黄芪多糖对内毒素刺激体外培养肠上皮细胞间黏附分子-1的调节作用

Effect of Astragalus mongholicus polysaccharides(黄芪多糖) on intercellular adhesion molecule-1 secreted by in vitro intestinal epithelial cell induced by lipopolysaccharide

目的观察黄芪多糖对内毒素脂多糖（LPS）体外刺激小肠上皮IEC-6细胞株产生细胞间黏附分子-1（ICAM-1）的调节作用，探讨黄芪多糖对损伤IEC-6细胞的免疫保护机制。方法以IEC-6细胞株为研究对象，将培养的细胞分别加入50、100、200和500mg／L不同浓度的黄芪多糖，孵育1h，以10mg／L的LPS刺激1～4h后，采用逆转录-聚合酶链反应（RT—PCR）方法检测ICAM-1 mRNA的表达变化。结果LPS刺激IEC-6细胞后ICAM-1 mRNA表达水平较正常对照组显著升高（0．74±0．06比1．45±0．07，P〈0．01）；黄芪多糖100、200和500mg／L时的ICAM-1 mRNA表达量分别为0．97±0．06、0．82±0．07和0．65±0．05；黄芪多糖500mg／L作用1h和4h的ICAM-1 mRNA抑制率分别为32．7％（1．19±0．06和0．80±0．10）和36．3％（0．93±0．07和0．72±0．08），说明黄芪多糖呈浓度和时间依赖性地抑制了LPS诱导IEC-6细胞表达ICAM-1 mRNA的水平（P均〈0．01）。结论黄芪多糖具有抑制LPS刺激IEC-6细胞分泌ICAM-1的作用，对LPS所致的肠道损伤具有保护作用。

Objective To explore the regulatory effect of Astragalus mongholicus polysaccharides （黄芪多糖, APS） on lipopolysaccharide （LPS） -induced intercellular adhesion molecule-1 （ICAM-1） gene expression in small intestinal epithelial cells （IEC-6） in vitro, and to approach the mechanism of immune protective effect of APS on IEC-6 injury. Methods The cultured IEC-6 were observed. They were added 50, 100, 200, and 500 mg/L of APS in different cultures respectively for 1 hour, and then were induced by LPS of 10 mg/L for 1 - 4 hours. The expression of ICAM-1 mRNA was determined by reverse transcriptionpolymerase chain reaction （RT-PCR）. Results After IEC-6 were stimulated by LPS, the level of ICAM-1 mRNA was significantly higher than that in the normal control group （0. 74 ± 0.06 vs. 1.45 ± 0.07, P〈 0.01）. The expressions of ICAM-1 mRNA in the cultures of APS 100, 200 and 500 mg/L were 0. 97±0. 06, 0.82±0. 07 and 0.65±0.05, respectively. The inhibition rate of ICAM-1 mRNA under APS 500 mg/L at 1 hour and 4 hours were 32.7% （1.19±0.06 vs. 0.80±0.10） and 36.3% （0.93±0.07 vs. 0.72±0.08）, respectively. Moreover, APS significantly abrogated LPS-induced ICAM-1 at mRNA level in a concentration and time dependent manner （all P〈0.01）. Conclusion APS can inhibit LPS-induced production of ICAM-1 mRNA, and has protective effect on the intestinal tract injury from LPS.