摘要
目的:探讨黄芪多糖(APS)在内毒素-脂多糖(LPS)损伤小肠上皮细胞(IEC-6)中的作用机制及对细胞因子和核因子-κB(NF-κB)表达的影响.方法:以小肠上皮细胞株IEC-6为研究对象,将培养的细胞分为6组:对照组、LPS组、LPS+APS 50 mg/L组、LPS+APS 100 mg/L组、LPS+APS 200 mg/L组和LPS+APS 500 mg/L组.采用RT-PCR法检测细胞因子TNF-α和IL-8 mRNA的表达,采用凝胶电泳迁移率法分析NF-κB蛋白活性.结果:LPS损伤IEC-6细胞后,TNF-α,IL-8 mRNA水平和NF-κB蛋白定量表达均升高,均显著高于对照组(TNF-α:1.26±0.06 vs 0.65±0.05,IL-8 mRNA:1.19±0.05 vs 0.57±0.06.NF-κB:2.76±0.07 vs 0.07±0.03,P均<0.01).而黄芪多糖呈浓度和时间依赖性地抑制LPS诱导IEC-6细胞分泌的TNF-α,IL-8等细胞因子的mRNA的表达水平(P<0.01),并能降低NF-κB的表达活性(P<0.01).结论:APS具有抑制LPS刺激IEC-6细胞产生的TNF-α,IL-8炎性因子的作用,并能降低NF-κB的表达活性,其对LPS所致的肠道损伤具有保护作用.
AIM： To explore the mechanism of the action and impact of Astragalus mongholicus polysaccharides （APS） on lipopolysaccharide （LPS）-induced inflammatory factors gene expression and nuclear factor （NF）-κB transcriptional activity in intestinal epithelial cells （IEC-6）.
METHODS： Intestinal epithelial cells （IEC-6） were divided into six groups： controls, LPS, LPS ＋ APS 50 mg/L, LPS ＋ APS 100 mg/L, LPS ＋ APS 200 mg/L, LPS ＋ APS 500 mg/L. Expression of tumor necrosis factor （TNF）-α and interleukin （IL）-8 mRNA was determined by RT-PCR. Expression of NF-κB protein was determined by electrophoretic mobility shift assay.
RESULTS： The levels of TNF-α, IL-8 mRNA and NF-κB protein were significantly higher in the LPS-damaged group than those in the control group （TNF-α： 1.26 ±0.06 vs 0.65± 0.05, IL-8 mRNA： 1.19 ± 0.05 vs 0.57± 0.06, NF-κB： 2.76 ±0.07 vs 0.07 ±0.03, P 〈 0.01）. Moreover, APS significantly inhibited LPS-induced TNF-α nd IL-8 at the mRNA level and reduced the production of NF-κB protein in a concentration- and timedependent manner （P 〈 0.01）.
CONCLUSION： APS can inhibit LPS-induced production of TNF-α and IL-8 mRNA, perhaps via suppression of the NF-κB signaling pathway. Modulation of bacterial product-mediated NF- κB signaling by APS may represent an attractive strategy for the prevention and treatment of intestinal inflammation.
出处
《世界华人消化杂志》
CAS
北大核心
2008年第1期15-19,共5页
World Chinese Journal of Digestology
关键词
黄芪多糖
小肠上皮细胞株
肿瘤坏死因子Α
白细胞介素-8
核因子-ΚB
Astragalus mongholicus polysaccharides
Intestinal epithelial cells
Tumor necrosis factor-α
Interleukin-8
Nuclear factor kappa B
