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Protective effects of a combination of quercetin and vitamin E against cyclosporine A‐induced oxidative stress and hepatotoxicity in rats
Author(s) -
Mostafavi–Pour Zohreh,
Zal Fatemeh,
Monabati Ahmad,
Vessal Mahmood
Publication year - 2008
Publication title -
hepatology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.123
H-Index - 75
eISSN - 1872-034X
pISSN - 1386-6346
DOI - 10.1111/j.1872-034x.2007.00273.x
Subject(s) - tbars , oxidative stress , vitamin e , pharmacology , thiobarbituric acid , chemistry , glutathione peroxidase , lipid peroxidation , antioxidant , reactive oxygen species , quercetin , glutathione , vitamin c , alkaline phosphatase , catalase , biochemistry , endocrinology , medicine , enzyme
Aim: Cyclosporine A (CsA) is the most widely used immunosuppressive drug in transplant surgery. It is able to generate reactive oxygen species (ROS) and cause lipid peroxidation (thiobarbituric acid‐reacting substances [TBARS]), which will directly result in CsA hepatotoxicity. Methods: In this study, the potential of quercetin (Q) and vitamin E (E), in attenuating CsA‐induced liver dysfunction in rats was investigated. Male Sprague–Dawley rats were divided into six groups and treated with either olive oil, ethanol + olive oil, CsA, CsA + E, CsA + Q, or CsA + E + Q for both 4 and 8 weeks. Hepatotoxicity was assessed by morphological alterations in tissue architecture and by reduced serum total protein and increased serum alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase. Results: The results indicated that CsA treatment increases TBARS and decreases activities of catalase (CAT) and glutathione peroxidase (GPx) in the rat liver. The co‐administration of E and Q with CsA treatment improved both liver morphology changes and function. A combination of these antioxidants significantly reduced TBARS and increased CAT and GPx activities in the hepatic tissue. Conclusion: Our data demonstrates that E + Q plays a protective role against the imbalance elicited by CsA between the production of free radicals and antioxidant defence systems, and suggests that a combination of these two antioxidants may find clinical application where cellular damage is a consequence of ROS.