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作 者:蒋荣[1] 张倩倩[1] 张久丹 卢斌[1] 臧璞[1] 刘隽[1] 柏晓勇[1] 杜宏[1]
机构地区:[1]南京大学医学院临床学院内分泌科(南京军区总医院内分泌科),210002
出 处:《中国糖尿病杂志》2015年第6期546-549,共4页Chinese Journal of Diabetes
基 金:国家自然科学基金(81173622);江苏省自然科学基金(BK2011664)
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-α40ng/ml(TNF-α)组、Rhein100μg/ml+TNF-α40ng/ml(Rhein100)组、Rhein 50μg/ml+TNF-α40ng/ml(Rhein50)组、Rhein 10μg/ml+TNF-α40ng/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[(2.88±0.04)vs(1.27±0.32),(1.28±0.17),(1.32±0.25),P<0.05或P<0.01];Rhein100和Rhein50组ICAM-1mRNA的水平下降[(2.12±0.24)vs(1.19±0.17),(1.26±0.23),P<0.05或P<0.01];在黏附性实验中,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,可能是Rhein对HUVECs的保护机制之一。Objective 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:only HUVECs(HUVECs group),TNF-α(treated with TNF-α40ng/ml),Rhein100(treated with Rhein 100μg/ml plus TNF-α40ng/ml),Rhein50(treated with Rhein 50μg/ml plus TNF-α40ng/ml),Rhein10(treated with Rhein 10μg/ml plus TNF-α40ng/ml).The mRNA and protein expressions of intercellular adhersionmolecule-1(ICAM-1)were detected by RTPCR and Western blot respectively,the adhesive function of HUVECs was detected by monocytic THP-1cells.Results Compared with TNF-αgroup,the expression of ICAM-1protein was decreased in Rhein100,Rhein 50,and Rhein 10group[(2.88±0.04)vs(1.27±0.32),(1.28±0.17),(1.32±0.25),P〈0.05 or P〈0.01];the levels of ICAM-1mRNA were decreased in Rhein 100 and Rhein 50 group [(2.12±0.24)vs(1.19±0.17),(1.26±0.23),P〈0.05 or P〈0.01],and the number of adhesive monocytic THP-1cells was decreased in Rhein 100 group[(1.28±0.07)vs(1.07±0.14),P 〈0.01].Conclusion Rhein can inhibit TNF-αinduced ICAM-1 expression in HUVECs,which is a potential mechanism for Rhein associated vascular protection.
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