作者: Meltem Kuruş , Mukaddes Eşrefoğlu , Aysun Bay , Feral Öztürk
DOI: 10.1007/S11255-004-0011-5
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摘要: Background: One of the major adverse effects long term cyclosporine A (CyA) administration is chronic nephrotoxicity. Several studies have suggested that alterations L-arginine (L-Arg) nitric oxide (NO) pathway may be involved in pathogenesis CyA-induced kidney damage. Aim: We postulated vivo activation L-Arg-NO might a beneficial effect on renal Conditions NO enhancement was established with L-Arg supplementation and blockade N-nitro-L-Arg methyl ester (L-NAME). tested hypothesis that, if CyA alters intrarenal synthesis, then exogenous could limit injury, contrary, L-NAME, potent competitive inhibitor enhance Harmful indirectly supports model Methods: Rats were administered vehicle (VH), (7.5 mg/kg/day), + (2g/kg/day), L-NAME (5 mg/100 ml/day), VH L-Arg, sacrificed at end experiment. Body weight, serum creatinine, blood urea nitrogen (BUN) levels determined. Tubular injury interstitial fibrosis evaluated semiquantitatively using scoring systems paraffin sections stained hematoxylin/eosin (H/E), Masson’s trichromic periodic acid-Schiff (PAS). Results: The group developed marked characterized by significant increase creatinine BUN, histopathological including tubular dilatation, vacuolization, necrosis, cell infiltration tubulointerstitial fibrosis. reduced level. treatment significantly enhanced biosynthesis protected animals from In contrast strikingly level, worsened biochemical alterations. Conclusion: Chronic nephrotoxicity can aggravated ameliorated suggesting protective