A single dose of carbon monoxide intraperitoneal administration protects rat intestine from injury induced by lipopolysaccharide

Liu, Shaohua; Ma, Ke; Xu, Xiaoling; Xu, Bing

doi:10.1007/s12192-010-0183-0

Cited by 52 publications

(36 citation statements)

References 35 publications

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“…ROS and apoptosis are the major mechanisms of I/R injury. The use of antioxidants and antiapoptosis agents decreased the effects of reperfusion on the intestinal mucosa [5,16].…”

Section: Discussionmentioning

confidence: 99%

Salvianolic Acid A Protects Against Oxidative Stress and Apoptosis Induced by Intestinal Ischemia-Reperfusion Injury Through Activation of Nrf2/HO-1 Pathways

Zhou

Che

et al. 2018

Cell Physiol Biochem

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Background/Aims: Ischemia-reperfusion (I/R) adversely affects the intestinal mucosa. The major mechanisms of I/R are the generation of reactive oxygen species (ROS) and apoptosis. Salvianolic acid A (SalA) is suggested to be an effective antioxidative and antiapoptotic agent in numerous pathological injuries. The present study investigated the protective role of SalA in I/R of the intestine. Methods: Adult male Sprague-Dawley rats were subjected to intestinal I/R injury in vivo. In vitro experiments were performed in IEC-6 cells subjected to hypoxia/ reoxygenation (H/R) stimulation to simulate intestinal I/R. TNF-α, IL-1β, and IL-6 levels were measured using enzyme-linked immunosorbent assay. Malondialdehyde and myeloperoxidase and glutathione peroxidase levels were measured using biochemical analysis. Apoptosis was measured by terminal deoxynucleotidyl transferase mediated dUTP nick-end labeling staining or flow cytometry in vivo and in vitro. The level of reactive oxygen species (ROS) was measured by dichlorodihydrofluorescin diacetate (DCFH-DA) staining. Western blotting was performed to determine the expression of heme oxygenase-1 (HO-1), Nrf2 and proteins associated with apoptosis. The mRNA expressions of Nrf2 and HO-1 were detected by quantitative real-time polymerase chain reaction in vivo and in vitro. Results: Malondialdehyde level and myeloperoxidase and glutathione peroxidase, TNF-α, IL-1β, and IL-6 levels group in intestinal tissue decreased significantly in the SalA pretreatment groups compared to the I/R group. SalA markedly abolished intestinal injury compared to the I/R group. SalA significantly attenuated apoptosis and increased Nrf2/HO-1 expression in vivo and in vitro. However, Nrf2 siRNA treatment partially abrogated the above mentioned effects of SalA in H/R-induced ROS and apoptosis in IEC-6 cells. Conclusion: The present study demonstrated that SalA ameliorated oxidation, inhibited the release of pro-inflammatory cytokines and alleviated apoptosis in I/R-induced injury and that these protective effects may partially occur via regulation of the Nrf2/ HO-1 pathways.

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“…ROS and apoptosis are the major mechanisms of I/R injury. The use of antioxidants and antiapoptosis agents decreased the effects of reperfusion on the intestinal mucosa [5,16].…”

Section: Discussionmentioning

confidence: 99%

Salvianolic Acid A Protects Against Oxidative Stress and Apoptosis Induced by Intestinal Ischemia-Reperfusion Injury Through Activation of Nrf2/HO-1 Pathways

Zhou

Che

et al. 2018

Cell Physiol Biochem

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“…There are no published data to suggest that a luminal polysaccharide might mediate acute neural actions of gut microbiota, although lipopolysaccharide (LPS) from pathogenic bacteria activate spinal sensory neurons upon direct exposure 19 . The zwitterionic capsular exopolysaccharide A, from the anaerobic symbiotic Gram-negative gut bacterium, Bacteroides fragilis (BF) could be a candidate.…”

mentioning

confidence: 99%

Bacteroides fragilis polysaccharide A is necessary and sufficient for acute activation of intestinal sensory neurons

et al. 2013

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Symbionts or probiotics are known to affect the nervous system. To understand the mechanisms involved, it is important to measure sensory neuron responses and identify molecules responsible for this interaction. Here we test the effects of adding Lactobacillus rhamnosus (JB-1) and Bacteroides fragilis to the epithelium while making voltage recordings from intestinal primary afferent neurons. Sensory responses are recorded within 8 s of applying JB-1 and excitability facilitated within 15 min. Bacteroides fragilis produces similar results, as does its isolated, capsular exopolysaccharide, polysaccharide A. Lipopolysaccharide-free polysaccharide A completely mimics the neuronal effects of the parent organism. Experiments with a mutant Bacteroides fragilis devoid of polysaccharide A shows that polysaccharide A is necessary and sufficient for the neuronal effects. Complex carbohydrates have not been reported before as candidates for such signalling between symbionts and the host. These observations indicate new neuronal targets and invite further study of bacterial carbohydrates as inter-kingdom signalling molecules between beneficial bacteria and sensory neurons.

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“…20 effects support the new paradigm that, at low concentrations, CO functions as a signaling molecule that exerts significant cytopro tective and antiinflammatory actions. Similar to the effects observed with HO-1, CO has been reported to mediate potent cytoprotective and anti-inflammatory effects against intestinal I/R injuries, LPS-induced intestinal injury, [91][92][93] or postoperative ileus [94][95][96][97] (Table 2). Nakao et al 15,98,99 have shown the efficacy of CO gas inhalation for the prevention of cold intestinal I/R injury using a small intestinal transplantation model.…”

Section: Role Of Co In the Small Intestinementioning

confidence: 56%

The role of heme oxygenase and carbon monoxide in inflammatory bowel disease

et al. 2010

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Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease, is a chronic and recurrent inflammatory disorder of the intestinal tract. Since the precise pathogenesis of IBD remains unclear, it is important to investigate the pathogenesis of IBD and to evaluate new anti-inflammatory strategies. Recent evidence suggests that heme oxygenase-1 (HO-1) plays a critical protective role during the development of intestinal inflammation. In fact, it has been demonstrated that the activation of HO-1 may act as an endogenous defensive mechanism to reduce inflammation and tissue injury in various animal intestinal injury models induced by ischemia-reperfusion, indomethacin, lipopolysaccharide-associated sepsis, trinitrobenzene sulfonic acid or dextran sulfate sodium. In addition, carbon monoxide (CO) derived from HO-1 has been shown to be involved in the regulation of intestinal inflammation. Furthermore, administration of a low concentration of exogenous CO has a protective effect against intestinal inflammation. These data suggest that HO-1 and CO may be novel therapeutic molecules for patients with gastrointestinal inflammatory diseases. In this review, we present what is currently known regarding the role of HO-1 and CO in intestinal inflammation.

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A single dose of carbon monoxide intraperitoneal administration protects rat intestine from injury induced by lipopolysaccharide

Cited by 52 publications

References 35 publications

Salvianolic Acid A Protects Against Oxidative Stress and Apoptosis Induced by Intestinal Ischemia-Reperfusion Injury Through Activation of Nrf2/HO-1 Pathways

Salvianolic Acid A Protects Against Oxidative Stress and Apoptosis Induced by Intestinal Ischemia-Reperfusion Injury Through Activation of Nrf2/HO-1 Pathways

Bacteroides fragilis polysaccharide A is necessary and sufficient for acute activation of intestinal sensory neurons

The role of heme oxygenase and carbon monoxide in inflammatory bowel disease

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