%0 Journal Article
%T Astragalus mongholicus polysaccharide inhibits lipopolysaccharide-induced production of TNF-¦Á and interleukin-8
%A Yuan Yuan
%A Mei Sun
%A Ke-Shen Li
%J World Journal of Gastroenterology
%D 2009
%I Baishideng Publishing Group Co. Limited
%X 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 ¦Ìg/mL APS group, LPS+ 100 ¦Ìg/mL APS group, LPS+ 200 ¦Ìg/mL APS group, and LPS+ 500 ¦Ìg/mL APS group. Levels of mRNAs in LPS-induced inflammatory factors, tumor necrosis factor (TNF)-¦Á 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-¦Á 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-¦Á 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-¦Á 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.
%K Astragalus mongholicus polysaccharide
%K Intestinal epithelial cells
%K Tumor necrosis factor-¦Á
%K Interleukin-8
%K Extracellular signal-regulated kinase
%K C Jun amino-terminal kinase
%K p38 kinase
%U http://www.wjgnet.com/1007-9327/full/v15/i29/3676.htm