Carbon Monoxide Releasing Molecule-2 Protects Intestinal Mucosal Barrier Function of Rat Undergoing Cardiopulmonary Resuscitation via Attenuation of TNF-α/NF-κB Signaling

Abstract The unique features of post–cardiac arrest pathophysiology are often superimposed on the disease or injury, causing the cardiac arrest, as well as underlying comorbidities. Exogenous carbon monoxide (CO) was reported to reduce ischemia-reperfusion injury (IRI). This study aimed to assess the effects of CO releasing molecule-2 (CORM-2) on intestinal mucosal barrier function after cardiopulmonary resuscitation (CPR) in rats. For this purpose, we established a rat model of asphyxiation-induced cardiac arrest and resuscitation to study intestinal IRI, and measured the serum level of intestinal fatty-acid binding protein (I-FABP). The expression levels of claudin-3, occludin, ZO-1, tumor necrosis factor-alpha (TNF-α), interleukin-10 (IL-10), and nuclear factor kappa B (NF-κB) p65 were detected by Western blotting. CORM-2 up-regulated the expression levels of tight junction proteins (claudin-3, occludin, and ZO-1) in intestinal mucosa, leading to the reduction of the permeability of intestinal mucosa and reduced the release of proinflammatory cytokines. Besides, the CORM-2 exhibited anti-inflammatory effects by regulating the TNF-α/NF-κB pathway. In conclusion, CORM-2 treatment is clinically significant, preventing intestinal mucosal damage as a result of IRI during CPR.

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Methamphetamine-induced alterations in intestinal mucosal barrier function occur via the microRNA-181c/ TNF-α/tight junction axis

Toxicology Letters ◽

10.1016/j.toxlet.2019.12.020 ◽

2020 ◽

Vol 321 ◽

pp. 73-82 ◽

Cited By ~ 3

Author(s):

Simin Shen ◽

Jingjiao Zhao ◽

Yicong Dai ◽

Fengrong Chen ◽

Zunyue Zhang ◽

...

Keyword(s):

Tight Junction ◽

Barrier Function ◽

Mucosal Barrier ◽

Intestinal Mucosal Barrier ◽

Tnf Α ◽

Mucosal Barrier Function

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The influence of hyperbaric oxygen therapy on intestinal mucosal barrier function in rats with acute carbon monoxide poisoning

Toxicological and Environmental Chemistry ◽

10.1080/02772248.2015.1058382 ◽

2015 ◽

Vol 97 (5) ◽

pp. 609-618

Author(s):

Zhen Wang ◽

Zetian Shen ◽

Xiujian Chen ◽

Ping Jia ◽

Yadong Guan

Keyword(s):

Carbon Monoxide ◽

Hyperbaric Oxygen ◽

Hyperbaric Oxygen Therapy ◽

Barrier Function ◽

Oxygen Therapy ◽

Carbon Monoxide Poisoning ◽

Mucosal Barrier ◽

Intestinal Mucosal Barrier ◽

Acute Carbon Monoxide Poisoning ◽

Mucosal Barrier Function

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Chitosan Ameliorates DSS-Induced Ulcerative Colitis Mice by Enhancing Intestinal Barrier Function and Improving Microflora

International Journal of Molecular Sciences ◽

10.3390/ijms20225751 ◽

2019 ◽

Vol 20 (22) ◽

pp. 5751 ◽

Cited By ~ 8

Author(s):

Jia Wang ◽

Cuili Zhang ◽

Chunmei Guo ◽

Xinli Li

Keyword(s):

Barrier Function ◽

Intestinal Microflora ◽

Intestinal Barrier ◽

Mucosal Barrier ◽

Intestinal Barrier Function ◽

Tight Junction Proteins ◽

Intestinal Mucosal Barrier ◽

Tnf Α ◽

Mucosal Barrier Function ◽

Junction Proteins

Ulcerative colitis (UC) has been identified as one of the inflammatory diseases. Intestinal mucosal barrier function and microflora play major roles in UC. Modified-chitosan products have been consumed as effective and safe drugs to treat UC. The present work aimed to investigate the effect of chitosan (CS) on intestinal microflora and intestinal barrier function in dextran sulfate sodium (DSS)-induced UC mice and to explore the underlying mechanisms. KM (Kunming) mice received water/CS (250, 150 mg/kg) for 5 days, and then received 3% DSS for 5 days to induce UC. Subsequently, CS (250, 150 mg/kg) was administered daily for 5 days. Clinical signs, body weight, colon length, and histological changes were recorded. Alterations of intestinal microflora were analyzed by PCR-DGGE, expressions of TNF-α and tight junction proteins were detected by Western blotting. CS showed a significant effect against UC by the increased body weight and colon length, decreased DAI (disease activity index) and histological injury scores, and alleviated histopathological changes. CS reduced the expression of TNF-α, promoted the expressions of tight junction proteins such as claudin-1, occludin, and ZO-1 to maintain the intestinal mucosal barrier function for attenuating UC in mice. Furthermore, Parabacteroides, Blautia, Lactobacillus, and Prevotella were dominant organisms in the intestinal tract. Blautia and Lactobacillus decreased with DSS treatment, but increased obviously with CS treatment. This is the first time that the effect of original CS against UC in mice has been reported and it is through promoting dominant intestinal microflora such as Blautia, mitigating intestinal microflora dysbiosis, and regulating the expressions of TNF-α, claudin-1, occludin, and ZO-1. CS can be developed as an effective food and health care product for the prevention and treatment of UC.

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