scholarly journals Remediation of Hemorrhagic Shock-Induced Intestinal Barrier Dysfunction by Treatment with Diphenyldihaloketones EF24 and CLEFMA

2014 ◽  
Vol 351 (2) ◽  
pp. 413-422 ◽  
Author(s):  
Vivek R. Yadav ◽  
Alamdar Hussain ◽  
Kaustuv Sahoo ◽  
Vibhudutta Awasthi
Keyword(s):  
Hemorrhagic Shock ◽  
Intestinal Barrier ◽  
Barrier Dysfunction ◽  
Intestinal Barrier Dysfunction

Blockade of Stellate Ganglion Remediates Hemorrhagic Shock–Induced Intestinal Barrier Dysfunction

2019 ◽  
Vol 244 ◽  
pp. 69-76
Author(s):  
Jing Zhang ◽  
Xue-Rong Lin ◽  
Yu-Ping Zhang ◽  
Li-Min Zhang ◽  
Hui-Bo Du ◽  
...  
Keyword(s):  
Hemorrhagic Shock ◽  
Stellate Ganglion ◽  
Intestinal Barrier ◽  
Barrier Dysfunction ◽  
Intestinal Barrier Dysfunction

The role of RAGE in the pathogenesis of intestinal barrier dysfunction after hemorrhagic shock

2006 ◽  
Vol 291 (4) ◽  
pp. G556-G565 ◽  
Author(s):  
Kathleen G. Raman ◽  
Penny L. Sappington ◽  
Runkuan Yang ◽  
Ryan M. Levy ◽  
Jose M. Prince ◽  
...  
Keyword(s):  
Hemorrhagic Shock ◽  
Bacterial Translocation ◽  
Intestinal Barrier ◽  
High Plasma ◽  
Mucosal Barrier ◽  
Barrier Dysfunction ◽  
Mesenteric Lymph Nodes ◽  
Mucosal Permeability ◽  
Intestinal Barrier Dysfunction ◽  
Soluble Rage

The receptor for advanced glycation end products (RAGE) has been implicated in the pathogenesis of numerous conditions associated with excessive inflammation. To determine whether RAGE-dependent signaling is important in the development of intestinal barrier dysfunction after hemorrhagic shock and resuscitation (HS/R), C57Bl/6, rage−/−, or congenic rage+/+ mice were subjected to HS/R (mean arterial pressure of 25 mmHg for 3 h) or a sham procedure. Twenty-four hours later, bacterial translocation to mesenteric lymph nodes and ileal mucosal permeability to FITC-labeled dextran were assessed. Additionally, samples of ileum were obtained for immunofluorescence microscopy, and plasma was collected for measuring IL-6 and IL-10 levels. HS/R in C57Bl/6 mice was associated with increased bacterial translocation, ileal mucosal hyperpermeability, and high circulating levels of IL-6. All of these effects were prevented when C57Bl/6 mice were treated with recombinant human soluble RAGE (sRAGE; the extracellular ligand-binding domain of RAGE). HS/R induced bacterial translocation, ileal mucosal hyperpermeability, and high plasma IL-6 levels in rage+/+ but not rage−/− mice. Circulating IL-10 levels were higher in rage−/− compared with rage+/+ mice. These results suggest that activation of RAGE-dependent signaling is a key factor leading to gut mucosal barrier dysfunction after HS/R.

scholarly journals SGB Postconditioning Improves Intestinal Barrier Function by Inhibiting Autophagy in Conscious Rats Following Hemorrhagic Shock and Resuscitation

2021 ◽  
Author(s):  
Zhong-Hua Li ◽  
Wen-Di Wang ◽  
Qi Sun ◽  
Ting-Jiao Suo ◽  
Jia-Yi Zhai ◽  
...  
Keyword(s):  
Blood Flow ◽  
Hemorrhagic Shock ◽  
Intestinal Barrier ◽  
Haemorrhagic Shock ◽  
Intestinal Morphology ◽  
Intestinal Loop ◽  
Post Processing ◽  
Barrier Dysfunction ◽  
Intestinal Barrier Dysfunction

Abstract Background Intestinal barrier dysfunction is the critical link of distant organ injury caused by hemorrhagic shock. The role of autophagy in ischemic intestinal injury has been paid more and more attention. Prophylactic treatment of stellate ganglion block (SGB) reduces intestinal barrier dysfunction induced by haemorrhagic shock. This study investigated the role of SGB post-processing on improved bowel barrier function and autophagy-related mechanisms of action after haemorrhagic shock. Methods The model of hemorrhagic shock in conscious rats was established, and the rats were treated with SGB, autophagy inhibitor 3- methyladenine (3-MA) at the time of fluid resuscitation. We detected the survival rate, intestinal loop blood flow, intestinal barrier permeability, intestinal morphology, wet/dry ratio (W/D), the intestinal barrier and autophagy marker proteins. Simultaneously, we also observed the effect of autophagy activator rapamycin (RAPA) on SGB. Results SGB postconditioning significantly prolonged the overall survival and enhanced survival rate of 72 hours in rats after hemorrhagic shock. SGB post-processing and 3-MA administration improved the intestinal morphology and intestinal permeability, increased the intestinal loop blood flow and expression of ZO1, Occludin and Claudin-1, and decreased the intestinal W/D and LC3 and Beclin-1 expressions, expected for increased P62. Meanwhile, RAPA partially inhibited the effect of SGB on above indices in haemorrhagic shock rats. Conclusion SGB postconditioning alleviates the intestinal barrier dysfunction caused by haemorrhagic shock, which is related to the inhibition of excessive autophagy.

Confirmation and Prevention of Intestinal Barrier Dysfunction and Bacterial Translocation Caused by Methotrexate

2006 ◽  
Vol 51 (9) ◽  
pp. 1549-1556 ◽  
Author(s):  
Desheng Song ◽  
Bin Shi ◽  
Hua Xue ◽  
Yousheng Li ◽  
Xiaodong Yang ◽  
...  
Keyword(s):  
Bacterial Translocation ◽  
Intestinal Barrier ◽  
Barrier Dysfunction ◽  
Intestinal Barrier Dysfunction

Oxygen supplementation during airway instrumentation improves intestinal barrier dysfunction

2006 ◽  
Vol 41 (8) ◽  
pp. 1386-1391 ◽  
Author(s):  
Ali Nayci ◽  
Sibel Atis ◽  
Gulden Ersoz ◽  
Ayse Polat ◽  
Derya Talas
Keyword(s):  
Intestinal Barrier ◽  
Barrier Dysfunction ◽  
Oxygen Supplementation ◽  
Intestinal Barrier Dysfunction

scholarly journals Cystine reduces tight junction permeability and intestinal inflammation induced by oxidative stress in Caco-2 cells

Amino Acids ◽  
2021 ◽  
Author(s):  
Tatsuya Hasegawa ◽  
Ami Mizugaki ◽  
Yoshiko Inoue ◽  
Hiroyuki Kato ◽  
Hitoshi Murakami
Keyword(s):  
Oxidative Stress ◽  
Tight Junction ◽  
Mrna Expression ◽  
Inflammatory Cytokines ◽  
Inflammatory Responses ◽  
Intestinal Barrier ◽  
Barrier Dysfunction ◽  
Whole Cells ◽  
Intestinal Barrier Dysfunction ◽  
Pro Inflammatory Cytokines

AbstractIntestinal oxidative stress produces pro-inflammatory cytokines, which increase tight junction (TJ) permeability, leading to intestinal and systemic inflammation. Cystine (Cys2) is a substrate of glutathione (GSH) and inhibits inflammation, however, it is unclear whether Cys2 locally improves intestinal barrier dysfunction. Thus, we investigated the local effects of Cys2 on oxidative stress-induced TJ permeability and intestinal inflammatory responses. Caco-2 cells were cultured in a Cys2-supplemented medium for 24 h and then treated with H2O2 for 2 h. We assessed TJ permeability by measuring transepithelial electrical resistance and the paracellular flux of fluorescein isothiocyanate–dextran 4 kDa. We measured the concentration of Cys2 and GSH after Cys2 pretreatment. The mRNA expression of pro-inflammatory cytokines was assessed. In addition, the levels of TJ proteins were assessed by measuring the expression of TJ proteins in the whole cells and the ratio of TJ proteins in the detergent-insoluble fractions to soluble fractions (IS/S ratio). Cys2 treatment reduced H2O2-induced TJ permeability. Cys2 did not change the expression of TJ proteins in the whole cells, however, suppressed the IS/S ratio of claudin-4. Intercellular levels of Cys2 and GSH significantly increased in cells treated with Cys2. Cys2 treatment suppressed the mRNA expression of pro-inflammatory cytokines, and the mRNA levels were significantly correlated with TJ permeability. In conclusion, Cys2 treatment locally reduced oxidative stress-induced intestinal barrier dysfunction possively due to the mitigation of claudin-4 dislocalization. Furthermore, the effect of Cys2 on the improvement of intestinal barrier function is related to the local suppression of oxidative stress-induced pro-inflammatory responses.

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