scholarly journals Evaluation of Combined Effects of Vitamin E and Methylprednisolone in Ischemia and Reperfusion Injury of the Testicle Post Torsion and Detorsion in West African Dwarf Goats

2021 ◽  
Author(s):  
Udegbunam Sunday Ositadinma ◽  
Okoro Emmanuel Ikechukwu ◽  
C. Onuba Augustine ◽  
Okereke Henry Nnamdi ◽  
Udegbunam Rita Ijeoma ◽  
...  
Keyword(s):  
Vitamin E ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
West African ◽  
Cellular Damage ◽  
Ischemia And Reperfusion ◽  
Ischemia And Reperfusion Injury ◽  
West African Dwarf ◽  
Germinal Cells

Background: To investigate the protective effects of vitamin E and methylprednisolone on ischemia and reperfusion testicular injury after testicular torsion and detorsion in West African dwarf (WAD) goats. Methods: Thirty-two male WAD goats were randomly allocated into four groups (n=8); group A was treated with vitamin E, group B with methylprednisolone, group C with combo-therapy of vitamin E and methylprednisolone and group D was the control. The levels of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), total tissue protein (TTP) and catalase (CAT) were assayed while tissue biopsies were harvested for evaluation of degeneration of germinal cells, desquamation in germinal cells, interstitial edema and haemorrhage. Result: Findings revealed that Vitamin E administered immediately post ligature application significantly (p less than 0.05) decreased MDA level in groups A and C. Vitamin E monotherapy and its combination with methylprednisolone respectively ameliorated more the cellular damage and histological alterations caused by ischaemia and reperfusion injury. This study, therefor, suggests that vitamin E monotherapy and its combination with methylprednisolone is more beneficial in the management of short and long term ischemia/reperfusion injury respectively.

scholarly journals Protective effects of berberine on intestinal ischemia and reperfusion injury in rats

2017 ◽  
Vol 69 (1) ◽  
pp. 45-51 ◽  
Author(s):  
Tanzhou Chen ◽  
Bin Lv
Keyword(s):  
Reperfusion Injury ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Immunoglobulin A ◽  
Male Rats ◽  
Ischemia And Reperfusion ◽  
Protective Effects ◽  
Ischemia And Reperfusion Injury ◽  
Intestinal Ischemia Reperfusion

This study aims to investigate the potential protective effects of berberine on ischemia and reperfusion (IR) injury in rats. Thirty male rats were randomly divided into three experimental groups as follows: the sham group, the IR group and the berberine+IR group. Intestinal ischemia-reperfusion was performed by occlusion of the superior mesenteric artery for 30 min, followed by 2-h reperfusion. The berberine+IR group of rats were administered 200 mg/kg of berberine once a day for 7 days before laparotomy. Compared with the IR group, rats pretreated with berberine prior to IR had significantly reduced intestinal ischemia/reperfusion injury and a significant reduction in Chiu?s score (p<0.05). The level of malondialdehyde and myeloperoxidase in the berberine+IR group was significantly decreased compared with the IR group (p<0.001). Superoxide dismutase activity in the berberine+IR group was significantly higher than in the IR group (p<0.001). Compared with the IR group, diamine oxidase was markedly decreased in the berberine+IR group (p<0.01). The level of secretory immunoglobulin A in the berberine+IR group was significantly increased when compared to the IR group (p<0.001). Our results suggest that berberine can protect from intestinal IR injury and that it can be beneficial in treating conditions associated with intestinal IR injury.

scholarly journals Eosinophils attenuate hepatic ischemia-reperfusion injury in mice through ST2-dependent IL-13 production

2021 ◽  
Vol 13 (579) ◽  
pp. eabb6576
Author(s):  
Yaochun Wang ◽  
Yang Yang ◽  
Meng Wang ◽  
Shuhong Wang ◽  
Jong-Min Jeong ◽  
...  
Keyword(s):  
Liver Injury ◽  
Reperfusion Injury ◽  
Adoptive Transfer ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Cell Subpopulation ◽  
Ischemia And Reperfusion ◽  
Ischemia And Reperfusion Injury ◽  
Hepatic Ischemia

Eosinophils are a myeloid cell subpopulation that mediates type 2 T helper cell immune responses. Unexpectedly, we identified a rapid accumulation of eosinophils in 22 human liver grafts after hepatic transplantation. In contrast, no eosinophils were detectable in healthy liver tissues before transplantation. Studies with two genetic mouse models of eosinophil deficiency and a mouse model of antibody-mediated eosinophil depletion revealed exacerbated liver injury after hepatic ischemia and reperfusion. Adoptive transfer of bone marrow–derived eosinophils normalized liver injury of eosinophil-deficient mice and reduced hepatic ischemia and reperfusion injury in wild-type mice. Mechanistic studies combining genetic and adoptive transfer approaches identified a critical role of suppression of tumorigenicity (ST2)–dependent production of interleukin-13 by eosinophils in the hepatoprotection against ischemia-reperfusion–induced injury. Together, these data provide insight into a mechanism of eosinophil-mediated liver protection that could serve as a therapeutic target to improve outcomes of patients undergoing liver transplantation.

Comprehensive analysis of circRNAs from steatotic livers after ischemia and reperfusion injury by next generation RNA sequencing

2020 ◽  
Author(s):  
Xiaoye Qu ◽  
Chao Zheng ◽  
Bingrui Wang ◽  
Fang Wang ◽  
Xuehua Sun ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Rna Sequencing ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Circular Rnas ◽  
Organ Shortage ◽  
Ischemia And Reperfusion ◽  
Sequencing Data ◽  
Ischemia And Reperfusion Injury ◽  
Rnase R

Abstract Background Global organ shortage has enabled the permission of fatty livers for transplantation purpose, taking the risk of graft dysfunction related to the rapider ischemia/reperfusion injury (IRI) progress. Increasing evidence supports the role of circular RNAs as essential regulators of this progress. However, data about circular RNAs in ischemia and reperfusion injured steatotic livers are practically nonexistent. Methods In the present study, high-fat diet (HFD)-fed mice model was used to generate hepatic steatosis mice. RNA-sequencing was performed on IRI model or sham liver tissues both in HFD-fed mice to screen the significant differentially expressed circular RNAs. GO and KEGG analysis were applied to figure out the potential function of these screened circular RNAs. Results From this, we successfully found the expression of some circular RNAs were significantly altered in IRI livers after HFD-fed mouse models. To further validate sequencing data, one up-regulated circRNA and four down-regulated circular RNAs were examined in steatotic mice livers after IRI. The RNase R digestion experiment exhibited these circRNAs possessed high stability compared with linear RNAs and sequence alignment of their junction positions provided identical sequences by sanger sequencing following gel electrophoresis, demonstrating the circularity of these circular RNAs. The expression of four stable circRNAs undigested by RNase R were further validated by quantitative PCR. Conclusion In summary, this study reveals that circular RNAs emerge as novel and potentially efficient targets which involve in more severe damage of steatotic livers to IRI.

CHIP, a cochaperone/ubiquitin ligase that regulates protein quality control, is required for maximal cardioprotection after myocardial infarction in mice

2005 ◽  
Vol 288 (6) ◽  
pp. H2836-H2842 ◽  
Author(s):  
Chunlian Zhang ◽  
Zhelong Xu ◽  
Xiao-Rui He ◽  
Lloyd H. Michael ◽  
Cam Patterson
Keyword(s):  
Myocardial Infarction ◽  
Quality Control ◽  
Reperfusion Injury ◽  
Ubiquitin Ligase ◽  
Protein Quality ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ischemia And Reperfusion ◽  
Ischemia And Reperfusion Injury ◽  
Response To Stress

Limitation of damage after ischemia and reperfusion injury to the myocardium remains an elusive clinical goal. Previous studies have suggested that molecular chaperones, which include members of the heat shock protein (Hsp) family, may have cardioprotective effects, although the protective role of endogenous chaperones has not been well documented. CHIP (carboxyl terminus of Hsp70-interacting protein) is a cochaperone/ubiquitin ligase that integrates the response to stress at multiple levels. We tested the response of CHIP(−/−) mice to in vivo ischemia and reperfusion injury induced by left anterior descending coronary artery ligation. Compared with wild-type littermates, CHIP(−/−) mice had decreased survival and increased incidence of arrhythmias during reperfusion. The size of myocardial infarction, as assessed by the ratio of infarct area to area at risk, was 50% greater in CHIP(−/−) mice. Increased infarct size was accompanied by impaired upregulation of the chaperone Hsp70 after ischemia-reperfusion injury. In situ analysis also indicated that hearts of CHIP(−/−) mice were more prone to develop apoptosis in cardiomyocytes and especially endothelial cells of intramural vessels. Previous studies have found that CHIP plays a central role in maintaining protein quality control and coordinating the response to stress. The present data indicate that these functions of CHIP provide a critical cardioprotective effect in the setting of ischemia-reperfusion injury due in part to increased apoptosis in cardiac cells. Quality control mechanisms therefore may be underappreciated clinical targets for maximizing myocardial protection after injury.

scholarly journals The protective effect of L-arginine, tadalafil, and their combination in rat testes after ischemia and reperfusion injury

2017 ◽  
Vol 11 (1-2) ◽  
pp. 19 ◽  
Author(s):  
Gokhun Ozmerdiven ◽  
Burhan Coskun ◽  
Onur Kaygisiz ◽  
Berna Aytac Vuruskan ◽  
Burak Asiltas ◽  
...  
Keyword(s):  
Protective Effect ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Combination Group ◽  
Control Group ◽  
Ischemia And Reperfusion ◽  
Contralateral Testis ◽  
Treatment Groups ◽  
Testis Torsion

Introduction: Nitric oxide (NO) plays an important role in the ischemia and reperfusion process. In this study, we aimed to examine the effect of L-arginine, tadalafil, and their combination for preventionof the ischemia reperfusion injury after testis torsion in rats.Methods: A total of 40 adult, male Sprague-Dawley rats were allocated into five groups. Three hours of left testicular torsion was performed in each group, excluding the control group. While the ischemia reperfusion (I/R) group had no treatment, I/R + Arg group received L-arginine, I/R + Td group received tadalafil and I/R + Arg + Td group received tadalafil and L-arginine 30 minutes before the detorsion. Then the left testis was untwisted for four hours of reperfusion. After bilateral orchiectomy, lipid peroxidation (LPx) and glutathione (GSH) activities were examined in testicular tissue.Spermatogenesis was evaluated with Johnsen’s score.Results: LPx levels of the I/R group were found to be significantly higher than for groups that received drugs for both testes (p<0.001). GSH levels of the combination group were higher than I/R group inipsilateral testis (p<0.01) and it was significantly higher than other groups for contralateral testis (p<0.001 for I/R group, p<0.01 for I/R + Arg, p<0.05 for I/R + Td). Mean Johnsen’s score of the I/Rgroup was found to be significantly lower than treatment groups in ipsilateral testis (p<0.001 for I/R + Arg + Td group, p<0.01 for other treatment goups) and contralateral testis (p<0.001). The meanJohnsen score of the combination group was significantly higher than that of other treatment groups in ipsilateral testis (p<0.05) and it was significantly higher than in the I/R + Td group in the contralateral testis (p<0.05).Conclusions: L-arginine, tadalafil, and combination of these two molecules showed protective effect against ischemia/reperfusion injury for both testes after unilateral testis torsion.

Effects of Nitric Oxide Donor Antioxidants Containing the Phenol Vitamin E Substructure and a Furoxan Moiety on Ischemia/Reperfusion Injury

2011 ◽  
Vol 59 (03) ◽  
pp. 111-116
Author(s):  
Antonella Di Stilo ◽  
Konstantin Chegaev ◽  
Loretta Lazzarato ◽  
Roberta Fruttero ◽  
Alberto Gasco ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vitamin E ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nitric Oxide Donor

scholarly journals Fenofibrate Ameliorates Hepatic Ischemia/Reperfusion Injury in Mice: Involvements of Apoptosis, Autophagy, and PPAR-α Activation

PPAR Research ◽  
2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Jie Zhang ◽  
Ping Cheng ◽  
Weiqi Dai ◽  
Jie Ji ◽  
Liwei Wu ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
Hepatocyte Apoptosis ◽  
Ischemia And Reperfusion Injury ◽  
Hepatic Ischemia ◽  
Tissue Samples ◽  
Hepatic Ischemia Reperfusion ◽  
And Oxidative Stress

Hepatic ischemia and reperfusion injury is characterized by hepatocyte apoptosis, impaired autophagy, and oxidative stress. Fenofibrate, a commonly used antilipidemic drug, has been verified to exert hepatic protective effects in other cells and animal models. The purpose of this study was to identify the function of fenofibrate on mouse hepatic IR injury and discuss the possible mechanisms. A segmental (70%) hepatic warm ischemia model was established in Balb/c mice. Serum and liver tissue samples were collected for detecting pathological changes at 2, 8, and 24 h after reperfusion, while fenofibrate (50 mg/kg, 100 mg/kg) was injected intraperitoneally 1 hour prior to surgery. Compared to the IR group, pretreatment of FF could reduce the inflammatory response and inhibit apoptosis and autophagy. Furthermore, fenofibrate can activate PPAR-α, which is associated with the phosphorylation of AMPK.

Mucosal arachidonate metabolism and intestinal ischemia-reperfusion injury

1989 ◽  
Vol 257 (2) ◽  
pp. G299-G307 ◽  
Author(s):  
M. J. Mangino ◽  
C. B. Anderson ◽  
M. K. Murphy ◽  
E. Brunt ◽  
J. Turk
Keyword(s):  
Blood Flow ◽  
Reperfusion Injury ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Leukotriene B4 ◽  
Time Dependent ◽  
Ischemia And Reperfusion ◽  
Synthesis Inhibitor ◽  
Intestinal Ischemia Reperfusion

Mucosal arachidonic acid metabolism was examined after 3 h of ischemia and 1 h of reperfusion in isolated ileal segments in the dog. The cyclooxygenase products thromboxane B2, 6-ketoprostaglandin F1 alpha, and prostaglandin E2 increased by 365%, 97%, and 158%, respectively, after ischemia and reperfusion but were not altered after 3 h of ischemia alone. The potent chemotactic lipoxygenase product leukotriene B4 (LTB4) increased by 687% after ischemia and reperfusion and was not affected by ischemia without reperfusion. In addition, tissue production of the thiol ether leukotrienes (LTC4, LTD4, and LTE4) increased threefold after ischemia and reperfusion. Quantitation of regionally isomeric hydroxy acids produced from arachidonate revealed a 300% increase in 12-hydroxyeicosatetraenoate (12-HETE) after intestinal ischemia and reperfusion without a change in other isomers (15-HETE and 5-HETE). Stereochemical analysis of 12-HETE demonstrated exclusive synthesis of the S-enantiomer. A significant and time-dependent decrease in intestinal blood flow also occurred during reperfusion. Administration of the dual cyclooxygenase-lipoxygenase synthesis inhibitor BW755C (1 mg/kg ia) did not alter time-dependent decreases in blood flow and failed to inhibit eicosanoid synthesis. Histologic examinations of intestinal samples revealed significant mucosal damage associated with ischemia alone and ischemia after reperfusion. This study indicates that intestinal ischemia-reperfusion injury is associated with dramatic alterations in mucosal production of vasoactive eicosanoids and with changes in blood flow that occur during reperfusion but not during ischemia alone. These events may be involved in the pathology characteristic of this injury.

scholarly journals RNA-Seq identifies condition-specific biological signatures of ischemia-reperfusion injury in the human kidney

2020 ◽  
Vol 21 (S1) ◽  
Author(s):  
Meeyoung Park ◽  
Chae Hwa Kwon ◽  
Hong Koo Ha ◽  
Miyeun Han ◽  
Sang Heon Song
Keyword(s):  
Immune Response ◽  
Cell Growth ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Human Kidney ◽  
Biological Pathways ◽  
Ischemia And Reperfusion ◽  
Som Clustering ◽  
And Migration

Abstract Background Acute kidney injury (AKI) is defined as a sudden event of kidney failure or kidney damage within a short period. Ischemia-reperfusion injury (IRI) is a critical factor associated with severe AKI and end-stage kidney disease (ESKD). However, the biological mechanisms underlying ischemia and reperfusion are incompletely understood, owing to the complexity of these pathophysiological processes. We aimed to investigate the key biological pathways individually affected by ischemia and reperfusion at the transcriptome level. Results We analyzed the steady-state gene expression pattern of human kidney tissues from normal (pre-ischemia), ischemia, and reperfusion conditions using RNA-sequencing. Conventional differential expression and self-organizing map (SOM) clustering analyses followed by pathway analysis were performed. Differential expression analysis revealed the metabolic pathways dysregulated in ischemia. Cellular assembly, development and migration, and immune response-related pathways were dysregulated in reperfusion. SOM clustering analysis highlighted the ischemia-mediated significant dysregulation in metabolism, apoptosis, and fibrosis-related pathways, while cell growth, migration, and immune response-related pathways were highly dysregulated by reperfusion after ischemia. The expression of pro-apoptotic genes and death receptors was downregulated during ischemia, indicating the existence of a protective mechanism against ischemic injury. Reperfusion induced alterations in the expression of the genes associated with immune response such as inflammasome and antigen representing genes. Further, the genes related to cell growth and migration, such as AKT, KRAS, and those related to Rho signaling, were downregulated, suggestive of injury responses during reperfusion. Semaphorin 4D and plexin B1 levels were also downregulated. Conclusions We show that specific biological pathways were distinctively involved in ischemia and reperfusion during IRI, indicating that condition-specific therapeutic strategies may be imperative to prevent severe kidney damage after IRI in the clinical setting.

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