The nuclear protein high-mobility group box 1 (HMGB1) is a key trigger for the inflammatory reaction during liver ischemia reperfusion injury (IRI). Hydrogen treatment was recently associated with down-regulation of the expression of HMGB1 and pro-inflammatory cytokines during sepsis and myocardial IRI, but it is not known whether hydrogen has an effect on HMGB1 in liver IRI. A rat model of 60 minutes 70% partial liver ischemia reperfusion injury was used. Hydrogen enriched saline (2.5, 5 or 10 ml/kg) was injected intraperitoneally 10 minutes before hepatic reperfusion. Liver injury was assessed by serum alanine aminotransferase (ALT) enzyme levels and histological changes. We also measured malondialdehyde (MDA), hydroxynonenal (HNE) and 8-hydroxy-guanosine (8-OH-G) levels as markers of the peroxidation injury induced by reactive oxygen species (ROS). In addition, pro-inflammatory cytokines including TNF-α and IL-6, and high mobility group box B1 protein (HMGB1) were measured as markers of post
TY - JOUR. T1 - Pirfenidone alleviates lung ischemia-reperfusion injury in a rat model. AU - Saito, Masao. AU - Chen-Yoshikawa, Toyofumi F.. AU - Suetsugu, Kimitaka. AU - Okabe, Ryo. AU - Takahagi, Akihiro. AU - Masuda, Satohiro. AU - Date, Hiroshi. PY - 2019/7. Y1 - 2019/7. N2 - Objective: Lung ischemia-reperfusion injury is among the complications seen after lung transplantation, resulting in morbidity and mortality. Pirfenidone, an antifibrotic agent for the treatment of idiopathic pulmonary fibrosis, is reported to have cytoprotective properties in various disease models. The purpose of this study was to investigate the effect of pirfenidone on lung ischemia-reperfusion injury. Methods: Male Lewis rats (260-290 g) were divided into 3 groups: sham group (n = 5), warm ischemia (WI) group (n = 10), and WI plus pirfenidone (WI+PFD) group (n = 10). The sham group underwent 210 minutes of perfusion without ischemia. The WI and WI+PFD groups underwent 90 minutes of warm ischemia and 120 minutes of ...
TY - JOUR. T1 - Methane attenuates hepatic ischemia/reperfusion injury in rats through antiapoptotic, anti-inflammatory, and antioxidative actions. AU - Ye, Zhouheng. AU - Chen, Quyang. AU - Zhang, Rongjia. AU - Nakao, Atsunori. AU - Fan, Danfeng. AU - Zhang, Ting. AU - Gu, Zhengyong. AU - Tao, Hengyi. AU - Sun, Xuejun. PY - 2015/9/1. Y1 - 2015/9/1. N2 - Hepatic ischemia/reperfusion (I/R) injury, which occurs in various diseases, introduces severe tissue damage and liver dysfunction. However, no promising therapies for such a significant condition currently exist. Methane has been suggested to exert a protective effect against intestinal I/R injury. In this study, we introduced methane to treat hepatic I/R injury to show its promising protective effect. Also, intraperitoneal injection with methane-rich saline, which could have potential clinical applications, was applied as a new method. Partial liver warm ischemia was applied in Sprague-Dawley rats for 60 min followed by succedent reperfusion. ...
TY - JOUR. T1 - Impact of epoxyeicosatrienoic acids in lung ischemia-reperfusion injury.. AU - Townsley, Mary I.. AU - Morisseau, Christophe. AU - Hammock, Bruce. AU - King, Judy A.. PY - 2010/2. Y1 - 2010/2. N2 - OBJECTIVE: Epoxyeicosatrienoic acids (EETs) are protective in both myocardial and brain ischemia, variously attributed to activation of K(ATP) channels or blockade of adhesion molecule upregulation. In this study, we tested whether EETs would be protective in lung ischemia-reperfusion injury. METHODS: The filtration coefficient (K(f)), a measure of endothelial permeability, and expression of the adhesion molecules vascular cell adhesion molecule (VCAM) and intercellular adhesion molecule (ICAM) were measured after 45 minutes ischemia and 30 minutes reperfusion in isolated rat lungs. RESULTS: K(f) increased significantly after ischemia-reperfusion alone vs time controls, an effect dependent upon extracellular Ca(2+) although not on the EET-regulated channel TRPV4. Inhibition of ...
TY - JOUR. T1 - (−)-Phenserine inhibits neuronal apoptosis following ischemia/reperfusion injury. AU - Chang, Cheng Fu. AU - Lai, Jing Huei. AU - Wu, John Chung Che. AU - Greig, Nigel H.. AU - Becker, Robert E.. AU - Luo, Yu. AU - Chen, Yen Hua. AU - Kang, Shuo Jhen. AU - Chiang, Yung Hsiao. AU - Chen, Kai Yun. PY - 2017/12/15. Y1 - 2017/12/15. N2 - Stroke commonly leads to adult disability and death worldwide. Its major symptoms are spastic hemiplegia and discordant motion, consequent to neuronal cell death induced by brain vessel occlusion. Acetylcholinesterase (AChE) is upregulated and allied with inflammation and apoptosis after stroke. Recent studies suggest that AChE inhibition ameliorates ischemia-reperfusion injury and has neuroprotective properties. (−)-Phenserine, a reversible AChE inhibitor, has a broad range of actions independent of its AChE properties, including neuroprotective ones. However, its protective effects and detailed mechanism of action in the rat middle cerebral ...
Protective Role of p70S6K in Intestinal Ischemia-Reperfusion Injury in Mice. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
Purpose: Liver ischemia reperfusion injury (IRI) remains a clinical problem associated with both surgical and non-surgical settings. Innate immune-dominated inflammation drives the pathogenesis of liver injuries. Although the activation of liver inflammation by IR have been studied extensively, few has been focused on the inflammation resolution in the disease process.. *Methods: In a murine liver partial warm ischemia model, we characterized the inflammation resolution during IR at histological, cellular and molecular levels. The role of Kupffer cells (KCs) was determined by clodronate-liposome (CL)-mediated depletion, and their functional mechanisms were explored by the inhibition of KC efferocytosis via TIM-4 blocking Abs, during the recovery stage of liver IRI (three doses at 24h, day 3 and day5 post reperfusion).. *Results: The restoration of liver homeostasis from a 90 min ischemia lasts for 7 days, as defined by: (i) repair of hepatocellular damage, (ii) clearance of infiltrating ...
TY - JOUR. T1 - Role of the bronchial circulation in ischemia-reperfusion lung injury. AU - Pearse, D. B.. AU - Wagner, E. M.. PY - 1994/1/1. Y1 - 1994/1/1. N2 - Bronchial arterial (BA) perfusion could modify pulmonary arterial (PA) ischemia-reperfusion (IR) injury by promoting clearance of peribronchial edema or limiting edema formation through maintenance of pulmonary vessel integrity via bronchopulmonary anastomotic or pulmonary vasa vasorum flow. The purpose of this study was to determine the effect of BA perfusion on IR injury in isolated sheep lungs. In 12 lungs (BA++) the BA was perfused throughout 30 min of PA ischemia and 180 min of reperfusion. In 12 lungs (BA- +) BA perfusion was begun with PA reperfusion, and in 15 lungs (BA--) the BA was never perfused. After 180 min, extravascular lung water was less (P , 0.05) in BA++ and BA-+ lungs [4.70 ± 0.16 and 4.57 ± 0.18 g/g blood-free dry lung (bfdl)] than in BA-- lungs (5.23 ± 0.19 g/g bfdl). The reflection coefficient for albumin was ...
TY - JOUR. T1 - Cannabinoid-2 receptor mediates protection against hepatic ischemia/reperfusion injury. AU - Bátkai, Sándor. AU - Osei-Hyiaman, Douglas. AU - Pan, Hao. AU - El-Assal, Osama. AU - Rajesh, Mohanraj. AU - Mukhopadhyay, Partha. AU - Hong, Feng. AU - Harvey-White, Judith. AU - Jafri, Anjum. AU - Haskó, G.. AU - Huffman, John W.. AU - Gao, Bin. AU - Kunos, George. AU - Pacher, Pál. PY - 2007/6. Y1 - 2007/6. N2 - Hepatic ischemia-reperfusion (I/R) injury continues to be a fatal complication that can follow liver surgery or transplantation. We have investigated the involvement of the endocannabinoid system in hepatic I/R injury using an in vivo mouse model. Here we report that I/R triggers several-fold increases in the hepatic levels of the endocannabinoids anandamide and 2-arachidonoylglycerol, which originate from hepatocytes, Kupffer, and endothelial cells. The I/R-induced increased tissue endocannabinoid levels positively correlate with the degree of hepatic damage and serum ...
TY - JOUR. T1 - Adenosine and inosine exert cytoprotective effects in an in vitro model of liver ischemia-reperfusion injury. AU - Modis, Katalin. AU - Gero, Domokos. AU - Stangl, Rita. AU - Rosero, Olivér. AU - Szijártó, Attila. AU - Lotz, Gábor. AU - Mohácsik, Petra. AU - Szoleczky, Petra. AU - Coletta, Ciro. AU - Szabo, Csaba. PY - 2013/2. Y1 - 2013/2. N2 - Liver ischemia represents a common clinical problem. In the present study, using an in vitro model of hepatic ischemia-reperfusion injury, we evaluated the potential cyto-protective effect of the purine metabolites, such as adenosine and inosine, and studied the mode of their pharmacological actions. The human hepatocellular carcinoma-derived cell line HepG2 was subjected to combined oxygen-glucose deprivation (COGD; 0-14-24 h), followed by re-oxygenation (0-4-24 h). Adenosine or inosine (300-1,000 μM) were applied in pretreatment. Cell viability and cytotoxicity were measured by the 3-(4,5-dimethyl-2-thiazolyl)-2, ...
Discussion. In this study, we used the ischemia/reperfusion model developed for kidney function and injury studies at the Department of Anesthesiology, Botucatu Medical School. This model consists of right nephrectomy in all animals, followed by randomization of the animals into four groups of 10 animals per group: Ischemia, Ischemia + drug, Non-ischemia, and Non-ischemia + drug. Thus, parecoxib was tested in two groups, in the presence and absence of I/R (IP and NIP groups), and NGAL levels were measured in all groups at four times to evaluate renal function.. Nephrectomy followed by ischemia/reperfusion may trigger mechanisms of renal preconditioning, reducing histological lesions and preserving or facilitating recovery of renal function in the ischemic kidney. For instance, animals that had not been nephrectomized prior to ischemia/reperfusion had oliguric renal failure, whereas animals that had been nephrectomized prior to I/R developed polyuric renal failure with better prognosis and ...
The Hamid Rabb Lab is involved in translational research aimed at understanding the molecular pathogenesis of kidney ischemia/reperfusion injury. Were interested in the development of novel treatments for kidney IRI.. Research Areas: kidney diseases, kidney ischemia/reperfusion injuries, nephrology ...
BACKGROUND: In contrast with various pre-clinical studies, recent clinical trials suggest that high dose erythropoietin (EPO) treatment following kidney transplantation does not improve short-term outcome and that it even increases the risk of thrombotic events. ARA290 is a non-erythropoietic EPO derivative and does not increase the risk of cardiovascular events, but potentially has cytoprotective capacities in prevention of renal ischemia/reperfusion injury. METHODS: Eight female Dutch Landrace pigs were exposed to unilateral renal ischemia for 45 minutes with simultaneous cannulation of the ureter of the ischemic kidney. ARA290 or saline was administered by an intravenous injection at 0, 2, 4 and 6 hours post-reperfusion. The animals were sacrificed seven days post-reperfusion. RESULTS: ARA290 increased glomerular filtration rate during the observation period of seven days. Furthermore, ARA290 tended to reduce MCP-1 and IL-6 expression 15 minutes post-reperfusion. Seven days post-reperfusion ARA290
To explore the effects of propofol post-conditioning (PPC) on hepatic ischaemia/reperfusion injury (HIRI) and the potential mechanisms that might be involved in the interaction of Brahma-related gene1(BRG1) and Nuclear-related factor 2(Nrf2). Patients were randomized into PPC(n = 16) and non-PPC(NPC)( n = 21) groups. Propofol(2 mg/kg) was infused within 10 min. of the onset of liver reperfusion during liver transplantation in the PPC group. Liver function tests, as well as Brg1, Nrf2, Heme oxygenase-1(HO-1) and NADPH:quinone oxidoreductase1(NQO1) expression levels were evaluated. CMV-Brg1 mice were designed to investigate the role of Brg1 overexpression during HIRI. Brg1 and Nrf2 siRNA were used to examine the relationship between Brg1 and Nrf2/HO-1 pathways in propofol-mediated effects in a human hepatocyte(L02) hypoxia/reoxygenation(H/R) model. In patients, PPC attenuated both donor liver pathological and function injury, and reducing oxidative stress markers, compared to the NPC group, 24 hrs ...
Myocardial infarction (MI) induces cardiac remodeling. This may increase the susceptibility of the infarcted heart to subsequent ischemic events. While chronic angiotensin II blockade is cardioprotective post-MI, the acute effects of angiotensin II i
1. Aihara T, Shiraishi M, Hiroyasu S, Hatsuse K, Mochizuki H, Seki S. et al. Ulinastatin, a protease inhibitor, attenuates hepatic ischemia/reperfusion injury by downregulating TNF-alpha in the liver. Transplant Proc. 1998;30:3732-4 doi:S0041-1345(98)01214-7 [pii] 2. Yang YL, Li JP, Xu XP, Dou KF, Yue SQ, Li KZ. Protective effects of tumor necrosis factor alpha antibody and ulinastatin on liver ischemic reperfusion in rats. World J Gastroenterol. 2004;10:3161-4 3. Klune JR, Dhupar R, Cardinal J, Billiar TR, Tsung A. HMGB1: endogenous danger signaling. Mol Med. 2008;14:476-84 doi:10.2119/2008-00034.Klune 4. Kang R, Livesey KM, Zeh HJ 3rd, Lotze MT, Tang D. HMGB1 as an autophagy sensor in oxidative stress. Autophagy. 2011;7:904-6 doi:15704 [pii] 5. Fan J, Li Y, Levy RM, Fan JJ, Hackam DJ, Vodovotz Y. et al. Hemorrhagic shock induces NAD(P)H oxidase activation in neutrophils: role of HMGB1-TLR4 signaling. J Immunol. 2007;178:6573-80 6. Tang D, Shi Y, Kang R, Li T, Xiao W, Wang H. et al. Hydrogen ...
TY - JOUR. T1 - Interleukin-10 delivery via mesenchymal stem cells. T2 - A novel gene therapy approach to prevent lung ischemia-reperfusion injury. AU - Manning, Eddie. AU - Pham, Si. AU - Li, Sen. AU - Vazquez-Padron, Roberto I. AU - Mathew, James. AU - Ruiz, Phillip. AU - Salgar, Shashikumar K.. PY - 2010/6/1. Y1 - 2010/6/1. N2 - Ischemia-reperfusion (IR) injury is an important cause of primary graft failure in lung transplantation. In this study, viral interleukin-10 (vIL-10)-engineered mesenchymal stem cells (MSCs) were tested for their ability to prevent lung IR injury. Bone marrow-derived MSCs were transduced with rvIL-10-retrovirus. After 120min of warm left lung ischemia, rats received ∼15×106 vIL-10-engineered MSCs (MSC-vIL-10), empty vector-engineered MSCs (MSC-vec), or saline intravenously. Mean blood oxygenation (PaO2/FiO2 ratio, mmHg) was measured at 4hr, 24hr, 72hr, and 7 days. As early as 4hr post-IR injury with MSC-vIL-10 treatment, blood oxygenation was significantly (p,0.05) ...
Objective To evaluate the impact of miR-148a on hepatic ischemia/reperfusion (I/R) injury via inhibiting Ca(2+)/calmodulin-dependent protein kinase IIα (CaMKIIα), and analyze the potential mechanism. Methods Liver I/R model was built in mice. Expression of CaMKIIα was detected in the hepatic tissues by Western blotting. The mRNA levels of miR-148a, CaMKIIα, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were analyzed by quantitative real-time PCR (qRT-PCR). HE staining was performed to observe morphological changes of the livers in each group. TUNEL was used to evaluate the degree of hepatocellular apoptosis in each group. Results After hepatic I/R injury, the expression of miR-148a increased, and it was negatively correlated with CaMKIIα. After therapy with exogenous miR-148a mimics, the protein expression of CaMKIIα, the mRNA levels of TNF-α and IL-1β, the degree of inflammatory cell infiltration and liver cell necrosis, and the level of hepatocellular apoptosis were all
TY - JOUR. T1 - Reduced ischemia and reperfusion injury following exercise training. AU - Libonati, Joseph R.. AU - Gaughan, John P.. AU - Hefner, Colleen A.. AU - Gow, Andrew. AU - Paolone, Albert M.. AU - Houser, Steven R.. PY - 1997. Y1 - 1997. N2 - We examined the effects of two exercise training modalities, i.e., low intensity endurance and sprint running, on in vitro, isovolumic myocardial performance following ischemia and reperfusion. Rats ran on a treadmill 5 d · wk-1 for 6 wk at the following levels: endurance; 20 m · min-1, 0% grade, 60 min · d-1 and sprint; five 1-min runs at 75 m · min-1, 15% grade interspersed with 1-min active recovery runs at 20 m · min-1, 15% grade. Both endurance and sprint training significantly improved exercise tolerance relative to control (P ,0.05) on two graded exercise tests. Buffer perfused hearts of control (N = 18), endurance (N = 20), and sprint (N = 13) trained animals underwent no-flow ischemia (20 min) and reperfusion (30 min) in a ...
We used COX-2-deficient mice to investigate the role of COX-2 in the mechanisms of liver I/R injury. Our data demonstrate that COX-2−/− mice, compared with their WT counterparts, were significantly less susceptible to liver I/R reperfusion injury. COX-2−/− mice showed reduced sGPT and sGOT levels after I/R injury, which indicate that liver damage was reduced in these mice as compared with WT controls. Inflammatory processes are mediated by multiple molecular mechanisms, and COX-2 is a major inflammatory mediator (44). Our observation that the lack of COX-2 confers a protective role in liver I/R injury is supported by our own celecoxib studies, in which selective COX-2 inhibition ameliorated mouse liver I/R injury. This observation is also supported by other publications, in which COX-2 inhibition was beneficial in rat liver I/R injury (22, 23).. Bcl-2 and Bcl-xL play an important role in inhibition of apoptotic cell death and are essential for maintenance of major organ systems (49). ...
TY - JOUR. T1 - Dexamethasone protects from renal ischemia/reperfusion injury. T2 - A possible association with SGK-1. AU - Rusai, Krisztina. AU - Prokai, A.. AU - Juanxing, C.. AU - Meszaros, K.. AU - Szalay, B.. AU - Pásti, K.. AU - Müller, V.. AU - Heemann, U.. AU - Lutz, J.. AU - Tulassay, T.. AU - Szabo, A.. PY - 2013/6/1. Y1 - 2013/6/1. N2 - Previous experimental data suggest that steroids might have protective effects during hypoxic/ischemic injury of various organs. In this study, the association between dexamethason (Dexa) treatment and the anti-apoptotic SGK-1 was tested in ischemic renal injury. In vitro, HK-2 cells were exposed to 24 h hypoxia, and the effect of Dexa incubation on SGK-1 expression / activation and on cell death was studied. In an in vivo rat model of unilateral renal IR, animals were treated with Dexa, and serum renal function parameters, tissue injury and SGK-1 expression and localization were examined after different reperfusion times (2 h, 4 h and 24 h). Dexa at ...
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TY - JOUR. T1 - Absence of glutathione peroxidase-1 exacerbates cerebral ischemia-reperfusion injury by reducing post-ischemic microvascular perfusion. AU - Wong, Connie Hoi Yee. AU - Bozinovski, Steven. AU - Hertzog, Paul John. AU - Hickey, Michael John. AU - Crack, Peter J. PY - 2008. Y1 - 2008. N2 - Mice deficient in the anti-oxidant enzyme glutathione peroxidase-1 (Gpx1) have a greater susceptibility to cerebral injury following a localized ischemic event. Much of the response to ischemia-reperfusion is caused by aberrant responses within the microvasculature, including inflammation, diminished endothelial barrier function (increased vascular permeability), endothelial activation, and reduced microvascular perfusion. However, the role of Gpx1 in regulating these responses has not been investigated. Wild-type and Gpx1-/- mice underwent focal cerebral ischemia via mid-cerebral artery occlusion followed by measurement of cerebral perfusion via laser Doppler and intravital microscopy. ...
TY - JOUR. T1 - Ex vivo application of carbon monoxide in UW solution prevents transplant-induced renal ischemia/reperfusion injury in pigs. AU - Yoshida, J.. AU - Ozaki, K. S.. AU - Nalesnik, M. A.. AU - Ueki, S.. AU - Castillo-Rama, M.. AU - Faleo, G.. AU - Ezzelarab, M.. AU - Nakao, A.. AU - Ekser, B.. AU - Echeverri, G. J.. AU - Ross, M. A.. AU - Stolz, D. B.. AU - Murase, N.. PY - 2010/4. Y1 - 2010/4. N2 - I/R injury is a major deleterious factor of successful kidney transplantation (KTx). Carbon monoxide (CO) is an endogenous gaseous regulatory molecule, and exogenously delivered CO in low concentrations provides potent cytoprotection. This study evaluated efficacies of CO exposure to excised kidney grafts to inhibit I/R injury in the pig KTx model. Porcine kidneys were stored for 48 h in control UW or UW supplemented with CO (CO-UW) and autotransplanted in a 14-day follow-up study. In the control UW group, animal survival was 80% (4/5) with peak serum creatinine levels of 12.0 ± 5.1 ...
Abstract. Background: Increasing evidences suggest that innate immunity is involved in cerebral ischemia-reperfusion (I/R) injury, but the liable innate immune receptors have not been completely elucidated. Here, we explored the role of the nucleotide-binding oligomerization domain (NOD)2, a member of the cytosolic NOD-like receptor family, in acute focal cerebral I/R injury.. Methods: An in vivo middle cerebral artery occlusion (MCAO) model that in wild type (WT) and NOD2 deficient (NOD2-/-) mice and in vitro model of oxygen glucose deprivation and reoxygenation (OGD/R) in cultured primary microglia and astrocytes were used to investigate the expression of NOD2 and explore the roles of NOD2 in ischemic stroke.. Results: Our results showed that NOD2 expression was significantly increased in microglia and astrocytes in response to the I/R insult. Pretreatment with muramyl dipeptide, an extrinsic ligand of NOD2, significantly increased the infarct volume and neurological dysfunction in mice ...
The objective of the present study was to determine whether preischemic administration of syringic acid (SA) would attenuate renal ischemia-reperfusion injury (IRI). Rats were divided into three groups: Sham group; IR group; and IR + SA group. The effects of SA were examined using biochemical parameters including serum ischemia-modified albumin (IMA), total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), tissue superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and malondialdehyde (MDA). The apoptosis status and histopathological changes were evaluated. After calculating the score for each histopathological change, the total score was obtained by summing all the scores. In the SA group, MDA, IMA, TOS, and OSI decreased significantly compared to the IR group. After SA administration, the increase in GPx activity was found to be significant. Apoptosis decreased significantly in the SA group compared with the IR group. The total score ...
Principal Investigator:WAKIDA Yasushi, Project Period (FY):1995 - 1997, Research Category:Grant-in-Aid for Scientific Research (C), Section:一般, Research Field:Circulatory organs internal medicine
Protective Effect of Pharmacological Preconditioning of Total Flavones of Abelmoschl Manihot on Cerebral Ischemic Reperfusion Injury in Rats. The present study was to investigate the effect of pharmacological preconditioning of total flavones of Abelmoschl Manihot (TFA) on cerebral ischemic reperfusion injury in rats. Rat cerebral isch.... ...
TY - JOUR. T1 - Cloning and expression of rat caspase-6 and its localization in renal ischemia/reperfusion injury. AU - Singh, Amar B.. AU - Kaushal, Varsha. AU - Megyesi, Judit K.. AU - Shah, Sudhir V.. AU - Kaushal, Gur P.. PY - 2002/1/1. Y1 - 2002/1/1. N2 - Background. Caspase-6 is an important member of the executioner caspases in the caspase family of cell death proteases. The executioner caspases are the major active caspases detected in apoptotic cells and are generally considered to mediate the execution of apoptosis by cleaving and inactivating intracellular proteins. However, the complete characterization of mRNA and protein of caspase-6 in rat and its expression in normal kidney and in disease state has not been previously elucidated. Methods. A rat kidney cortex λgt10 cDNA library was screened to isolate the full-length caspase-6 cDNA. The recombinant caspase-6 protein was characterized by expression in bacteria and by transient transfection in mammalian cells. The expression in ...
Ischemia/reperfusion injury (IRI) remains a major problem in organ transplantation, which represents the main cause of graft dysfunction posttransplantation. Hepatic IRI is characterized by an excessive inflammatory response within the liver. Mesenchymal stem cells (MSCs) have been shown to be immunomodulatory cells and have the therapeutic action on IRI in several organs. However, the mechanism of regulatory effect of MSCs on IRI remains unclear. In the present study, we examined the impact of MSCs on hepatic inflammatory response such as neutrophil influx and liver damage in a rat model of 70% hepatic IRI. Treatment with MSCs protected rat against hepatic IRI, with significantly decreased serum levels of liver enzymes, attenuated hepatic neutrophil infiltration, reduced expression of apoptosis-associated proteins, and ameliorated liver pathological injury. MSCs also significantly enhanced the intracellular activation of p38 MAPK phosphorylation, which led to decreased expression of CXCR2 on the
Abstract: : Purpose: To evaluate the expression of heme oxygenase-1 (HO-1), which is a heme-catabolizing enzyme induced by oxidative stress and acts against oxidant-induced tissue injury, on ischemia-reperfusion injury in the rat retina. Methods: Retinal ischemia was induced in male 8weeks SD rats by increasing the intraocular pressure to 110 mmHg for 45 minutes. At 6, 12, 24, and 48 hours after reperfusion, rat eyes were enucleated. Expression of HO-1 and HO-2, a constitutive isoform, in mRNA level in the retina was determined by using RT-PCR and that of protein levels were also studied by using Western blotting analysis. For immunohistochemical double-labeling, sections were incubated with antibodies against HO-1 and S-100. To evaluate possible neuroprotective effects of hemin, an inducer of HO-1, we injected 150 mg/kg of hemin intraperitoneally before the ischemia. The degree of retinal damage was assessed by electroretinogram (ERG) recording on 1, 2 and 4 weeks thereafter, by measuring the ...
Introduction/Aim Ischemia Reperfusion injury is a poorly understood entity with wide-ranging clinical implications touching on most fields of clinical medicine. Using skin flap and hind limb models of injury in the mouse we attempt to reduce ischemia reperfusion injury by targeting different parts of the ischemia reperfusion injury pathway. Methods Dorsal lateral thoracic artery island skin flaps (3.5x1.5 cm) were elevated in C57BL/6 mice and rendered ischemic for 10 hours by placing a 7 mm microclamp on the vascular pedicle followed by 7 days of reperfusion. Hind-limb ischemia (was achieved with orthodontic rubber bands applied above the greater trochanter of male C57BL/6 mice using a McGivney Haemorrhoid Ligator. Limbs underwent ischemia for two hours followed by 24 hours reperfusion prior to euthanasia. Animals were treated with intravenous Poloxamer 188 and P8 IgM-binding protein to assess their effect on ischemiareperfusion injury. Results Administration of P188 prior to ischemia gave an ...
AngII (angiotensin II), ACE (angiotensin I-converting enzyme) and the AT(1) receptor (AngII type I receptor) are associated with the inflammatory process and microvascular dysfunction of AKI (acute kidney injury) induced by renal I/R (ischaemia/reperfusion). However, Ang-(1-7) [angiotensin-(1-7)], ACE2 (angiotensin I-converting enzyme 2) and the Mas receptor also play a role in renal disease models. Therefore, in the present study, we have examined the renal profile of Ang-(1-7), ACE2 and the Mas receptor in renal I/R and compared them with that of AngII, ACE and the AT(1) receptor. Male Wistar rats were submitted to left nephrectomy and ischaemia (45 min) followed by reperfusion (2 or 4 h) in the right kidney. At 4 h of reperfusion, renal AngII was increased (P , 0.01) and renal Ang-(1-7) was decreased substantially (P , 0.05), although plasma levels of both angiotensins were unchanged. in addition, renal I/R decreased the renal mRNA expression of renin (P , 0.05), AT(1) receptors (P , 0.001) ...
The present study aimed to investigate the protective effects of rhein on cerebral ischemic/reperfusion (I/R) injury in rats. The present study focused on the effect of rhein on oxidative stress and apoptotic factors, which are considered to serve an important role in the onset of I/R injury. Sprague‑Dawley rats were subjected to middle cerebral artery occlusion. Neurological functional scores (NFSs) were evaluated according to the Zea Longas score criteria and the area of brain infarct was determined by triphenyltetrazolium chloride staining. The morphology of the nerve cells in the cortex was observed following hematoxylin and eosin staining. In addition, levels of oxidative stress were assessed by measuring the levels of superoxide dismutase (SOD), glutathione‑peroxidase (GSH‑Px), catalase (CAT) and malondialdehyde (MDA). Levels of B‑cell lymphoma-2 (Bcl‑2), apoptosis regulator Bax (BAX), caspase-9, caspase‑3 and cleaved caspase‑3 expression were analyzed using western blot ...
TY - JOUR. T1 - Activation of BNIP3-mediated mitophagy protects against renal ischemia-reperfusion injury. AU - Tang, Chengyuan. AU - Han, Hailong. AU - Liu, Zhiwen. AU - Liu, Yuxue. AU - Yin, Lijun. AU - Cai, Juan. AU - He, Liyu. AU - Liu, Yu. AU - Chen, Guochun. AU - Zhang, Zhuohua. AU - Yin, Xiao-Ming. AU - Dong, Zheng. PY - 2019/9/12. Y1 - 2019/9/12. N2 - Acute kidney injury (AKI) is a syndrome of abrupt loss of renal functions. The underlying pathological mechanisms of AKI remain largely unknown. BCL2-interacting protein 3 (BNIP3) has dual functions of regulating cell death and mitophagy, but its pathophysiological role in AKI remains unclear. Here, we demonstrated an increase of BNIP3 expression in cultured renal proximal tubular epithelial cells following oxygen-glucose deprivation-reperfusion (OGD-R) and in renal tubules after renal ischemia-reperfusion (IR)-induced injury in mice. Functionally, silencing Bnip3 by specific short hairpin RNAs in cultured renal tubular cells reduced ...
The principal objectives of this were to determine whether hepatocyte membrane potentials (PD) are altered during liver transplantation and whether such changes may be of pathophysiologic importance in ischemia/reperfusion injury and graft survival. Livers of adult male Sprague-Dawley rats (N = 3-4/group) were impaled with intracellular microelectrodes prior to and at various time periods for six hours following complete hepatic resection. Just prior to resection each liver was perfused with preservation solutions associated with high (normal saline, NS), moderate (Eurocollins, EC) and low (University of Wisconsin solution, UW) risks of reperfusion injury. To determine whether changes are of pathophysiologic importance, the NS solution was modified (addition of 0.1% ethanol) to achieve similar PD changes as those observed with UW. Liver transplants were then performed using a nonarterialized, cuff technique in adult Lewis rats where the donor livers had been perfused and preserved for six hours ...
The pathophysiologic mechanisms leading to acute ischemic renal failure are not completely understood. Melatonin, a compound with well-known antioxidant properties, reduces IR-induced renal injury. The purpose of the present study was to investigate the changes in levels of tumor necrosis factor (TNF)-alpha, IL-beta, and IL-6 in postischemic reperfused renal tissue, and to determine whether the protective effect of melatonin is related the modulation of the production of these inflammatory molecules. Male Wistar albino rats were unilaterally nephrectomized and subjected to 1 hr of renal pedicle occlusion followed by 2 hr or 24 hr of reperfusion. Melatonin (10 mg/kg, i.p.) or vehicle was administrated at 10 min prior to ischemia. After 24 hr of the reperfusion, following decapitation, kidney samples were taken both for histologic examination and for the determination of malondialdehyde (MDA), myeloperoxidase (MPO) activity, total antioxidant capacity (TAC), total oxidative stress (TOS), ...
TY - JOUR. T1 - Rat Liver Ischemia/Reperfusion Induced Proinflammatory Mediator and Antioxidant Expressions Analyzed by Gene Chips and Real-Time Polymerase Chain Reactions. AU - Hsu, Y. C.. AU - Chou, T. Y.. AU - Chen, C. F.. AU - Wang, D.. AU - Su, C. L.. AU - Hu, R. T.. PY - 2008/9. Y1 - 2008/9. N2 - Objective: Ischemia/reperfusion (I/R) of the rat liver induces injury; however, few studies have investigated gene expressions associated with this phenomenon. In this study, gene chip and real-time polymerase chain reactions (PCR) were used to study the expressions of the proinflammatory mediators and antioxidants after I/R. Materials and Methods: Ischemia was induced by clamping the common hepatic artery and portal vein for 40 minutes followed by 90 minutes reperfusion. Blood samples collected before ischemia and after reperfusion were analyzed for alanine amino transferase, lactic dehydrogenase, hydroxyl radicals, nitric oxide (NO), and tumor necrosis factor α (TNFα). Expressions of TNFα, ...
BACKGROUND: Acute myocardial infarction is one of the leading causes of death. It is caused by a blockage of a coronary artery leading to reduced blood flow to the myocardium and hence ischemic damage. In addition, a second wave of damage after the flow has been restored, named reperfusion injury greatly exacerbate the damage. For the latter, no medical treatment exist. In this study the aim was to characterize Ca(2+) sensitivity in coronary arteries following experimental ischemia/reperfusion injury.. METHODS: Arteries were isolated from hearts exposed to a well-established rat ischemia/reperfusion model. Wire myograph combined with FURA2-AM measurements was applied to study the Ca(2+) dependency of the vasoconstriction.. RESULTS: The results presented herein show that ETB receptors (R) have much weaker Ca(2+)-sensitizing effect than ETA-R and that ETB-R appear to be more dependent on Ca(2+) influx presumably through voltage-gated Ca(2+) channels (VGCC). In addition, we show that there is an ...
Nutr Metab Cardiovasc Dis. 2009 Jan;19(1):20-6. doi: 10.1016/j.numecd.2008.01.004. Epub 2008 May 2. Research Support, Non-U.S. Govt
Introduction: Glutathione (GSH) protects the tissue and cell from oxidative injury. Objectives: In the current study, we investigated the possible effects of GSH on liver markers, oxidative stress and inflammatory indices in rat with renal ischemia reperfusion (RIR) injury. Materials and Methods: Twenty-four adult male Wistar rats were divided into 3 groups (n=8). Group I (the control group), group II (the RIR group) received saline (0.25 mL/d, intraperitoneally; i.p.), group III as the RIR group that received GSH (100 mg/kg/d, i.p.). The treatment with saline or GSH began daily 14 days before RIR induction. RIR was induced by clamping renal pedicles for 45 minutes and 24 hours of reperfusion. Results: RIR significantly increased the serum level of nitric oxide (NO), the serum activities of aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyltransferase (GGT), the serum and renal levels of malondialdehyde (MDA), and the serum activity of myeloperoxidase (MPO). However, RIR
The gut is a critical target organ after severe insult such as shock, trauma, sepsis, and surgery. During these severe stress states, it is known that blood flow to the gut is disproportionately decreased to preserve central hemodynamic stability and that it could cause intestinal I/R, leading to the loss of gut barrier function (17). Dysfunction of the gut barrier after severe insults has been implicated as a major contributor to systemic inflammatory response syndrome, resulting in acute respiratory distress syndrome or multiple-organ dysfunction syndrome (18). Gut commensal bacteria are known to play important roles in maintaining the gut mucosal barrier and the intestinal immune system (32). Gut microbiota stimulate the normal development of the humoral and cellular mucosal immune system during neonatal life and maintain homeostasis of intestinal immune system thereafter (11, 61). Under normal conditions, the gastrointestinal tract provides resistance to both beneficial commensals and ...
Effects of In Vivo Hepatic Ischemia-Reperfusion Injury on the Hepatobiliary Disposition of Rhodamine 123 and its Metabolites in Isolated Perfused Rat Livers
OBJECTIVE Ischemia reperfusion injury is partly responsible for the high mortality associated with induced myocardial injury and the reduction in the full benefit of myocardial reperfusion. Remote ischemic preconditioning, perconditioning, and postconditioning have all been shown to be cardioprotective. However, it is still unknown which one is the most beneficial. To examine this issue, we used adult male Wistar rat ischemia reperfusion models to compare the cardioprotective effect of these three approaches applied on double-sided hind limbs. METHODS The rats were randomly distributed to the following five groups: sham, ischemia reperfusion, remote preconditioning, remote perconditioning, and remote post-conditioning. The ischemia/reperfusion model was established by sternotomy followed by a 30-min ligation of the left coronary artery and a subsequent 3-h reperfusion. Remote conditioning was induced with three 5-min ischemia/5-min reperfusion cycles of the double-sided hind limbs using a tourniquet.
TY - JOUR. T1 - Delayed onset of apoptosis following ischemia/reperfusion in rat liver. T2 - Downregulation of BAX gene. AU - Lai, W. Y.. AU - Chien, C. T.. AU - Cheng, C. L.. AU - Yang, B. C.. AU - Hsu, S. M.. AU - Lee, P. H.. PY - 1999/11/1. Y1 - 1999/11/1. UR - http://www.scopus.com/inward/record.url?scp=0032720663&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0032720663&partnerID=8YFLogxK. U2 - 10.1016/S0041-1345(99)00616-8. DO - 10.1016/S0041-1345(99)00616-8. M3 - Article. C2 - 10578340. AN - SCOPUS:0032720663. VL - 31. SP - 2924. EP - 2925. JO - Transplantation Proceedings. JF - Transplantation Proceedings. SN - 0041-1345. IS - 7. ER - ...
There is vast literature on the topic of ischemia-reperfusion injury. A summative discussion of the complex pathogenicity will aid practicing physicians in diagnosis and management. We offer a review of this literature as well as a discussion on a rare case of tense edematous bullae as a presentation of ischemia-reperfusion injury. A 65-year-old male underwent a right femoropopliteal bypass for rest pain that had not improved after iliac stent placement. He presented three days after discharge with blistering lesions on the reperfused limb that resembled bullous pemphigoid. This case describes the variability in the presentation of reperfusion injury, as well as the necessity to educate those managing atypical presentations of reperfusion injury.
3- Lima-Posada I, Portas-Cortés C, Pérez-Villalva R, Fontana F, Rodríguez-Romo R, Prieto R, Sánchez-Navarro A, Rodríguez-González G, Gamba G, Zambrano E, Bobadilla N. Gender Differences in the Acute Kidney Injury to Chronic Kidney Disease Transition. Sci Rep. 2017;7(1) [Crossref] ...
In this study, the role of intraepithelial lymphocytes (IEL) was analyzed in Graft-versus-Host disease, small bowel transplantation, sepsis and inflammatory bowel disease. Furthermore, the influence of oxidative stress and endogenous protective mechanisms on the development of intestinal ischemia/reperfusion injury was determined. The phenotypic and functional characteristics of IEL in these diseases indicated that only specific T-cell subsets selectively migrate and/or survive in the intestinal mucosa. In addition, it was demonstrated that IEL display several functions in the intestinal barrier system: they are cytolytic effector cells, but do also exert regulatory functions on the expression of mucosal host defense mechanisms such as NOS-2 expression. The investigations on intestinal ischemia / reperfusion injury revealed that selective intestinal ischemia induces tissue injury not only in the intestine, but in the liver as well. In both organs, oxidative stress plays a predominant role in the ...
Based on our findings and the divergent results of previous animal and human studies, it can be concluded that the renoprotective effects of rIPC are minimal, if any, and are not robustly detectable.
Our serial in vivo and in vitro studies showed that circulating sFGL2 was increased in kidney injuries and contributed to TEC apoptosis[11]. Here, we further investigated the dynamic change of sFGL2 in the kidney and circulation throughout 2-week duration of renal IR injury in a porcine auto-transplantation model. This study revealed that renal dysfunction and histological damage was maximized from day 2 to 5 post-transplantation and followed by a gradual recovery, while the expression of sFGL2 and its receptor FcγRIIB exhibited a delayed peak at day 5 to 10. These results indicate that sFGL2 might be involved in the process of renal repairing and remodeling and exert protective effects.. sFGL2, as an immunoregulatory effector of Treg, has been proved a capacity of TEC apoptotic induction. TECs compromise over 80% of renal parenchymal cells and play an important role in maintaining normal kidney function[14]. TEC apoptosis is closely related with IR injury, delayed graft function and early ...