Effects of Lipopolysaccharide on Intestinal Injury: Potential Role of Nitric Oxide and Lipid Peroxidation

Mercer, David; Smith, Gregory S.; Cross, James M.; Russell, Diane Haddock; Chang, Lily; Cacioppo, Jason

doi:10.1006/jsre.1996.0245

Cited by 68 publications

(58 citation statements)

References 4 publications

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“…LPS is a potent endotoxin found in the cell membrane of all gram-negative bacteria. LPS induced intestinal morphological injury, enhanced mucosal permeability and bacterial translocation and caused symptoms of acute bacterial infection, including anorexia, hypersomnia and fever (Mercer et al, 1996). These effects of LPS were associated with its ability to stimulate the rapid synthesis and release of pro-inflammatory cytokines.…”

Section: Discussionmentioning

confidence: 99%

PEGylated porcine glucagon-like peptide-2 improved the intestinal digestive function and prevented inflammation of weaning piglets challenged with LPS

Deng

et al. 2015

Animal

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This study was conducted to determine the effects on intestinal function, anti-inflammatory role and possible mechanism of polyethylene glycosylated (PEGylated) porcine glucagon-like peptide-2 (pGLP-2), a long-acting form of pGLP-2, in weaning piglets challenged with Escherichia coli lipopolysaccharide (LPS). We divided 18 weaned piglets on day 21 into three groups (control, LPS and LPS + PEG-pGLP-2; n = 6). The piglets from the LPS + PEG-pGLP-2 group were injected with PEG-pGLP-2 at 10 nmol/kg BW from 5 to 7 days of the trials daily. On 8 th day, the piglets in the LPS and LPS + PEG-pGLP-2 groups were intraperitoneally administered with 100 µg LPS/kg. The control group was administered with the same volume of saline solution. The piglets were then sacrificed on day 28. Afterwards, serum, duodenum, jejunum and ileum samples were collected for analysis of structural and functional endpoints. LPS + PEG-pGLP-2 treatment increased ( P < 0.05) lactase activities in the duodenum and the jejunum compared with LPS treatment. LPS + PEG-pGLP-2 treatment also significantly increased sucrase activity in the jejunum compared with LPS treatment. Furthermore, LPS treatment increased ( P < 0.05) the mRNA expression levels of interleukin (IL)-8, tumour necrosis factor-α (TNF-α) and IL-10 in the ileum compared with the control treatment. By contrast, LPS + PEG-pGLP-2 treatment decreased ( P < 0.05) the mRNA expression levels of IL-8, IL-10 and TNF-α in the ileum compared with the LPS treatment. LPS treatment also increased ( P < 0.05) the mRNA expression level of GLP-2 receptor (GLP-2R) and the percentage of GLP-2R-positive cells in the ileum; by comparison, these results were ( P < 0.05) reduced by LPS + PEG-pGLP-2 treatment. Moreover, LPS + PEGpGLP-2 treatment increased ( P < 0.05) the content of serum keratinocyte growth factor compared with the control group and the LPS group. The protective effects of PEG-pGLP-2 on intestinal digestive function were associated with the release of GLP-2R mediator (keratinocyte growth factor) and the decrease in the expressions of intestinal pro-inflammatory cytokines.

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Section: Discussionmentioning

confidence: 99%

PEGylated porcine glucagon-like peptide-2 improved the intestinal digestive function and prevented inflammation of weaning piglets challenged with LPS

Deng

et al. 2015

Animal

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“…The pathogenesis of intestinal mucosa barrier damage is unclear. It may be due to the increased lipid peroxidation reaction in intestinal tissue and intestinal mucosa damage caused by endotoxin [28] . It needs to be further studied.…”

Section: Discussionmentioning

confidence: 99%

Change of intestinal mucosa barrier function in the progress of non-alcoholic steatohepatitis in rats

Sheng¹,

Wu²,

He³

et al. 2008

WJG

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AIM:To explore the change of intestinal mucosa barrier function in the progress of non-alcoholic steatohepatitis (NASH) in rats. METHODS: Thirty-two Sprague-Dawley (SD) rats were randomly divided into control group and model group. Rats in the control group were given normal diet, and rats in the model group were given fat-rich diet. Eight rats in each group were killed at end of the 8th and 12th wk, respectively. The levels of endotoxin, D-xylose, TG, TC, ALT and AST, intestinal tissue SOD and MDA as well as intestinal mucus secretory IgA (sIgA) were measured. The pathology of liver was observed by HE staining. RESULTS: At end of the 8th wk, there was no marked difference in the levels of endotoxin, D-xylose and sIgA between the two groups. At end of the 12th wk, rats in the model group developed steatohepatitis and had a higher serum level of endotoxin (P = 0.01) and D-xylose (P = 0.00) and a lower serum level of sIgA (P = 0.007). CONCLUSION: Intestinal mucosa barrier malfunction may exist in NASH rats and may be an important promoter of NASH in rats.

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“…Sepsis was induced by intraperitoneal administration of lipopolysaccharide from Escherichia coli serotype 0111:B4, given in doses of 5 or 20 mg/kg body weight while controls received a comparable volume of saline (0.9%). Both doses of LPS have been previously demonstrated to increase iNOS immunoreactivity in the rat ileum 5 h after its administration [9]. Consequently, 5 h after receiving saline or LPS, rats were randomized to one of the several experimental protocols described below.…”

Section: Methodsmentioning

confidence: 99%

Does Upregulation of Inducible Nitric Oxide Synthase (iNOS) Render the Stomach More Susceptible to Damage?

Castaneda

Denning

Chang

et al. 1999

Journal of Surgical Research

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Effects of Lipopolysaccharide on Intestinal Injury: Potential Role of Nitric Oxide and Lipid Peroxidation

Cited by 68 publications

References 4 publications

PEGylated porcine glucagon-like peptide-2 improved the intestinal digestive function and prevented inflammation of weaning piglets challenged with LPS

PEGylated porcine glucagon-like peptide-2 improved the intestinal digestive function and prevented inflammation of weaning piglets challenged with LPS

Change of intestinal mucosa barrier function in the progress of non-alcoholic steatohepatitis in rats

Does Upregulation of Inducible Nitric Oxide Synthase (iNOS) Render the Stomach More Susceptible to Damage?

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