scholarly journals Molecular Mechanisms Underlying Intestinal Ischemia/Reperfusion Injury: Bioinformatics Analysis and In Vivo Validation

2020 ◽  
Vol 26 ◽  
Author(s):  
Fengshou Chen ◽  
Dan Wang ◽  
Xiaoqian Li ◽  
He Wang
Keyword(s):  
Reperfusion Injury ◽  
Intestinal Ischemia ◽  
Molecular Mechanisms ◽  
Bioinformatics Analysis ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Intestinal Ischemia Reperfusion ◽  
In Vivo Validation

scholarly journals Antioxidant-Based Therapy Reduces Early-Stage Intestinal Ischemia-Reperfusion Injury in Rats

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 853
Author(s):  
Gaizka Gutiérrez-Sánchez ◽  
Ignacio García-Alonso ◽  
Jorge Gutiérrez Sáenz de Santa María ◽  
Ana Alonso-Varona ◽  
Borja Herrero de la Parte
Keyword(s):  
Reperfusion Injury ◽  
Intestinal Ischemia ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion Injury ◽  
Early Stage ◽  
Ischemia Reperfusion ◽  
Mucosal Damage ◽  
Intestinal Damage ◽  
Oxygen Species ◽  
Intestinal Ischemia Reperfusion

Intestinal ischemia-reperfusion injury (i-IRI) is a rare disorder with a high mortality rate, resulting from the loss of blood flow to an intestinal segment. Most of the damage is triggered by the restoration of flow and the arrival of cytokines and reactive oxygen species (ROS), among others. Inactivation of these molecules before tissue reperfusion could reduce intestinal damage. The aim of this work was to analyze the preventive effect of allopurinol and nitroindazole on intestinal mucosal damage after i-IRI. Wag/RijHsd rats were subjected to i-IRI by clamping the superior mesenteric artery (for 1 or 2 h) followed by a 30 min period of reperfusion. Histopathological intestinal damage (HID) was assessed by microscopic examination of histological sections obtained from injured intestine. HID was increased by almost 20% by doubling the ischemia time (from 1 to 2 h). Nitroindazole reduced HID in both the 1 and 2 h period of ischemia by approximately 30% and 60%, respectively (p < 0.001). Our preliminary results demonstrate that nitroindazole has a preventive/protective effect against tissue damage in the early stages of i-IRI. However, to better understand the molecular mechanisms underlying this phenomenon, further studies are needed.

scholarly journals Sulforaphane Elicits Protective Effects in Intestinal Ischemia Reperfusion Injury

2020 ◽  
Vol 21 (15) ◽  
pp. 5189
Author(s):  
Zhiquan Chen ◽  
Annika Mohr ◽  
Barbara Heitplatz ◽  
Uwe Hansen ◽  
Andreas Pascher ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ex Vivo ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
Cellular Interactions ◽  
Morphological Alterations ◽  
Intestinal Ischemia Reperfusion

Intestinal ischemia reperfusion injury (IRI) is an inherent, unavoidable event of intestinal transplantation, contributing to allograft failure and rejection. The inflammatory state elicited by intestinal IRI is characterized by heightened leukocyte recruitment to the gut, which is amplified by a cross-talk with platelets at the endothelial border. Sulforaphane (SFN), a naturally occurring isothiocyanate, exhibits anti-inflammatory characteristics and has been shown to reduce platelet activation and block leukocyte adhesion. Thus, the aim of this study was to investigate protective effects and mechanism of action of SFN in a murine model of intestinal IRI. Intestinal IRI was induced by superior mesenteric artery occlusion for 30 min, followed by reperfusion for 2 h, 8 h or 24 h. To investigate cellular interactions, leukocytes were in vivo stained with rhodamine and platelets were harvested from donor animals and ex vivo stained. Mice (C57BL/6J) were divided into three groups: (1) control, (2) SFN treatment 24 h prior to reperfusion and (3) SFN treatment 24 h prior to platelet donation. Leukocyte and platelet recruitment was analyzed via intravital microscopy. Tissue was analyzed for morphological alterations in intestinal mucosa, barrier permeability, and leukocyte infiltration. Leukocyte rolling and adhesion was significantly reduced 2 h and 8 h after reperfusion. Mice receiving SFN treated platelets exhibited significantly decreased leukocyte and platelet recruitment. SFN showed protection for intestinal tissue with less damage observed in histopathological and ultrastructural evaluation. In summary, the data presented provide evidence for SFN as a potential therapeutic strategy against intestinal IRI.

Role of JNK phosphorylation in intestinal ischemia/reperfusion injury in mice

2010 ◽  
Vol 30 (2) ◽  
pp. 140-143
Author(s):  
De-yi ZHENG ◽  
Jian-ming WNAG ◽  
Yi-tao JIA ◽  
Jin-feng FU ◽  
Kai-yang LU ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Intestinal Ischemia Reperfusion

Dynamic metabolomic analysis of intestinal ischemia–reperfusion injury in rats

IUBMB Life ◽  
2020 ◽  
Vol 72 (5) ◽  
pp. 1001-1011 ◽  
Author(s):  
Die Dai ◽  
Jingchao Chen ◽  
Menglu Jin ◽  
Zunjian Zhang ◽  
Wei‐Hua Chen ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Metabolomic Analysis ◽  
Intestinal Ischemia Reperfusion

scholarly journals Murine Model of Intestinal Ischemia-reperfusion Injury

10.3791/53881 ◽  
2016 ◽  
Author(s):  
Ekaterina O. Gubernatorova ◽  
Ernesto Perez-Chanona ◽  
Ekaterina P. Koroleva ◽  
Christian Jobin ◽  
Alexei V. Tumanov
Keyword(s):  
Reperfusion Injury ◽  
Murine Model ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Intestinal Ischemia Reperfusion
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