• Sprague-Dawley (SD) rats were subjected to bilateral renal artery clamping for 45 min followed by perfusion restoration for establishing a simulated renal IRI model. (frontiersin.org)
  • Thus, pioglitazone ameliorates renal IRI by inhibiting the NF-κB signaling pathway and inflammatory response in rats. (frontiersin.org)
  • In two models of partial renal IR with and without ischemia preconditioning (IPC) and using Mas receptor (MasR) blockade, A779 or its vehicle, the renal vascular responses to angiotensin II (Ang II) administration in two-kidney-one-clip (2K1C) hypertensive rats were determined. (hindawi.com)
  • The rats in the IR group underwent 45 min partial kidney ischemia, and the animals in the IPC + IR group underwent two 5 min cycles of partial kidney ischemia followed by 10 min reperfusion and partial kidney ischemia for 45 min. (hindawi.com)
  • In the present work, a hypoxia/reoxygenation (H/R) model in NRK-52E cells and ischemia-reperfusion model in rats were used. (mdpi.com)
  • To investigate the effect of sevoflurane on renal ischemia-reperfusion injury (IRI) in rats and its regulatory effect on reperfusion injury salvage kinase (RISK) signaling pathway. (ajol.info)
  • Sevoflurane represses the release of inflammatory factors, lowers ROS level and apoptosis of renal cells and improves renal function through activation of RISK signaling pathway in kidney tissues of rats with renal IRI. (ajol.info)
  • Therefore, we were curious to know if Anwu can have a protective effect on remote organ injury after II/R. The purpose of the present study was to examine the effect of Anwu on the remote renal injury induced by II/R in rats and investigate its mechanism. (phcog.com)
  • After reperfusion or sham operation, blood and kidneys were collected from the rats for the detection of relative biochemical parameters. (phcog.com)
  • Anwu has a protective effect against the II/R-induced remote renal injury in rats, which may be related to its regulation of antioxidant, anti-inflammatory, and antiapoptotic pathways. (phcog.com)
  • Renal damage in rats induced by myocardi. (sdu.edu.tr)
  • Ischemia/reperfusion-induced renal failure in rats as a model for evaluating cell therapies. (wakehealth.edu)
  • In this research the protective effects of the methanolic extract of S. multicaulis was evaluated in renal ischaemia-reperfusion injuries in rats. (healthbiotechpharm.org)
  • In the treatment groups 1-3, before causing ischemia in the kidneys, rats received 50, 100, and 150 mg/kg/day doses of the extract orally for 20 days, then ischaemia was created. (healthbiotechpharm.org)
  • Investigating the protective effect of the methanolic extract of Salvia multicaulis on renal ischemia-reperfusion injuries in rats', Health Biotechnology and Biopharma (HBB) , 7(1), pp. 60-77. (healthbiotechpharm.org)
  • Eighty male and female rats were assigned into 8 groups, 4 groups in each gender including: sham, renal ischemia for 45min by clamping renal vessels followed by 3, 24 or 48h reperfusion. (phypha.ir)
  • 8. Dehghani A, Saberi S, Nematbakhsh M. Role of Mas receptor antagonist A799 in renal blood flow response to Ang 1-7 after bradykinin administration in ovariectomized estradiol-treated rats. (phypha.ir)
  • Gender difference in the development of cardiac lesions following acute ischemic-reperfusion renal injury in albino rats. (phypha.ir)
  • The protective effect of erythropoietin on renal injury induced by abdominal aortic-ischemia-reperfusion in rats. (phypha.ir)
  • Materials and Methods: Sprague-Dawley rats (200-300 g) were subjected to 40 minutes of renal warm ischemia. (elsevierpure.com)
  • We evaluated the effect of DEX-MVs on NRK-52E cells migration, hypoxia/reoxygenation (H/R)-induced cell death, and reactive oxygen species (ROS) amount and renal IR model in rats. (ntnu.edu.tw)
  • The objective of this study was to determine whether homing of endothelial progenitor cells (EPCs) induced by ischemic preconditioning (IPC) contributed to the protection of renal acute ischemia-reperfusion injury (IRI) in male rats. (annalsoftransplantation.com)
  • Rats, subjected to bilateral renal ischemia (45 min) followed by reperfusion (6 h), were administered EUK-134 (0.3 and 3 mg/kg, i.v.) prior to and during reperfusion, after which biochemical and histological indicators of renal dysfunction and injury were measured. (scienceopen.com)
  • The effects of EUK-134 on serum levels of NO in rats subjected to renal I/R or on NO production by PTCs incubated with interferon-γ (IFN-γ, 100 IU/ml) and bacterial lipopolysaccharide (LPS, 10 µg/ml) in combination for 24 h were also measured. (scienceopen.com)
  • However, EUK-134 also reduced nitrosative stress caused by I/R in vivo (reduction of iNOS expression and nitrotyrosine formation), which was reflected by a significant reduction in serum NO levels in rats subjected to renal I/R. Specifically, serum NO levels were reduced from 57 ± 12 (n = 12, I/R only) to 23 ± 3 m M (n = 12, I/R +3 mg/kg EUK-134). (scienceopen.com)
  • One of the primary causes of ARF is ischemia/reperfusion (I/R). Inflammatory process and oxidative stress are thought to be the major mechanisms causing I/R. MK-886 is a potent inhibitor of leukotrienes biosynthesis which may have anti-inflammatory and antioxidant effects through inhibition of polymorphonuclear leukocytes (PMNs) infiltration into renal tissues. (biomedcentral.com)
  • Inhibition of oxidative stress in renal ischemia-reperfusion injury. (phypha.ir)
  • We propose that EUK-134 reduces renal I/R injury not only via reduction of oxidative stress, but also by reducing nitrosative stress caused by renal I/R. (scienceopen.com)
  • Therefore, in the present study, we evaluated the effect of mitochondrial complex 1 inhibition by rotenone on the chronic renal damage induced by acute ischemia-reperfusion. (oncotarget.com)
  • Furthermore, we examined the effect of inhibition of complement-factor C5 on renal I/R injury. (maastrichtuniversity.nl)
  • abstract = "Inhibition of complement factor C5 protects against renal ischemia-reperfusion injury: inhibition of late apoptosis and inflammation.De Vries B, Matthijsen RA, Wolfs TG, Van Bijnen AA, Heeringa P, Buurman WA.Department of General Surgery, Nutrition and Toxicology Research Institute Maastricht (NUTRIM), Maastricht University, Maastricht, The Netherlands.BACKGROUND: Complement has been implicated in the pathophysiology of renal ischemia-reperfusion (I/R) injury. (maastrichtuniversity.nl)
  • Inhibition of renal Rho kinase attenuates ischemia/reperfusion-induced injury. (rug.nl)
  • In this review we discuss current evidence that complement activation contributes to progression of CKD, how complement could cause renal inflammation and whether complement inhibition would slow progression of renal disease. (wjgnet.com)
  • In support of the integral involvement of NHE activity during organ ischemia, NHE1 inhibition has been shown to exert a protective effect during cardiac ischemia . (tocris.com)
  • Inhibition of α v ß 5 Integrin Attenuates Vascular Permeability and Protects against Renal Ischemia-Reperfusion Injury. (bvsalud.org)
  • 11. Hassoun HT, Lie ML, Grigoryev DN, Liu M, Tuder RM, Rabb H. Kidney ischemia-reperfusion injury induces caspase-dependent pulmonary apoptosis. (phypha.ir)
  • Consistently, DEX-MVs were better than MV in increasing CD44 expression, improving IR-depressed renal hemodynamics and renal erythropoietin expression, inhibiting IR-enhanced renal ROS level, tubular injury score, miR-122-5p expression, pNF-κB expression, Bax/caspase 3/poly(ADP-ribose) polymerase (PARP)-mediated apoptosis, blood urea nitrogen, and creatinine levels. (ntnu.edu.tw)
  • In summary, intrarenal arterial DEX-MV conferred further therapeutic potential to reduce renal IR injury through the miR-122-5p/erythropoietin/apoptosis axis. (ntnu.edu.tw)
  • Over the last few decades, it has been studied that the mechanisms of cisplatin-induced kidney damage are complex and involved numerous cellular and molecular processes including inflammation, apoptosis, accumulation of cisplatin in renal tubular cells via renal drug transporters, Ctr1 and OCT2, and involvement of mitogen-activated protein kinases (MAPK) pathways [ 3 ] [ 4 ]. (thieme-connect.com)
  • 9 ] reported curcumin administration provided protection against cisplatin-induced renal tubular cell apoptosis. (thieme-connect.com)
  • Background: It has been demonstrated that myocardial ischemia/reperfusion (MI/R) causes renal damage. (sdu.edu.tr)
  • However, reperfusion following a period of prolonged ischemia can often cause myocardial ischemia-reperfusion (I/R) injury, leading to damage of cardiac tissues ( 5 ). (spandidos-publications.com)
  • Moreover, BB5.1 treatment significantly protected against I/R-induced renal dysfunction. (maastrichtuniversity.nl)
  • Here we investigate the effect of EUK-134, a synthetic superoxide dismutase and catalase mimetic, (i) on renal dysfunction and injury caused by I/R in vivo and (ii) on proximal tubular cell (PTC) injury and death caused by oxidative and nitrosative stress. (scienceopen.com)
  • EUK-134 produced a significant reduction in renal dysfunction and injury caused by I/R. Specifically, serum creatinine levels, an indicator of renal dysfunction, were reduced from 227 ± 11 (n = 12, I/R only) to 146 ± 9 µ M (n = 12, I/R +3 mg/kg EUK-134). (scienceopen.com)
  • The findings emphasize the role of concomitant oxidative and nitrosative stress and the role of peroxynitrite in the ensuing renal dysfunction. (scienceopen.com)
  • These sequelae of renal ischemia are a result of endothelial dysfunction, which is most probably responsible for the 'no-reflow' phenomenon and further aggravation of tubular ischemia during the early reperfusion period. (scienceopen.com)
  • In conclusion, the intricate relations between endothelial and epithelial cells, based in part on the relations between endothelial and inducible nitric oxide synthases, are perturbed in renal ischemia primarily as a result of endothelial dysfunction precipitating epithelial injury. (scienceopen.com)
  • Nitric oxide production (by iNOS) may play several roles in renal pathophysiology, including induction of tubular damage. (biomedcentral.com)
  • Nitric oxide in acute renal failure: NOS versus NOS. (scienceopen.com)
  • This overview provides information on the pathophysiology of the inducible nitric oxide synthase/nitric oxide (iNOS/NO) system in the injury to cultured renal tubular epithelia, freshly isolated proximal tubules, and the whole organ after hypoxic or ischemic insult. (scienceopen.com)
  • BACKGROUND: Complement has been implicated in the pathophysiology of renal ischemia-reperfusion (I/R) injury. (maastrichtuniversity.nl)
  • Serum creatinine measurement is not reliably indicative of underlying pathophysiology (ie, it does not allow differentiation of hemodynamically mediated changes in kidney function, such as prerenal azotemia from intrinsic renal failure or obstructive uropathy from structural kidney damage). (medscape.com)
  • In this study, we investigated the role of the NF-κB signaling pathway and inflammation in the amelioration of renal IRI using pioglitazone. (frontiersin.org)
  • Therefore, in this study, we aimed to investigate the molecular mechanisms underlying pioglitazone hydrochloride-mediated amelioration of renal IRI with respect to the nuclear factor-kappaB (NF-κB) signaling pathway and inflammatory response using a rat model. (frontiersin.org)
  • METHODS: Five pigs were subjected to 60 min of focal kidney ischemia. (au.dk)
  • MATERIALS AND METHODS: We randomly divided 34 Macaca cynomolgus monkeys into groups 1 and 2, which received a renal autograft after 2 hours of cold ischemia, and groups 3 and 4, which received the autograft after 24 hours of cold ischemia. (unica.it)
  • ARA290 Protects Against Renal Ischemia/Reperfusion Injury. (ox.ac.uk)
  • The microvascular and parenchymal organ damage induced upon ischemia tissue reperfusion is mainly attributed to the reactive oxygen-free radicals, and it has been demonstrated in many organs. (frontiersin.org)
  • CONCLUSIONS: Renal I/R is followed by activation of the complement system and intrarenal deposition of C3 and MAC. (maastrichtuniversity.nl)
  • Cell-specific delivery of a transforming growth factor-beta type I receptor kinase inhibitor to proximal tubular cells for the treatment of renal fibrosis. (rug.nl)
  • Renal targeting of kinase inhibitors. (rug.nl)
  • The renin-angiotensin system (RAS) and hypertension also may be influenced by renal IR injury. (hindawi.com)
  • In contrast to the negative effects of Ang II on the renal circulation, Ang1-7 as a renoprotective agent improves endothelial function, which increases RBF and decreases renal vascular resistance (RVR) [ 16 ]. (hindawi.com)
  • Studies in animal models indicate that ischemia triggers alterations in endothelial function that contribute significantly to the overall degree and severity of a kidney injury. (eurekaselect.com)
  • Interestingly, PTX3 deposits co-localized with activation of the terminal Complement complex (C5b-9) on endothelial cells, indicating that PTX3-mediated Complement activation occurred mainly at the renal vascular level. (unicatt.it)
  • In rat renal tissue, pioglitazone treatment decreased the serum levels of post-renal IRI creatinine and urea nitrogen, as well as necrosis. (frontiersin.org)
  • It is considered as a major cause of acute renal failure and the main factor in early recovery of renal graft function and long-term survival post renal transplantation. (frontiersin.org)
  • We examined whether intrarenal arterial transplantation of dexmedetomidine (DEX) preconditioning ADSC-derived microvesicles (DEX-MVs) could promote further therapeutic potential to reduce renal IR injury. (ntnu.edu.tw)
  • Acute renal failure (ARF) is an important clinical problem with a high mortality and morbidity. (biomedcentral.com)
  • Progressive AKI leads to acute renal failure (ARF)[ 1 ]. (biomedcentral.com)
  • Acute kidney injury (AKI) is a common clinical syndrome characterized by rapid deterioration of renal function. (biomedcentral.com)
  • In our previous study, we found that Anwu can improve the intestinal function after ischemia/reperfusion. (phcog.com)
  • PURPOSE: We established a primate model to investigate the effects of the antileukocyte function associated antigen 1 (CD 11a) mAb odulimomab (Imtix-Sangstad, Lyon, France) for preventing renal ischemia-reperfusion injury. (unica.it)
  • Groups 1 and 3 monkeys were treated with an antileukocyte function associated antigen 1 mAb before cold ischemia and then for 3 days, while groups 2 and 4 monkeys received an IgG1 isotype control. (unica.it)
  • RESULTS: A decrease in renal function was shown after 2 hours of cold ischemia with tubular necrosis and mild cell infiltration, while after 24 hours of cold ischemia there was severe renal failure with tubular and glomerular necrosis, and leukocyte infiltration. (unica.it)
  • A significant improvement in renal function and decrease in kidney lactoferrin content was evident in group 1 compared to group 2 at 72 hours, while no significant difference was noted in groups 3 and 4. (unica.it)
  • The protective effects of antileukocyte function associated antigen 1 mAb on renal injury was not as dramatic as in rodent models but a significant improvement in renal function was observed in treated animals after 2 hours of cold ischemia. (unica.it)
  • Serum creatinine may not become elevated before substantial kidney function has been lost due to renal reserve. (medscape.com)
  • renal adenosine A1 receptor activation during the renal ischemia-reperfusion injury is detrimental to renal function. (eurekamag.com)
  • [ 1 ] At present, serum creatinine, which is used to measure the glomerular filtration rate (GFR), is the most commonly used marker of renal function. (medscape.com)
  • [ 24 ] Small increases in postoperative serum creatinine levels after cardiac surgery have been reported to be associated with increased morbidity and mortality even if the renal function has returned to normal at discharge. (medscape.com)
  • Restoration of blood supply, termed reperfusion, has been used to treat ischemic myocardium and prevent further tissue damage. (spandidos-publications.com)
  • CABG may be performed as an emergency procedure in the context of an ST-segment elevation MI (STEMI) in cases where it has not been possible to perform percutaneous coronary intervention (PCI) or where PCI has failed and there is persistent pain and ischemia threatening a significant area of myocardium despite medical therapy. (medscape.com)
  • One of the primary causes of ARF is I/R which is a drop in blood flow leading to inadequate supply of oxygen and nutrients to renal tissue which can be caused by, amongst others, surgery, organ transplantation and shock [ 1 ]. (biomedcentral.com)
  • Attenuation of ischemia-reperfusion injury in a canine model of autologous renal transplantation. (musc.edu)
  • Future large and well-designed randomized trails should explore the more appropriate dose of dexmedetomidine to maximize its renal protective effect with less side effects affecting prognosis. (medscape.com)
  • Renal IRI models were created in model and sevoflurane groups, while sham group had no ligation. (ajol.info)
  • Here, we assessed the metabolic alterations following subclinical focal ischemia-reperfusion injury with hyperpolarized [1- 13 C]pyruvate MRI in a porcine model. (au.dk)
  • To investigate the involvement of complement in I/R injury, we studied the activation and deposition of complement in a murine model of renal I/R injury. (maastrichtuniversity.nl)
  • CONCLUSIONS: This study provides evidence for the validity of this ischemia-reperfusion injury model in primates. (unica.it)
  • Our study investigated the role of PTX3 as possible modulator of Complement activation in a swine model of renal ischemia/reperfusion (I/R) injury. (unicatt.it)
  • The renal vascular responses to graded Ang II (30, 100, 300, and 1000 ng kg −1 .min −1 ) infusion using A779 or its vehicle were measured at constant renal perfusion pressure. (hindawi.com)
  • No significant differences were detected between the groups in renal blood flow (RBF) or renal vascular resistance (RVR) responses to Ang II infusion when MasR was not blocked. (hindawi.com)
  • IR promotes a cascade of molecular events that lead to renal vascular and tubular damage and, ultimately, acute kidney injury (AKI) [ 2 - 4 ]. (hindawi.com)
  • In addition, there is discussion of how intrinsic damage to the endothelium impairs homeostatic responses in vascular tone as well as promotes leukocyte adhesion and exacerbating the reduction in renal blood flow. (eurekaselect.com)
  • RATIONALE AND OBJECTIVE: Vascular cell adhesion molecule-1 (VCAM-1) is upregulated in ischemia reperfusion injury (IRI), persisting after restoration of blood flow. (ox.ac.uk)
  • At 24 h post-operatively, we assessed the serum levels of creatinine and urea nitrogen, expression levels of peroxisome proliferator-activated receptor gamma (PPAR-γ) and NF-κB-related (p-IKK-β and IκB-α) proteins, and mRNA expression levels of the inflammatory cytokines, including TNF-α and MCP-1, in the renal tissue of various study groups. (frontiersin.org)
  • Dexmedetomidine is widely used for perioperative anesthesia/analgesia, and may have a more profound renal protection by stabilizing the sympathetic system, exerting anti-inflammatory effects and attenuating ischemia/reperfusion (I/R) injury. (medscape.com)
  • Intravenous adipose mesenchymal stem cells (ADSCs) attenuate renal ischemia/reperfusion (IR) injury but with major drawbacks, including the lack of a specific homing effect after systemic infusion, cell trapping in the lung, and early cell death in the damaged microenvironment. (ntnu.edu.tw)
  • In vivo quantification of VCAM-1 expression in renal ischemia reperfusion injury using non-invasive magnetic resonance molecular imaging. (ox.ac.uk)
  • 15. Kher A, Meldrum KK, Wang M, Tsai BM, Pitcher JM, Meldrum DR. Cellular and molecular mechanisms of sex differences in renal ischemia-reperfusion injury. (phypha.ir)
  • Renal indexes were not significantly different among all groups. (phcog.com)
  • However, the mechanism underlying complement-mediated renal I/R injury is thus far unknown. (maastrichtuniversity.nl)
  • Reperfusion injury and reactive oxygen species: the evolution of a concept. (phypha.ir)
  • Unlike the other NHE isoforms, NHE3 is recycled between apical membranes and the endosomal compartment of epithelial cells where it has a significant involvement in renal and intestinal Na + absorption. (tocris.com)
  • Intestinal ischemia/reperfusion (II/R) can cause injury of remote organs, including acute renal injury. (phcog.com)