摘要
目的探讨血管生成素1调节内皮祖细胞炎症因子的可能的信号传导通路。方法采用肿瘤坏死因子α诱导内皮祖细胞炎症,以慢病毒为载体将血管生成素1导入内皮祖细胞中,使用特异性抑制剂吡咯烷二硫代氨基甲酸盐抑制核因子κB,通过Western blot检测内皮祖细胞中血管生成素1蛋白和核因子κB蛋白的表达情况,随后采用荧光定量聚合酶链反应、酶联免疫吸附法检测各组内皮祖细胞中黏附分子细胞间黏附分子1、血管细胞黏附分子1的表达水平。结果转染血管生成素1基因内皮祖细胞中能够成功表达血管生成素1蛋白,而经吡咯烷二硫代氨基甲酸盐抑制后核因子κB蛋白未见明显表达。与肿瘤坏死因子α组相比,血管生成素1组、吡咯烷二硫代氨基甲酸盐组、血管生成素1+吡咯烷二硫代氨基甲酸盐组细胞间黏附分子1、血管细胞黏附分子1的mRNA和蛋白表达水平均明显下调(P<0.05),三组间无明显差异(P>0.05)。结论血管生成素1可能通过核因子κB信号传导通路影响肿瘤坏死因子α诱导的内皮祖细胞的炎症反应。
Ahn To investigate the possible signaling pathway in angiopoietin-1 (Ang-1) regulated inflammatory factors of endothelial progenitor cells. Methods We transformated Ang-1 into tumor necrosis factor-or (TNF-α) induced endothelial progenitor cell ( EPC), used the specific inhibitor pyrrolidine dithio carbamate (PDTC) to inhibit nuclear factor-kappa B (NF-κB). Western blot was used to detect the protein expression of Ang-1 and NF-κB, real-time poly- merase chain reaction (real-time PCR) and enzyme-linked immunosorbent assay (ELISA) were used to detect the mRNA and protein expression of intercellular cell adhesion molecule-1 ( ICAM-1 ) and vascular cellular adhesion molecule-1 ( VCAM-1 ) in EPC. Results Ang-1 protein expressed while no significant NF-κB protein expressed in EPC. Real- time PCR and ELISA show that compared to the TNF-α group, the expressions of ICAM-1 and VCAM-1 in Ang-1 group, PDTC group and Ang-1 +PDTC group significantly decreased (P 〈0. 05), but there were no significant differences among the three groups (P 〉 0. 05). Conclusions Ang-1 maybe affects adhesion molecules expression in TNF-α induced EPC through NF-κBsignaling pathway.
出处
《中国动脉硬化杂志》
CAS
CSCD
北大核心
2012年第4期309-314,共6页
Chinese Journal of Arteriosclerosis
基金
福建省自然科学基金计划项目(13081062)
关键词
血管生成素1
内皮祖细胞
炎症
核因子ΚB
Angiopoietin-1
Endothelial Progenitor Cell
Inflammation
Nuclear Factor-kappa B