N-acetyl glucosamine improves intestinal mucosal barrier function in rat

Authors

  • Yanxia Liu Bio-wave Research Center, Department of Laboratory Medicine, Third Military Medical University, Chongqing 400038
  • Weiwei Xu Bio-wave Research Center, Department of Laboratory Medicine, Third Military Medical University, Chongqing 400038
  • Lei Liu Bio-wave Research Center, Department of Laboratory Medicine, Third Military Medical University, Chongqing 400038
  • Linming Guo Bio-wave Research Center, Department of Laboratory Medicine, Third Military Medical University, Chongqing 400038
  • Yu Deng Bio-wave Research Center, Department of Laboratory Medicine, Third Military Medical University, Chongqing 400038
  • Junkang Liu Bio-wave Research Center, Department of Laboratory Medicine, Third Military Medical University, Chongqing 400038

DOI:

https://doi.org/10.3329/bjp.v7i4.12806

Keywords:

N-acetyl glucosamine, Intestinal mucosal barrier, Rat

Abstract

Our study investigated the effect of N-acetylglucosamine (GlcNAc) on the intestinal mucosal barrier function in rats. Rats were randomly assigned into normal control group, diarrhea-predominant irritable bowel syndrome (IBS-D) group and GlcNAc group. IBS-D was introduced into the IBS-D group without any treatment. The GlcNAc group were treated with GlcNAc. Microvilli and tight junctions of intestinal epithelial cells were detected. The D-lactic acid level and diamine oxidase (DAO) activity in the serum were determined. Compared with normal rats, microvilli were sparsely distributed on the intestinal epithelial cells, the tight junction gap also widened, and D-lactic acid level and DAO activity were significantly higher in the IBS-D group. After GlcNAc treatment, the microscopic structure of the intestinal mucosa became largely normal, and the level of D-lactic acid and the DAO activity were lowered. In conclusion, GlcNAc can effectively improve the intestinal mucosal barrier dysfunction, perhaps through enhancing the cellular metabolism.

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References

Al-Sadi R, Ye D, Said HM, Ma TY. IL-1?-Induced Increase in Intestinal Epithelial Tight Junction Permeability Is Mediated by MEKK-1 Activation of Canonical NF-?B Pathway Original Research Article. Am J Pathol. 2010; 177: 2310-22.

Berkes J, Viswanathan VK, Savkovic SD, Hecht G. Intestinal epithelial responses to enteric pathogens: Effects on the tight junction barrier, ion transport, and inflammation. Gut 2003; 52: 439-51.

Chatham JC, Nöt LG, Fülöp N, Marchase RB. Marchase, Hexosamine biosynthesis and protein O-glycosylation: The first line of defense against stress, ischemia, and trauma. Shock 2008; 29: 431-40.

Ciszewicz M, Wu G, Tam P, Polubinska A, Breborowicz A. Changes in peritoneal mesothelial cells phenotype after chronic exposure to glucose or N-acetylglucosamine. Translational Research. 2007; 150: 337-42.

Dunlop SP, Hebden J, Campbell E, Naesdal J, Olbe L, Perkins AC, Spiller RC. Abnormal intestinal permeability in subgroups of diarrhea-predominant irritable bowel syndromes. Am J Gastroenterol. 2006; 101: 1288-94.

Fasano A, Nataro JP. Intestinal epithelial tight junctions as targets for enteric bacteria-derived toxins. Adv Drug Deliv Rev. 2004; 56: 795-807.

Fennessy GJ, Warrillow SJ. Gastrointestinal problems in intensive care. Anaest Int Care Med. 2012; 13: 152-57.

Garrido D, Ruiz-Moyano S, Mills DA. Mills. Release and utilization of N-acetyl-d-glucosamine from human milk oligosaccharides by Bifidobacterium longum subsp.infantis. Anaerobe. 2012; 18: 430-35.

Hart GW, Housley MP, Slawson C. Cycling of O-linked beta-N-acetylglucosamine on nucleocytoplasmic proteins. Nature. 2007; 446: 1017-22.

Liu JK, Hu JC, Huang M. Study on the Influence of AWA on ATP Content of Intestinal Epithelia of IBS Rats. Biowave Sci Appl Oncol. 2007; 1: 29-31.

Liu JK, Hou WN, Wang J. Experimental study on choosing stimulating methods of establishing animal model. Biowave Sci Appl Oncol. 2007; 1: 15-17.

Longstreth GF, Thompson WG, Chey WD, Houghton LA, Mearin F, Spiller RC. Functional bowel disorders. Gastroenterology 2006; 130: 1480-91.

Ludmila Khailova, Andrew Maynard, Katerina Dvorak, Kelly M. Arganbright, Melissa Halpern, Toshi Kinouchi, Masako Yajima, Bohuslav Dvorak. W1774 Bifidobacterium Bifidum Improves Intestinal Barrier Function in Experimental Necrotizing Enterocolitis. Gastroenterology. 2008; 134: A-712-A-713.

Liu Jk, Wu XL, Chen J, Xu QW. Effect of GlcNAc against activation of bacterial cryptic growth cells to mast cells. Acta Acad Med Mil Tert. 2007; 29: 579-81.

Nielsen C, Lindholt JS, Erlandsen EJ, Mortensen FV. D-lactate as a marker of venous-induced intestinal ischemia: An experimental study in pigs. Int J Surg. 2011; 9: 428-32.

Sadik R, Bjornsson E, Simren M. The relationship between symptoms, body mass index, gastrointestinal transit and stool frequency in patients with irritable bowel syndrome. Eur J Gastroenterol Hepatol. 2010; 22: 10208.

Shikhman AR, Kuhn K, Alaaeddine N, Lotz M. N-acetylglucosamine prevents IL-1-mediated activation of human chondrocytes. J Immunol. 2001; 166: 515560.

Schenk M, Mueller C. The mucosal immune system at the gastrointestinal barrier. Best Pract Res Clin Gastroenterol. 2008; 22: 391-409.

Turner JR, Rill BK, Carlson SL, Carnes D, Kerner R, Mrsny RJ, Madara JL. Physiological regulation of epithelial tight junctions is associated with myosin light-chain phosphorylation. Am J Physiol. 1997; 273: C1378-85.

Tsujikawa T, Uda K, Ihara T, Inoue T, Andoh A, Fujiyama Y, Bamba T. Changes in serum diamine oxidase activity during chemotherapy in patients with hematological malignancies. Cancer Lett. 1999; 147: 195-98.

Zawalich WS, Dye ES, Matschinsky FM. Metabolism and insulin releasing capabilities of glucosamine and N-acetylglucosamine in isolated rat islets. Biochem J. 1979; 180: 14552.

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Published

2012-12-04

How to Cite

Liu, Y., W. Xu, L. Liu, L. Guo, Y. Deng, and J. Liu. “N-Acetyl Glucosamine Improves Intestinal Mucosal Barrier Function in Rat”. Bangladesh Journal of Pharmacology, vol. 7, no. 4, Dec. 2012, pp. 281-4, doi:10.3329/bjp.v7i4.12806.

Issue

Vol. 7 No. 4 (2012)

Section

Research Articles

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