Astragalus mongholicus polysaccharide inhibits lipopolysaccharide-induced production of TNF-α and interleukin-8

查看全文 作　　者：Yuan [1,2]Yuan;Mei [1]Sun;Ke-Shen [3]Li

机构地区：[1]Department of Pediatrics, ShengjingAffiliated Hospital of China Medical University, Shenyang110004, Liaoning Province, China;[2]Department of Pediatrics, Chinese PLA 211Hospital, Harbin 150086, Heilongjiang Province, China;[3]Ke-Shen ki, Institute of BiomediCal Engineering, HarbinEngineering University, Harbin 150001, Heilongjiang Province,China

出　　处：《World Journal of Gastroenterology》索引2009年第15卷第29期,共5页

摘　　要：AIM: To explore the effect of Astragalus mongholicus polysaccharide (APS) on gene expression and mitogenactivated protein kinase (MAPK) transcriptional activity in intestinal epithelial cells (IEC). METHODS: IEC were divided into control group, lipopolysaccharide (LPS) group, LPS+ 50 μg/mL APS group, LPS+ 100 μg/mL APS group, LPS+ 200 μg/mL APS group, and LPS+ 500 μg/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 signalregulated 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 productmediated p38 signaling represents an attractive strategy for prevention and treatment ofintestinal inflammation. 关键词：TNF 脂多糖诱导比反转录聚合酶链反应细胞外信号调节激酶生产黄芪糖抑制

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Astragalus mongholicus polysaccharide inhibits lipopolysaccharide-induced production of TNF-α and interleukin-8

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