Ellagic Acid Antiinflammatory and Antiapoptotic Potential Mediate Renoprotection in Cisplatin Nephrotoxic Rats

ABSTRACT Ellagic acid (EA) renoprotective effect against cisplatin (CIS)‐induced nephrotoxicity remains elusive. Therefore, male Sprague–Dawley rats received CIS alone or EA (10 and 30 mg/kg, p.o.) for 5 days before and after CIS injection. CIS increased serum levels of blood urea nitrogen, creatini...

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Bibliographic Details
Published in:Journal of biochemical and molecular toxicology 2014-10, Vol.28 (10), p.472-479
Main Authors: El-Garhy, Amany M., Abd El-Raouf, Ola M., El-Sayeh, Bahia M., Fawzy, Hala M., Abdallah, Dalaal M.
Format: Article
Language:English
Subjects:
Animals
Anti-Inflammatory Agents - pharmacology
Apoptosis
Apoptosis - drug effects
Blood Urea Nitrogen
Caspase 3 - drug effects
Caspase 3 - metabolism
Chemokine CCL2 - analysis
Chemokine CCL2 - drug effects
Cisplatin
Cisplatin - toxicity
Creatinine - blood
Drug-Related Side Effects and Adverse Reactions - prevention & control
Ellagic Acid
Ellagic Acid - pharmacology
Endothelin-1 - blood
gamma-Glutamyltransferase - blood
Heme Oxygenase-1 - metabolism
Inflammation
Kidney - drug effects
Male
Nephrotoxicity
NF-kappa B - drug effects
NF-kappa B - metabolism
Nitric Oxide - analysis
Rats
Rats, Sprague-Dawley
Tumor Necrosis Factor-alpha - analysis
Tumor Necrosis Factor-alpha - drug effects
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Summary:ABSTRACT Ellagic acid (EA) renoprotective effect against cisplatin (CIS)‐induced nephrotoxicity remains elusive. Therefore, male Sprague–Dawley rats received CIS alone or EA (10 and 30 mg/kg, p.o.) for 5 days before and after CIS injection. CIS increased serum levels of blood urea nitrogen, creatinine, γ‐glutamyl transferase, and reduced those of albumin and total protein. It also raised serum endothelin‐1, as well as serum and renal nitric oxide, tumor necrosis factor‐α, and monocyte chemoattractant protein‐1. CIS enhanced the renal caspase‐3, hemeoxygenase (HO)‐1, nuclear factor‐κB, and inducible nitric oxide. EA hampered CIS‐induced nephrotoxicity manifested by an enhancement of the glomerular filtration rate which was associated by the reduction of inflammatory mediators and the apoptotic marker in the serum and/or kidney. The present study discloses that EA suppresses HO‐1 and, its renoprotection is also linked to its anti‐inflammatory and antiapoptotic properties, as well as the reduction of nitric oxide and endothelin‐1.
ISSN:1095-6670
1099-0461
DOI:10.1002/jbt.21587