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Ellagic Acid Mitigates Sodium Arsenite-Induced Renal and Hepatic Toxicity in Male Wistar Rats Publisher Pubmed



Mehrzadi S1 ; Fatemi I2, 3 ; Malayeri AR4 ; Khodadadi A5, 6 ; Mohammadi F7 ; Mansouri E8 ; Rashno M5, 6 ; Goudarzi M4, 9
Authors
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Authors Affiliations
  1. 1. Razi Drug Research Center, Iran University of Medical Sciences, Tehran, Iran
  2. 2. Department of Physiology and Pharmacology, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
  3. 3. Physiology-Pharmacology Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
  4. 4. Medicinal Plant Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
  5. 5. Cancer, Environmental and Petroleum Pollutants Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
  6. 6. Department of Immunology, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
  7. 7. Brain and Spinal Cord Injury Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran
  8. 8. Cellular and Molecular Research Center, Department of Anatomical Sciences, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
  9. 9. Student Research Committee, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

Source: Pharmacological Reports Published:2018


Abstract

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. © 2018 Institute of Pharmacology, Polish Academy of Sciences
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