Brief Articles
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World J Gastroenterol. Aug 7, 2009; 15(29): 3676-3680
Published online Aug 7, 2009. doi: 10.3748/wjg.15.3676
Astragalus mongholicus polysaccharide inhibits lipopolysaccharide-induced production of TNF-α and interleukin-8
Yuan Yuan, Mei Sun, Ke-Shen Li
Yuan Yuan, Mei Sun, Department of Pediatrics, Shengjing Affiliated Hospital of China Medical University, Shenyang 110004, Liaoning Province, China
Yuan Yuan, Department of Pediatrics, Chinese PLA 211 Hospital, Harbin 150086, Heilongjiang Province, China
Ke-Shen Li, Institute of Biomedical Engineering, Harbin Engineering University, Harbin 150001, Heilongjiang Province, China
Author contributions: Yuan Y and Sun M contributed equally to this work; Yuan Y and Li KS performed the research; Yuan Y and Sun M designed the research, provided the new reagents/analytic tools, analyzed the data and wrote the paper.
Correspondence to: Dr. Mei Sun, Department of Pediatrics, Shengjing Affiliated Hospital of China Medical University, Shenyang 110004, Liaoning Province, China. sunm@cmu2h.com
Telephone: +86-451-57752418
Fax: +86-451-57752418
Received: April 20, 2009
Revised: June 25, 2009
Accepted: July 2, 2009
Published online: August 7, 2009
Abstract

AIM: To explore the effect of Astragalus mongholicus polysaccharide (APS) on gene expression and mitogen-activated protein kinase (MAPK) transcriptional activity in intestinal epithelial cells (IEC).

METHODS: IEC were divided into control group, lipopolysaccharide (LPS) group, LPS+ 50 &mgr;g/mL APS group, LPS+ 100 &mgr;g/mL APS group, LPS+ 200 &mgr;g/mL APS group, and LPS+ 500 &mgr;g/mL APS group. Levels of mRNAs in LPS-induced inflammatory factors, tumor necrosis factor (TNF)-α and interleukin (IL)-8, were measured by reverse transcription-polymerase chain reaction. MAPK protein level was measured by Western blotting.

RESULTS: The levels of TNF-α and IL-8 mRNAs were significantly higher in IEC with LPS-induced damage than in control cells. APS significantly abrogated the LPS-induced expression of the TNF-α and IL-8 genes. APS did not block the activation of extracellular signal-regulated kinase or c Jun amino-terminal kinase, but inhibited the activation of p38, suggesting that APS inhibits LPS-induced production of TNF-α and IL-8 mRNAs, possibly by suppressing the p38 signaling pathway.

CONCLUSION: APS-modulated bacterial product-mediated p38 signaling represents an attractive strategy for prevention and treatment of intestinal inflammation.

Keywords: Astragalus mongholicus polysaccharide; Intestinal epithelial cells; Tumor necrosis factor-α; Interleukin-8; Extracellular signal-regulated kinase; C Jun amino-terminal kinase; p38 kinase