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机构地区:[1]中国医科大学附属盛京医院儿科 [2]大庆龙南医院儿科,黑龙江大庆163453
出 处:《中国中西医结合急救杂志》2008年第2期114-116,共3页Chinese Journal of Integrated Traditional and Western Medicine in Intensive and Critical Care
摘 要: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.
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