Ellagic acid mitigates sodium arsenite-induced renal and hepatic toxicity in male Wistar rats

被引:56
|
作者
Mehrzadi, Saeed [1 ]
Fatemi, Iman [2 ,3 ]
Malayeri, Ali Reza [4 ]
Khodadadi, Ali [5 ,6 ]
Mohammadi, Fatemeh [7 ]
Mansouri, Esrafil [8 ]
Rashno, Mohammad [5 ,6 ]
Goudarzi, Mehdi [4 ,9 ]
机构
[1] Iran Univ Med Sci, Razi Drug Res Ctr, Tehran, Iran
[2] Rafsanjan Univ Med Sci, Dept Physiol & Pharmacol, Rafsanjan, Iran
[3] Rafsanjan Univ Med Sci, Physiol Pharmacol Res Ctr, Rafsanjan, Iran
[4] Ahvaz Jundishapur Univ Med Sci, Med Plant Res Ctr, Ahvaz, Iran
[5] Ahvaz Jundishapur Univ Med Sci, Canc Environm & Petr Pollutants Res Ctr, Ahvaz, Iran
[6] Ahvaz Jundishapur Univ Med Sci, Fac Med, Dept Immunol, Ahvaz, Iran
[7] Univ Tehran Med Sci, Brain & Spinal Cord Injury Res Ctr, Neurosci Inst, Tehran, Iran
[8] Ahvaz Jundishapur Univ Med Sci, Fac Med, Cellular & Mol Res Ctr, Dept Anat Sci, Ahvaz, Iran
[9] Ahvaz Jundishapur Univ Med Sci, Student Res Comm, Ahvaz, Iran
关键词
Sodium arsenite; Oxidative stress; Ellagic acid; INDUCED OXIDATIVE DAMAGE; GENTAMICIN-INDUCED NEPHROTOXICITY; NITRIC-OXIDE; KAPPA-B; STRESS; LIVER; PROTECTS; EXPOSURE; TISSUE; METABOLISM;
D O I
10.1016/j.pharep.2018.02.007
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Background: The aim of this study was to investigate the effect of ellagic acid (EA) on arsenic-induced renal and hepatic toxicity in rats. Methods: A total number of 35 male Wistar rats were randomly divided into five experimental groups. Group 1 received normal saline (po). Group 2 received sodium arsenite (SA, 10 mg/kg, po) for 21 days. Group 3 received EA (30 mg/kg, po) for 14 days. Groups 4 and 5 received SA 7 days prior to EA (10 and 30 mg/kg respectively) treatment and continued up to 21 days simultaneous with SA administration. Various biochemical, histological and molecular biomarkers were measured in kidney and liver. Results: Treatment with EA (more potently at dose of 30 mg/kg) restored the SA-induced alterations in serum creatinine (Cr) and blood urine nitrogen (BUN) levels as well as the changes in aspartate aminotransferase (AST), alkaline phosphatase (ALP) and alanine aminotransferase (ALT) concentrations (all p <0.001). Elevated levels of malondialdehyde (MDA) and nitric oxide (NO) in renal and hepatic tissue was reduced by EA treatment (all p <0.001). Treatment with EA enhanced the glutathione (GSH) content in liver (p < 0.001) and up-regulated renal and hepatic superoxide dismutase (SOD) and glutathione peroxidase (GPx) mRNA expression (all p <0.001). The SA-induced histopathological alterations in kidney and liver were reduced by EA treatment. Conclusion: In conclusion, the presence of EA with SA alleviated its toxic effects and EA treatment might be an effective strategy for the management of arsenic-induced renal and hepatic damage. (C) 2018 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:712 / 719
页数:8
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