenuates Cisplatin-Induced Acute Renal Injury in Male Rats

被引:31
|
作者
Al-Kahtani, Mohamed A. [1 ]
Abdel-Moneim, Ashraf M. [1 ,2 ]
Elmenshawy, Omar M. [1 ,3 ]
El-Kersh, Andmohamed A. [4 ,5 ]
机构
[1] King Faisal Univ, Fac Sci, Dept Biol Sci, Al Hasa 31982, Saudi Arabia
[2] Univ Alexandria, Fac Sci, Dept Zool, Alexandria 21511, Egypt
[3] Al Azhar Univ, Fac Sci, Dept Zool, Nasr City 11884, Egypt
[4] King Faisal Univ, Fac Sci, Dept Chem, Al Hasa 31982, Saudi Arabia
[5] Alexandria Univ, Fac Sci, Dept Biochem, Alexandria 21511, Egypt
关键词
INDUCED ACUTE NEPHROTOXICITY; NITRIC-OXIDE; OXIDATIVE STRESS; SPECTROPHOTOMETRIC ASSAY; OXYGENASE-1; INDUCTION; INDUCED KIDNEY; PEROXYNITRITE; GENTAMICIN; DAMAGE; GENE;
D O I
10.1155/2014/476430
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Background. The aim of this study is to investigate the protective effects of hemin (the heme oxygenase-1 [OH-1] inducer) against nephrotoxic effects induced by cisplatin [cis-diamminedichloroplatinum II (CP)] in male rats. Methods. The evaluation was performed through monitoring renal redox parameters: lipid peroxidation (LPO), glutathione peroxidase (GPx), superoxide dismutase (SOD), glutathione reductase (GR), and reduced glutathione (GSH). The work also examined renal function tests (urea and creatinine), tissue proinflammatory mediator like nitric oxide (NO), and kidney cytopathology. Results. Asingle intraperitoneal dose of CP (10 mg/kg b.w.) caused significant elevation of blood urea, serum creatinine, and renal LPO and NO, along with significant decline of the activities of GPx and GR, but renal SOD activity and GSH level were statistically insignificant as compared to control group. Subcutaneous injection of hemin (40 mu mol/kg b.w.) partially ameliorated CP-induced renal damage, based on suppression of blood urea, serum creatinine, the renal MDA and NO levels, and increased antioxidant capacity in CP-treated rats. The results of histopathological and ultrastructural investigations supported the renoprotective effect of hemin against CP-induced acute toxicity. Conclusion. The induction of HO-1 by hemin is a promising approach in the treatment of CP-induced nephrotoxicity. However, further preclinical studies are warranted to test effectiveness of CP/hemin on the outcome of tumor chemotherapy.
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页数:9
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