| Abstrakt: |
Background: Cyclosporine A (CsA) is an immunosuppression agent used frequently in fields of organs transplantation and autoimmune diseases. However, CsA-induced kidney injury is a major clinical problem associated with CsA therapy in which the conceivable accountable mechanism is oxidative stress (OS). The present study evaluated the protective and ameliorated effects of fucoidan (FU) as an antioxidant and an anti-inflammatory agent against CsA-induced kidney injury. Methods: Male rats were randomly divided into three groups. The first group was served as a control group that administered olive oil orally and normal saline subcutaneously, the second group (CA) was treated with CsA orally, and the third group (CA + FU) was treated with CsA orally in concomitant with FU subcutaneously. Experimental animals were sacrificed 20 days following the treatment period and serum samples were analyzed for creatinine test. The homogenate of renal tissues was prepared for OS assessment. Light and ultrastructure microscopic kidney sections were prepared for histopathological examination. Results: Treatment of rats with CsA alone produced a significant increase in the levels of creatinine, nitric oxide (NO), and malondialdehyde (MDA), as well as the activities of superoxide dismutase (SOD), catalase (CAT), and glucose 6 phosphate dehydrogenase (G6PD), whereas the level of glutathione reduced (GSH) was decreased. Some histopathological changes of the kidney tissue including tubular epithelial hypertrophy, vacuolizations, necrotic glomerulus cell, capillaries network shrinking, vascular congestion, interstitial infiltration, loss of apical microvilli, and deteriorated mitochondria were observed in CA group. Concomitant FU administration with CsA enhanced renal function, as indicated by the low level of creatinine. Moreover, FU ameliorated the oxidative status in kidney tissue as well as it provided histological protection against CsA-induced kidney injury. Conclusion: FU can develop a protective mechanism against kidney injury induced by CsA that mediated by OS. [ABSTRACT FROM AUTHOR] |
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