Literature DB >> 16858688

Spirulina attenuates cyclosporine-induced nephrotoxicity in rats.

Mahmood Khan1, Jagdish Chandra Shobha, Iyyapu Krishna Mohan, Madireddy Umamaheswara Rao Naidu, Aruna Prayag, Vijay Kumar Kutala.   

Abstract

Cyclosporine (CsA) causes a dose-related decrease in renal function in experimental animals and humans. The generation of reactive oxygen species (ROS) has been implicated in CsA-induced nephrotoxicity. It was previously shown that Spirulina, a blue-green algae, with antioxidant properties effectively attenuated the doxorubicin-induced cardiotoxicity in mice and cisplatin-induced nephrotoxicity in rat. The present study investigated the nephroprotective role of Spirulina against CsA-induced nephrotoxicity in rats. Spirulina (500 mg kg(-1) b.w.) was administered orally for 3 days before and 14 days concurrently with CsA (50 mg kg-1 b.w.). Rats treated with CsA showed nephrotoxicity as evidenced from a significant elevation in plasma urea, creatinine, urinary N-acetyl-beta-D-glucosaminidase (beta-NAG) and a decrease in creatinine and lithium clearance. Pretreatment with Spirulina protected the rats from CsA-induced nephrotoxicity. The CsA-induced rise in plasma urea and creatinine and the decrease in creatinine and lithium clearance were attenuated by Spirulina. There was a significant increase in plasma and kidney tissue MDA with CsA. Spirulina prevented the rise in plasma and kidney tissue MDA. Histopathology of the kidney from CsA-treated rats showed severe isometric vacuolization and widening of the interstitium. However, pretreatment with Spirulina prevented such changes, and the kidney morphology was comparable to that of the control. Spirulina treatment did not alter the blood CsA levels. These results suggest that Spirulina has a protective effect against nephrotoxicity induced by CsA. This study further supports the crucial role of the antioxidant nature of Spirulina in protecting against CsA-induced oxidative stress. Copyright 2006 John Wiley & Sons, Ltd.

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Year:  2006        PMID: 16858688     DOI: 10.1002/jat.1159

Source DB:  PubMed          Journal:  J Appl Toxicol        ISSN: 0260-437X            Impact factor:   3.446


  14 in total

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