scholarly journals Effects of enteral nutrition on pro-inflammatory factors and intestinal barrier function in patients with acute severe pancreatitis

2019 ◽  
Vol 17 ◽  
pp. 205873921982721 ◽  
Author(s):  
Ying-Jie Chen ◽  
Yao-Dong Zhuang ◽  
Zhe Cai ◽  
You-Ni Zhang ◽  
Sen-Ren Guo
Keyword(s):  
Enteral Nutrition ◽  
Parenteral Nutrition ◽  
Barrier Function ◽  
Tumor Necrosis ◽  
Intestinal Barrier ◽  
Inflammatory Factors ◽  
Intestinal Barrier Function ◽  
Acute Severe Pancreatitis ◽  
Severe Pancreatitis ◽  
Necrosis Factor

The main objective of this study was to explore the effect of enteral nutrition on serum pro-inflammatory cytokines, tumor necrosis factor, and intestinal barrier function in patients with acute severe pancreatitis. A total number of 140 patients were recruited and divided randomly into parenteral nutrition (PN) and enteral nutrition (EN) groups. They received parenteral nutrition and enteral nutrition, respectively. The levels of serum total protein (TP) and albumin (ALB) in peripheral blood were detected in the two groups. Interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNFα) in the two groups were comparatively analyzed. The levels of pro-inflammatory factors (IL-1β, IL-6, and TNFα) for both groups were same, and there was no significant difference ( P < 0.05) between the two groups before treatment. However, after treatment, a significant reduction was found in EN group which were 31.16 ± 1.95, 36.09 ± 9.44, and 29.21 ± 3.85 ng/L, respectively, showing significant lower values as compared to PN group. The levels of TP and ALB in EN group were 64.46 ± 3.77 and 27.19 ± 1.56 g/L, respectively, after treatment, showing significantly ( P < 0.05) elevated values than PN group. The incidence rates of pancreatic necrosis and pancreatic abscess in EN group were 28.57% and 11.43%, respectively, which were found to be lower significantly than PN group. Enteral nutrition is found to be more effective than parenteral nutrition in the treatment of severe acute pancreatitis, which can significantly reduce the level of pro-inflammatory factors as well as the degree of systemic inflammatory response and protect the intestinal barrier function; thus, this study is worthy for awareness and application in clinical practice.

scholarly journals Enteral versus Parenteral Nutrition: Effect on Intestinal Barrier Function

2009 ◽  
Vol 1165 (1) ◽  
pp. 338-346 ◽  
Author(s):  
Hua Yang ◽  
Yongjia Feng ◽  
Xiaoyi Sun ◽  
Daniel H. Teitelbaum
Keyword(s):  
Parenteral Nutrition ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function

scholarly journals P38 MAPK Pharmacological Inhibitor SB203580 Alleviates Total Parenteral Nutrition-Induced Loss of Intestinal Barrier Function but Promotes Hepatocyte Lipoapoptosis

2017 ◽  
Vol 41 (2) ◽  
pp. 623-634 ◽  
Author(s):  
Yong-Tao Xiao ◽  
Wei-Hui Yan ◽  
Yi Cao ◽  
Jun-Kai Yan ◽  
Wei Cai
Keyword(s):  
Parenteral Nutrition ◽  
Palmitic Acid ◽  
Total Parenteral Nutrition ◽  
P38 Mapk ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Mitogen Activated Protein Kinase ◽  
Intestinal Barrier Function ◽  
P38 Mapk Inhibitor ◽  
Mapk Inhibitor

Background & Aims: Our previous studies have provided evidence that p38 mitogen-activated protein kinase (MAPK) is involved in total parenteral nutrition (TPN)-associated complications, but its exact effects and mechanisms have not been fully understood. This study aimed to evaluate the roles of p38 MAPK inhibitor SB203580 in the TPN-induced loss of intestinal barrier function and liver disease. Methods: A rodent model of TPN was used to analyze the roles of SB203580 in TPN-associated complications.Intestinal barrier function was evaluated by transepithelial electrical resistance (TER) and paracellular permeability in Caco-2 cells. The palmitic acid (PA) was used to induce hepatic lipoapoptosis in vitro. The lipoapoptosis was detected using Caspase-3/7 and lipid staining. Results: In the present study, we showed that SB203580 treatment significantly suppressed TPN-mediated intestinal permeability in rats. SB203580 treatment significantly inhibited IL-1β-induced an increase in tight junction permeability of Caco-2 cells via repressing the p38/ATF-2 signaling. Unexpectedly, SB203580 treatment enhanced hepatic lipoapoptosis in the model of TPN. Palmitic acid (PA)-induced hepatic lipoapoptosis in human liver cells was significantly augmented by the SB203580 treatment. Conclusions: We demonstrate that the p38 MAPK inhibitor SB203508 ameliorates intestinal barrier function but promotes hepatic lipoapoptosis in model of TPN.

scholarly journals Betaine attenuates LPS-induced downregulation of Occludin and Claudin-1 and restores intestinal barrier function

2020 ◽  
Author(s):  
Jingtao Wu ◽  
Caimei He ◽  
Jie Bu ◽  
Yue Luo ◽  
Shuyuan Yang ◽  
...  
Keyword(s):  
Barrier Function ◽  
Intestinal Barrier ◽  
Protective Role ◽  
Vital Role ◽  
Inflammatory Factors ◽  
Intestinal Barrier Function ◽  
Epithelial Barrier ◽  
Epithelial Barriers ◽  
Vitro Model

Abstract Background：The intestinal epithelial barrier, which works as the first line of defense between the luminal environment and the host, once destroyed, it will cause serious inflammation or other intestinal diseases. Tight junctions (TJs) play a vital role to maintain the integrity of the epithelial barrier. Lipopolysaccharide (LPS), one of the most important inflammatory factors will downregulate specific TJ proteins including Occludin and Claudin-1 and impair integrity of the epithelial barrier. Betaine has excellent anti-inflammatory activity but whether betaine has any effect on TJ proteins, particularly on LPS-induced dysfunction of epithelial barriers remains unknown. The purpose of this study is to explore the pharmacological effect of betaine on improving intestinal barrier function represented by TJ proteins. Intestinal porcine epithelial cells (IPEC-J2) were used as an in vitro model. Results: The results demonstrated that betaine enhanced the expression of TJ proteins while LPS (1µg/mL) downregulates the expression of these proteins. Furthermore, betaine attenuates LPS-induced decreases of TJ proteins both shown by Western blot (WB) and Reverse transcription- polymerase chain reaction (RT-PCR). The immunofluorescent images consistently revealed that LPS induced the disruption of TJ protein Claudin-1 and reduced its expression while betaine could reverse these alterations. Similar protective role of betaine on intestinal barrier function was observed by transepithelial electrical resistance (TEER) approach. Conclusion: In conclusion, our research demonstrated that betaine attenuated LPS-induced downregulation of Occludin and Claudin-1 and restored the intestinal barrier function.

scholarly journals Rottlerin ameliorates DSS-induced colitis by improving intestinal barrier function via activation of the Epac-2/Rap-1 signaling pathway

2020 ◽  
Author(s):  
Xue Song ◽  
Lugen Zuo ◽  
Luyao Wang ◽  
Zihan Zhu ◽  
Jing Tao ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Inflammatory Factors ◽  
Intestinal Barrier Function ◽  
Control Group ◽  
Treatment Groups ◽  
Normal Feeding ◽  
Anti Inflammatory

ABSTRACTOBJECTIVESRottlerin, a pan PDE inhibitor, has a variety of pharmacological activities, including enhancing barrier function and mediating anti-inflammatory activity by changing the distribution of occludin and ZO-1. Nevertheless, the function of rottlerin on Crohn disease (CD) keep unknown. Our aim of the study is to investigate the role of rottlerin on CD-like colitis and its mechanism.METHODSWild-type mice which were 8-10 weeks old were randomly divided into three treatment groups: (i) the normal feeding, no administration (control) group, (ii) the group administered 3% dextran sodium sulfate (DSS) alone, and (iii) the group administered rottlerin (100 mg/kg) and 3% DSS. In this study, the effect of rottlerin on the function and structure of the intestinal barrier was investigated, and the possible mechanism was discussed. We performed signaling pathway analysis and flow cytometry to identify the detailed mechanisms by which rottlerin (10 μg/mL) treatment inhibits cell growth arrest and the attenuation of TJ proteins in LPS-treated FHs 74 int cells.RESULTSRottlerin treatment significantly ameliorated colitis induced by DSS in WT mice, which was manifested by a decrease in inflammation score, the attenuation of inflammatory factors and the inhibition of destruction on intestinal barrier structure. Rottlerin enhanced the levels of occludin and ZO-1, and improved the function of intestinal barrier, which may have been why rottlerin ameliorated colitis in WT mice. The anti-inflammatory effect of rottlerin may be partly due to the activation of Epac-2/Rap-1 signaling.CONCLUSIONSRottlerin may treat CD in humans via enhancing TJ proteins expression and improving the function of intestinal barrier.

Pretreatment With High-Fat Enteral Nutrition Reduces Endotoxin and Tumor Necrosis Factor-?? and Preserves Gut Barrier Function Early After Hemorrhagic Shock

Shock ◽  
2004 ◽  
Vol 21 (1) ◽  
pp. 65-71 ◽  
Author(s):  
Misha D. P. Luyer ◽  
Wim A. Buurman ◽  
M'hamed Hadfoune ◽  
Jan A. Jacobs ◽  
Sergey R. Konstantinov ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Enteral Nutrition ◽  
Hemorrhagic Shock ◽  
Barrier Function ◽  
Tumor Necrosis ◽  
High Fat ◽  
Gut Barrier ◽  
Gut Barrier Function ◽  
Necrosis Factor

scholarly journals Betaine attenuates LPS-induced downregulation of Occludin and Claudin-1 and restores intestinal barrier function

2020 ◽  
Author(s):  
Jingtao Wu ◽  
Caimei He ◽  
Jie Bu ◽  
Yue Luo ◽  
Shuyuan Yang ◽  
...  
Keyword(s):  
Barrier Function ◽  
Intestinal Barrier ◽  
Protective Role ◽  
Vital Role ◽  
Inflammatory Factors ◽  
Intestinal Barrier Function ◽  
Epithelial Barrier ◽  
Epithelial Barriers ◽  
Vitro Model

Abstract Background ： The intestinal epithelial barrier, which works as the first line of defense between the luminal environment and the host, once destroyed, it will cause serious inflammation or other intestinal diseases. Tight junctions (TJs) play a vital role to maintain the integrity of the epithelial barrier. Lipopolysaccharide (LPS), one of the most important inflammatory factors will downregulate specific TJ proteins including Occludin and Claudin-1 and impair integrity of the epithelial barrier. Betaine has excellent anti-inflammatory activity but whether betaine has any effect on TJ proteins, particularly on LPS-induced dysfunction of epithelial barriers remains unknown. The purpose of this study is to explore the pharmacological effect of betaine on improving intestinal barrier function represented by TJ proteins. Intestinal porcine epithelial cells (IPEC-J2) were used as an in vitro model. Results: The results demonstrated that betaine enhanced the expression of TJ proteins while LPS (1µg/mL) downregulates the expression of these proteins. Furthermore, betaine attenuates LPS-induced decreases of TJ proteins both shown by Western blot (WB) and Reverse transcription- polymerase chain reaction (RT-PCR). The immunofluorescent images consistently revealed that LPS induced the disruption of TJ protein Claudin-1 and reduced its expression while betaine could reverse these alterations. Similar protective role of betaine on intestinal barrier function was observed by transepithelial electrical resistance (TEER) approach. Conclusion: In conclusion, our research demonstrated that betaine attenuated LPS-induced downregulation of Occludin and Claudin-1 and restored the intestinal barrier function.

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