Glucagon‐like peptide 2 attenuates intestinal mucosal barrier injury through the MLCK/pMLC signaling pathway in a piglet model

2020 ◽  
Author(s):  
Yaqi Chang ◽  
Qiuhong Deng ◽  
Zhenyu Zhang ◽  
Hua Zhao ◽  
Jiayong Tang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Mucosal Barrier ◽  
Intestinal Mucosal Barrier ◽  
Mucosal Barrier Injury ◽  
Glucagon Like Peptide

Glucagon-Like Peptide-2 Improve Intestinal Mucosal Barrier Function in Aged Rats

2018 ◽  
Vol 22 (6) ◽  
pp. 731-738 ◽  
Author(s):  
Weiying Ren ◽  
Jiayu Wu ◽  
Li Li ◽  
Y. Lu ◽  
Y. Shao ◽  
...  
Keyword(s):  
Barrier Function ◽  
Mucosal Barrier ◽  
Aged Rats ◽  
Intestinal Mucosal Barrier ◽  
Mucosal Barrier Function ◽  
Glucagon Like Peptide

scholarly journals MiR-126 impairs the intestinal barrier function via inhibiting S1PR2 mediated activation of PI3K/AKT signaling pathway

2017 ◽  
Author(s):  
Tanzhou Chen ◽  
Haibo Xue ◽  
Ruoyang Lin ◽  
Zhiming Huang
Keyword(s):  
Signaling Pathway ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Akt Signaling ◽  
Mucosal Barrier ◽  
Intestinal Barrier Function ◽  
Luciferase Reporter ◽  
Akt Signaling Pathway ◽  
Intestinal Mucosal Barrier ◽  
Pathological Tissues

AbstractBackgroundAberrant expression of miRNAs was a critical element in the pathogenesis of inflammatory bowel disease (IBD). This study aimed to explore the involvement and mechanism of miR-126 in IBD.MethodsIn this study, the endogenous expressions of miR-126, S1PR2 and S1P in the pathological tissues of patients with IBD were detected using qRT-PCR and western blot assay, respectively. The luciferase reporter gene assay was performed to confirm the targeting regulatory relation between miR-126 and S1PR2. The transendothelial electrical resistance assay was used to measured the value of TEER.ResultsThe expressions of miR-126, S1PR2 and S1P in the pathological tissues of IBD patients were significantly higher than that of the control group. Moreover, miR-126 overexpression contributed to intestinal mucosal barrier dysfunction in vitro. S1PR2 was a direct target of miR-126, and S1PR2 expression was negatively regulated by miR-126 in Caco-2 cells. However, S1PR2 activated by S1P had the protection effect for the integrity and permeability of intestinal mucosal barrier via a PI3K/Akt dependent mechanism. MiR-126 silencing possessed obvious protective effects on the intestinal barrier function, but these effects could be reversed by JTE-013 or LY294002.ConclusionMiR-126 down-regulated S1PR2 and then prevented the activation of PI3K/AKT signaling pathway, which ultimately could damage intestinal mucosal barrier function.

scholarly journals Prospective study on the effect of abdominal hypertension on intestinal mucosal barrier injury during laparoscopic surgery

2019 ◽  
Author(s):  
Yong Yang ◽  
Xin kang ◽  
Xingjian Yang ◽  
Yi Hu ◽  
Rong Chen ◽  
...  
Keyword(s):  
Lactic Acid ◽  
Diamine Oxidase ◽  
Measurement Data ◽  
Postoperative Recovery ◽  
Mucosal Barrier ◽  
Co2 Pneumoperitoneum ◽  
Intestinal Mucosal Barrier ◽  
Mucosal Barrier Injury ◽  
Abdominal Hypertension ◽  
Group 1

Abstract Objective Prolonged and high intraperitoneal pressure may lead to impaired intestinal mucosal blood perfusion, increase the risk of surgery and complications, and affect the postoperative recovery of patients. However, the literature reports on the effect of abdominal hypertension on gastrointestinal function mainly focus on animal experiments, and there are few clinical reports. Our study intends to explore the effect of increased CO2 pneumoperitoneum pressure during laparoscopy on intestinal mucosal barrier injury. Methods A prospective study was conducted on 180 patients who underwent laparoscopic cholecystectomy in the First People's Hospital of Shuangliu District, Chengdu from October 2017 to March 2018. A randomized，single-blind，controlled study was performed in the 180 patients who were allocated into the 10 mmHg group(1 mmHg=0.133 kPa)，12 mmHg group and 15 mmHg group based on a random number table and setting value of intraoperative CO2 pneumoperitoneum pressure (10 mmHg，12 mmHg and 15 mmHg)．Main observation indexes such as intraoperative conditions and postoperative recovery were recorded, and the results of serum tumor necrosis factor alpha (TNF-α), interleukin 1 (IL-1), D-lactic acid, blood endotoxin levels，plasma diamine oxidase (DAO) activity were detected. The measurement data of normal distribution were expressed as mean ± standard deviation (x+S), and one-way analysis of variance was used for comparison between groups. The measurement data with non-normal distribution are represented by M (QR) and non-parametric test is adopted, count data were presented as the n(%), and comparison among groups was analyzed using the chi-square test. Results 180 patients were screened out, 60 patients in each group. Eight patients dropped out during the study (2 in 10 mmHg group, 1 in 12 mmHg group and 5 in 15 mmHg group). All patients in the three groups were cured and discharged without bleeding, secondary bile duct stones, bile leakage and reoperation. There was no significant difference in serum TNF-a, IL-1, D-lactic acid, endotoxin level and plasma diamine oxidase (DAO) among the three groups after operation (P>0.05).Conclusion Laparoscopic surgery under 15 mmHg CO2 pneumoperitoneum did not cause intestinal mucosal barrier damage, and the operation under the pneumoperitoneum was safe and reliable.Registry number of ChiCTR1900023936.

BRCC36 promotes intestinal mucosal barrier injury caused by BMP2 after ischemia-reperfusion via inhibiting PPARγ signaling

2021 ◽  
Author(s):  
Jin-Ming Zhang ◽  
Kun-Nan Wang ◽  
Yun Zhang ◽  
Jun-Ze Zhang ◽  
Xin-Pu Yuan ◽  
...  
Keyword(s):  
Ischemia Reperfusion ◽  
Bone Morphogenetic Protein 2 ◽  
Mucosal Barrier ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Intestinal Mucosal Barrier ◽  
Morphogenetic Protein ◽  
Mucosal Barrier Injury ◽  
Brca1 Brca2 ◽  
Intestinal Ischemia Reperfusion

Abstract As one of the most common pathological changes in trauma and surgery practice, intestinal ischemia-reperfusion (I/R) injury is regarded as a major precipitating factor in the occurrence and development of fatal diseases. BRCA1-BRCA2-containing complex subunit 36 (BRCC36), a deubiquitinase, has been proved important in a variety of pathophysiological processes such as DNA repair, cell cycle regulation, tumorigenesis and inflammatory response. However, the effect of BRCC36 on intestinal mucosal barrier injury after I/R has not been fully elucidated. Our research found that BRCC36 aggravated intestinal mucosal barrier injury caused by BMP2 (Bone morphogenetic protein 2) after I/R by downregulating PPARγ (Peroxisome proliferator-activated receptor-γ) signaling. These results suggested that BRCC36/PPARγ axis might serve as a potential therapeutic target for preventing intestinal mucosal barrier injury after I/R.

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