Astragalus mongholicus polysaccharide inhibits lipopolysaccharide-induced production of TNF-α and interleukin-8
Astragalus mongholicus polysaccharide inhibits lipopolysaccharide-induced production of TNF-α and interleukin-8
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DOI：
10.3748/wjg.15.3676
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发表时间：
2009-08-07
影响因子：
4.3
通讯作者：
Li, Ke-Shen
中科院分区：
文献类型：
--
作者：
Yuan, Yuan;Sun, Mei;Li, Ke-Shen
目的：探讨黄芪多糖（APS）对肠上皮细胞（IEC）基因表达及丝裂原活化蛋白激酶（MAPK）转录活性的影响。将IEC分为对照组、脂多糖（LPS）组、LPS+ 50 μ g/mL APS组、LPS+ 100 μ g/mL APS组、LPS+ 200 μ g/mL APS组，LPS+ 500 μ g/mL APS组。通过逆转录-聚合酶链反应测定LPS诱导的炎症因子、肿瘤坏死因子（TNF）-α和白细胞介素（IL）-8的mRNA水平。结果：LPS诱导IEC细胞损伤后，其TNF-α和IL-8 mRNA水平明显高于对照组。APS显著消除了LPS诱导的TNF-α和IL-8基因的表达。APS不阻断细胞外信号调节激酶或c-Jun氨基末端激酶的激活，但抑制p38的激活，提示APS可能通过抑制p38信号通路抑制LPS诱导的TNF-α和IL-8 mRNA的产生。结论：APS调节细菌产物介导的p38信号通路是一种有吸引力的预防和治疗肠道炎症的策略。(C)2009年，WIG出版社和百世登。All rights reserved.
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 mu g/mL APS group, LPS+ 100 mu g/ml APS group, LPS+ 200 mu g/mL APS group, and LPS+ 500 mu g/mL APS group. Levels of mRNAs in LPS-induced inflammatory factors, tumor necrosis factor (TNF)-alpha 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-alpha 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-alpha 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-alpha 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. (C) 2009 The WIG Press and Baishideng. All rights reserved.