The detail mechanisms in which renal ischemia reperfusion IRI happens are still indistinct. Various elements required in the pathogenesis include oxidative stress, inflammation, cellular necrosis, apoptosis, renal pathophysiological changes etc. To understand the pathway of ischemia reperfusion in renal we tested the hypothesis that GIT-27 attenuated renal ischemia reperfusion injury as specific Toll-like receptor inhibitors. Adult (3 to 5 month) male Sprague Dawely rats, and their weights ranged from 180 to 390 gm, were pre-treated with Git-27 intra peritoneal, plasma NGAL and cytokines mediator's in plasma and renal were analyzed by enzyme-linked immunosorbent assay (ELISA). And the pathological changes and cells injury in the renal were examined using hematoxylin and Eosin staining. Improvement of renal ischemia reperfusion by GIT-27 resulted in improved renal function and greater reductions in inflammatory mediators, and kidney injury. Taken together, GIT-27 significantly improved renal function following I/R through down-regulation of Tolllike receptor and serve as a potential therapeutic in ischemia reperfusion induced acute kidney injury.
Renal ischemia-reperfusion (Renal I/R) leads to acute kidney injury (AKI),a major kidney disease associated with an increasing prevalence and high mortality rates. A variety of experimental models,both in vitro and in vivo,have been used to study the pathogenic mechanisms of ischemic AKI and to test reno-protective strategies. Aim: To study potential protective effects of artesunate on renal I/R injury. Renal I/R injury was unilaterally induced in adult (3 to 5 months) male Sprague-Dawely rats,whose weights ranged from 180 to 390 g. Thereafter,the animals were pre-treated with artesunate intra-peritoneally,and at the end of reperfusion sacrificed humanely. Plasma,serum and tissue samples were obtained for analysis. Plasma concentrations of NGAL (neutrophil gelatinase associated lipocalin),an iron-trafficking protein involved in multiple processes such as apoptosis,innate immunity and renal development,and tissue concentrations of IL-18 (Interleukin-18) were measured via ELISA analysis. Serum urea and creatinine were also measured in the samples. Artesunate improved renal ischemia reperfusion,including renal function and brought about reductions in inflammatory mediators and kidney tissue injury. Plasma concentrations of NGAL and tissue concentrations of IL-18 were significantly (p < 0.05) lower in the artesunatepretreated group than in the vehicle and control groups. Furthermore,serum concentrations of urea and creatinine were significantly (p < 0.05) decreased in the pretreated group as compared to the control group. Artesunate can significantly improve renal function following I/R through down-regulation of inflammatory parameters and NGAL expression. Furthermore,it could serve as a potential therapy in ischemia reperfusion-induced acute kidney injury.
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