نتایج جستجو برای: renal ischemia reperfusion injury
تعداد نتایج: 597757 فیلتر نتایج به سال:
Tumor necrosis factor (TNF)-alpha plays a crucial role in the pathogenesis of ischemia/reperfusion-induced renal injury. We demonstrated recently that the preischemic treatment with resiniferatoxin, a transient receptor potential vanilloid 1 (TRPV1) agonist, attenuates renal TNF-alpha mRNA expression and improves ischemia/reperfusion-induced renal injury in rats. In addition, we found that SA13...
Long-term kidney graft survival is affected by different variables including donor condition, ischemia-reperfusion injury, and graft rejection during the transplantation process. The complement system is an important mediator of renal ischemia-reperfusion injury and in rejecting allografts. However, donor complement C3 seems to be crucial in renal transplantation-related injury as renal injury ...
Background: Renal injuries associated with ischemia/reperfusion are a prevalent clinical phenomenon that can cause the emergence of progressive kidney diseases, eventually leading to chronic kidney injuries. The present study was conducted to evaluate the results obtained from non-invasive imaging using small-animal SPECT and investigate the recovery process in an animal model of renal ischemia...
Renal ischemia as a course of renal transplantation is a common cause of renal dysfunction as renal failure. The purpose of this study was to investigate the influence of ascorbic acid on blood urea nitrogen (BUN), creatinine (Cr) and resistive index (RI) for dog models with renal ischemia-reperfusion (I/R) injury. Renal ischemia was induced on 6 Beagle dogs. The left kidney was exposed to norm...
CD4+ T cells contribute to the pathogenesis of ischemia-reperfusion injury, which is the primary cause of delayed graft failure after kidney transplantation. The TIM-1:TIM-4 pathway participates in the activation/differentiation of CD4+ T cells, suggesting that it may modulate ischemia-reperfusion injury. Here, we studied the role of TIM-1 in a murine uninephrectomized renal ischemia-reperfusio...
results the basic mechanism of hepatic ischemia – reperfusion injury is one of blood deprivation during ischemia, followed by the return of flow during reperfusion. it involves a complex series of events, such as mitochondrial deenergization, adenosine-5'-triphosphate depletion, alterations of electrolyte homeostasis, as well as kupffer cell activation, oxidative stress changes and upregulation...
Introduction: This study investigated the effect of berberine on renal dysfunction and histological damages of the lung induced by renal ischemia/ reperfusion at an early stage. Methods: There were four experimental groups of adult male rats (n=7). Seven days before induction of ischemia, the Ber+I/R group received oral (by gavage) berberine (15 mg/kg/day) while the I/R group received distil...
The volatile anesthetic isoflurane protects against renal ischemia and reperfusion injury by releasing renal tubular TGF-β1. As adenosine is a powerful cytoprotective molecule, we tested whether TGF-β1 generated by isoflurane induces renal tubular ecto-5'-nucleotidase (CD73) and adenosine to protect against renal ischemia and reperfusion injury. Isoflurane induced new CD73 synthesis and increas...
objectives: curcumin has anti-inflammatory and antioxidative properties. the objective of this study was to investigate the therapeutic effects of curcumin on functional disturbances, oxidative stress, and leukocyte infiltration induced by renal ischemia/reperfusion (i/r). materials and methods: animals were randomly divided into 9 groups. the groups with 24-h reperfusion consisted of sham-24h,...
ischemia-reperfusion injury is the tissue damage happened when blood supply returns to the tissue after a period of ischemia or shortage of oxygen. this brain injury initiates an inflammatory response involving the expression of adhesion molecules and cytokines. the aim of this study is investigating the effect of hydroalcoholic extract of cyperus rotundus l. on the expression of the bcl-x1 an...
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