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DA-9601, a standardized extract of Artemisia asiatica, blocks TNF-α-induced IL-8 and CCL20 production by inhibiting p38 kinase and NF-κ-B pathways in human gastric epithelial cells

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World Journal of Gastroenterology 2006年第30期12卷 4850-4858页

作者： Suck-Chei Choi Eun-Ju Choi Hyun-Mee Oh SungGa Lee Jeong-Kun Lee Meung-Su Lee Yong-Il Shin Suck-Jun Choi Jeong-Ryong Chae Kang-Min Lee Won-Jung Lee Jae-Sik park Chang-Yell Shin Tae-Young Oh Chang-Duk Jun Digestive Disease Research Institute Wonkwang University School of Medicine Iksan Chonbuk 570-749 Korea Department physical Education Kunsan National University Chonbuk 573-701 Korea Department of Life Science Gwangju Institute of Science and Technology Gwangju 500-712 Korea Department of Leisure Sports Wonkwang Health Science College Iksan Chonbuk 570-749 Korea Division of Biological Sciences College of Natural Science Chonbuk National University Jeonju Chonbuk 561-756 Korea Department of physiology Kyungpook National University School of Medicine Taegu 700-422 Korea Research Institute Dong-A Pharmaceutical Co. Ltd. Yongin 449-905 Korea

AIM: To investigate whether, or how, DA-9601, which is a new gastroprotective agent, inhibits TNF-α-induced inflammatory signals in gastric epithelial AGS cells. METHODS: Cell viability was determined by MTT assay. IL-8 and CCL20 promoter activities were determined by a luciferease reporter gene assay. NF-κB-dependent transcriptional activity was determined by I-κBαdegradation, NF-κB p65 nuclear translocation and a luciferase activity assay. IL-8 and CCL20 gene expression and protein secretion were determined by RT-pCR and an enzymelinked immunosorbent assay (ELISA). Total and phos-phorylated forms of mitogen-activated protein kinases (MApKs) were determined by Western blot. RESULTS: Treatment of AGS cells with DA-9601 reduced TNF-α-induced IL-8 and CCL20 promoter activities, as well as their gene expression and protein release. TNF-αalso induced NF-κB-dependent transcriptional activity in AGS cells. In contrast, in cells treated with DA-9601, TNF-α-induced NF-κB activity was significantly blocked. Although all three MAp kinase family members were phosphorylated in response to TNF-α, a selective inhibitor of p38 kinase SB203580 only could inhibit both NF-κB-dependent transcriptional activity and IL-8 and CCL20 production, suggesting a potential link between p38 kinase and NF-κB-dependent pathways in AGS cells. Interestingly, DA-9601 also selectively inhibited p38 kinase phosphorylation induced by TNF-α. CONCLUSION: DA-9601 blocked TNF-α-mediated inflammatory signals by potentially modulating the p38 kinase pathway and/or a signal leading to NF-κBdependent pathways in gastric epithelial cells.

关键词： CCL20 IL-8 Artemisia asiatica DA-9601 TNF-α p38 kinase NF-κB

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

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World Journal of Gastroenterology 2009年第29期15卷 3676-3680页

作者： Yuan Yuan Mei Sun Ke-Shen Li Department of pediatrics ShengjingAffiliated Hospital of China Medical University Shenyang110004 Liaoning Province China Department of pediatrics Chinese PLA 211Hospital Harbin 150086 Heilongjiang Province China Ke-Shen ki Institute of BiomediCal Engineering HarbinEngineering University Harbin 150001 Heilongjiang ProvinceChina

AIM： To explore the effect of Astraga/us 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 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 ***： ApS-modulated bacterial productmediated p38 signaling represents an attractive strategy for prevention and treatment of intestinal inflammation.

关键词： Astraga/us mongho/icus polysaccharide Intestinal epithelial cells Tumor necrosis factor-Q Interleukin-8 Extracellular signal-regulated kinase CJun amino-terminal kinase p38 kinase

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