Gastroduodenal defense

Ham, Maggie; Kaunitz, Jonathan D.

doi:10.1097/mog.0b013e3282f02607

Cited by 49 publications

(24 citation statements)

References 65 publications

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“…Mucous producing goblet cells secrete a thick layer of polysaccharide called mucin which coats the intestinal epithelial surface and provides a physical barrier suppressing epithelial-bacteria contact. This layer constitutes in part the unstirred layer covering the intestinal epithelium, slowing the movement of solutes and bulk fluid through the barrier [24]. The specific importance of mucins in protection against intestinal inflammation can be seen Muc2-deficient mice [25].…”

Section: Gut Barrier Function and Dysfunctionmentioning

confidence: 99%

Contribution of Gut Bacteria to Liver Pathobiology

Son

Kremer

Hines

2010

Gastroenterology Research and Practice

131

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Emerging evidence suggests a strong interaction between the gut microbiota and health and disease. The interactions of the gut microbiota and the liver have only recently been investigated in detail. Receiving approximately 70% of its blood supply from the intestinal venous outflow, the liver represents the first line of defense against gut-derived antigens and is equipped with a broad array of immune cells (i.e., macrophages, lymphocytes, natural killer cells, and dendritic cells) to accomplish this function. In the setting of tissue injury, whereby the liver is otherwise damaged (e.g., viral infection, toxin exposure, ischemic tissue damage, etc.), these same immune cell populations and their interactions with the infiltrating gut bacteria likely contribute to and promote these pathologies. The following paper will highlight recent studies investigating the relationship between the gut microbiota, liver biology, and pathobiology. Defining these connections will likely provide new targets for therapy or prevention of a wide variety of acute and chronic liver pathologies.

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Section: Gut Barrier Function and Dysfunctionmentioning

confidence: 99%

Contribution of Gut Bacteria to Liver Pathobiology

Son

Kremer

Hines

2010

Gastroenterology Research and Practice

131

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“…One of the proposed mechanisms of ethanol induced ulcers is by oxidative damage and stress along with depletion of anti-oxidants in gastrointestinal mucosa [3,4]. Etiology of these ulcers are not only related to extrinsic factors like alcohol but also to various intrinsic protective factors like gastric mucosal barrier, oxidative stress in mucosa and mucosal hypoperfusion [5]. Among all these factors, reactive oxygen species (ROS) due to oxidative stress generated in the mucosal is major contributor for gastric ulcers [6].…”

Section: Introductionmentioning

confidence: 99%

Cerium Oxide Nanoparticles Protects Gastrointestinal Mucosa From Ethanol Induced Gastric Ulcers in In-Vivo Animal Model

Prasad¹,

Davan²,

Jothi³

et al. 2013

Nano BioMed ENG

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Cerium oxide (CeO 2 ) nanoparticles having size range of 160 nm were prepared by using simple and effective sol-gel process and evaluated for their ulcer protective activity in an animal model. CeO 2 nanoparticles at a dose of 1mg/kg found to protect gastrointestinal mucosal from ethanol induced gastric ulcers. The ability of these nanoparticles to protect ethanol induced ulcers could be supported by increased amount of biomarkers in the native tissue like superoxide dismutase (SOD) (from 85.18 ± 0.24 to 103.18 ± 0.42) and Catalase (from 66.48 ± 0.71 to 85.88 ± 0.61) in Group 2 and Group 4. The percentage of ulcer inhibition of CeO 2 nanoparticles is 80.2% which is also close to the standard drug ranitidine (87.9%). The prepared nanoparticles were characterized by SEM and XRD. The probable mechanism may be due to the dual oxidation state of CeO 2 which will help in scavenging reactive oxygen species (ROS) and reduce oxidative stress locally and also mimicking the intrinsic intracellular enzymes like SOD. All these results and properties could be useful in protecting the gastrointestinal mucosa from oxidative stress generated by ethanol.

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“…The mucosal barrier consists of a pre-epithelial mucus layer, intercellular tight junctions connecting the epithelial cells, and submucosal acid sensors, prostaglandins, cytokines, enteric nerves and blood flow [2]. Disturbing the balance between aggressive and protective factors that control cell apoptosis and proliferation leads to gastric ulceration, which then activates the repairing system in the gastric mucosa.…”

Section: Introductionmentioning

confidence: 99%

Alpha-Lipoic Acid Improves Acetic Acid-Induced Gastric Ulcer Healing in Rats

et al. 2008

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To evaluate the role of ALA treatment on the healing of acetic acid-induced gastric ulcer, rats were given ALA (35 mg/kg/day) or saline for 3 days before the induction of ulcer and the treatment was continued twice daily for 2 days (early) or 10 days (late) until they were decapitated. Gastric ulcer index, microscopic score, elevated DNA fragmentation and chemiluminescence levels of the saline-treated ulcer groups were all reduced by ALA treatment. Likewise, ALA treatment inhibited chemiluminescence levels in both early and late ulcer groups. Marked reduction in glutathione levels of the saline-treated early ulcer group was reversed by ALA treatment, while ALA treatment was effective in depressing gastric myeloperoxidase activity in the late ulcer group. In conclusion, ALA treatment shows protective role in the healing of acetic acid-induced gastric injury in rats via the suppression of neutrophil accumulation, preservation of endogenous glutathione, inhibition of reactive oxidant generation and apoptosis.

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Gastroduodenal defense

Abstract: The continued elucidation of basic defense mechanisms has led to the development of several new compounds designed to enhance barrier function and repair mechanisms.

Cited by 49 publications

References 65 publications

Contribution of Gut Bacteria to Liver Pathobiology

Contribution of Gut Bacteria to Liver Pathobiology

Cerium Oxide Nanoparticles Protects Gastrointestinal Mucosa From Ethanol Induced Gastric Ulcers in In-Vivo Animal Model

Alpha-Lipoic Acid Improves Acetic Acid-Induced Gastric Ulcer Healing in Rats

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