Protective Effect of Aminoguanidine Against Cyclosporine Induced Nephrotoxicity and Hepatotoxicity in Rats: Histological and Biochemical Study
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- Category: Vol. 77, March 2009
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Protective Effect of Aminoguanidine Against Cyclosporine Induced Nephrotoxicity and Hepatotoxicity in Rats: Histological and Biochemical Study,KHALED M. ABDEL AAL, HEBA A.E. MUBARK, RANDA H. ABDEL HADY, WAFAA M. ABDEL MONEIM and ABEER M.R. HUSSEIN
Abstract
Cyclosporine A (CsA) is a potent and effective immuno-suppressive agent used to prevent rejection in organ transplant surgery and autoimmune diseases. Its use is frequently accom-panied by nephrotoxicity and hepatotoxicity. The present study was designed to investigate the possible protective effect of aminoguanidine on cyclosporine induced nephrotoxicity and hepatotoxicity in male albino rats. A total of sixty healthy adult male albino rats were used divided into four equal groups in this study. Group I rats served as control treated with distilled water orally only, group II was treated with CsA in a dose of 25mg/kg orally daily for 21 days, group III treated with CsA concurrently with aminoguanidine in doses of 25 and 20mg/kg orally daily for 21 days respectively and group IV was treated with olive oil orally (vehicle for CsA). Rats were sacrificed 24 hs after last dose, blood, kidney and liver samples were taken. Histopathological examination by light and electron microscopic, immunohistochemistry for active caspase-3 were done. Besides, biochemical measurement; serum nitric oxide level and kidney and liver functions tests were done. CsA oral administration for 21 days significantly increased serum nitric oxide level impaired the renal and hepatic function tests and markedly distorted the renal and hepatic morphology in light and electron microscopic exam-ination. Aminoguanidine administration improved serum nitric oxide level, kidney and liver function tests and preserved renal and hepatic morphological structures.
In Conclusion: Aminoguanidine has a protective effect against cyclosporine induced nephrotoxicity and hepatotoxicity.