·糖尿病基础研究·

　　【摘要】 目的 观察不同剂量的大黄酸(Rhein)对TNF-α诱导的人脐静脉内皮细胞(HUVECs)黏附作用的影响。 方法 将HUVECs分为单纯HUVECs组、单纯TNF-α40 ng/ml刺激(TNF-α)组、Rhein 100 μg/ml+TNF-α40 ng/ml刺激(Rhein100)组、Rhein 50 μg/ml+TNF-α40 ng/ml(Rhein50)组、Rhein 10 μg/ml+TNF-α40 ng/ml(Rhein10)组。采用Western blot和RT-PCR检测HUVECs细胞间黏附因子-1(ICAM-1)的蛋白和mRNA的水平。采用人单核细胞株(THP-1)和HUVECs的黏附性实验检测内皮细胞的黏附功能。 结果 与TNF-α组比较，Rhein100、Rhein50、Rhein10组ICAM-1蛋白相对表达量下降(P<0.05或P<0.01);Rhein100和Rhein50组ICAM-1 mRNA的水平下降(P<0.01或P<0.05);在黏附性试验中，Rhein100组HUVECs所黏附的单核细胞数目下降[(1.28±0.07) vs (1.07±0.14)，P<0.01]。 结论 Rhein能抑制TNF-α所诱导的HUVECs的ICAM-1的过度表达，这可能是Rhein对HUVECs的保护机制之一。

　　【关键词】 大黄酸;人脐静脉内皮细胞;细胞间黏附因子-1;

　　【Abstract】 Objectives To examine the effects of various concentrations of Rhein on adhesive function of Human umbilical vein endothelial cells(HUVECs) induced by Tumor Necrosis Factor-α(TNF-α). Methods HUVECs were divided into five groups of CTL(blank control), TNF-α(treated with TNF-α 40 ng/ml), Rhein100(treated with Rhein 100μg/ml plus TNF-α40 ng/ml), Rhein50(treated with Rhein 50μg/ml plus TNF-α40 ng/ml), Rhein10(treated with Rhein 10μg/ml plus TNF-α40 ng/ml). The mRNA and protein expressions of intercellular adhersion molecule-1(ICAM-1) were detected by RT-PCR and Western blotting respectively, the adhesive function of HUVECs were detected by monocytic THP-1 cells. Results Compared with group TNF-α, the expression of ICAM-1 protein was decreased in groups of Rhein100、Rhein50、Rhein10[(2.88±0.04) vs (1.27±0.32)，P<0.05;(2.88±0.04) vs (1.28±0.17)，P<0.01;(2.88±0.04) vs (1.32±0.25)，P<0.01];the levels of ICAM-1 mRNA were decreased in groups of C、D[(2.12±0.24) vs (1.19±0.17), P<0.01);(2.12±0.24) vs (1.26±0.23), P<0.05],and the number of adhesive monocytic THP-1 cells was decreased in group C[(1.28±0.07) vs (1.07±0.14), P<0.01]. Conclusions It is suggested that Rhein can inhibit TNF-α induced ICAM-1 expression in HUVECs, which provides a potential mechanism for vascular protection.

　　【Key words】 Rhein; Human umbilical vein endothelial cells(HUVECs); Intercellular Adhersion Molecule-1(ICAM-1)