油酰乙醇胺对人脐静脉内皮细胞血管细胞黏附分子-1表达的影响

Effect of oleoylethanolamide on expression of vascular cell adhesion molecule-1 in human umbilical vein endothelial cells

目的探讨油酰乙醇胺(OEA)对肿瘤坏死因子α(TNF-α)诱导的人脐静脉内皮细胞血管细胞黏附分子-1(VCAM-1)表达的影响。方法体外培养人脐静脉内皮细胞,分别加入3种不同浓度的OEA(10,50,100μmol/L)或非诺贝特(10,50,100μmol/L)共同孵育10 h,再加入TNF-α共同孵育6 h,采用实时定量逆转录聚合酶链式反应和酶联免疫吸附剂检测测定VCAM-1以及mRNA和蛋白的表达,并采用Western blot方法检测过氧化物酶体增殖物激活受体α(PPAR-α)的蛋白表达。结果与非诺贝特相比,不同浓度的OEA更加显著地抑制人脐静脉内皮细胞VCAM-1mRNA和蛋白的表达,随着浓度的增大,抑制作用逐渐增强。Western bolt结果显示OAE能明显增强PPAR-α蛋白的表达。结论OEA对TNF-α引起的内皮细胞受损起到保护作用,其机理可能与上调过PPAR-α有关。

Purpose To investigate the effect of oleoylethanolamide （OEA） on tumor necrosis factor a （TNF-α）induced the expression of vascular cell adhesion molecule-1 （VCAM-1） in human umbilical vein en- dothelial cells（HUVECs）. Methods OEA and fenofibrate of different concentrations were incorporated in HU- VECs for 10 hours respectively. Human recombinant TNF-α was then incubated with HUVECs for 6 hours. The expression of VCAM-1 in mRNA level and protein level was detected by real-time quantitative RT-PCR and enzyme linked immunosorbent assay. Protein level of peroxisome proliferator-activated receptor α（PPAR-α）was determined by Western bolt. Results Compared with fenofibrate, OEA significantly inhibited the expression of VCAM-1 mRNA and protein in a dose-dependant manner. The result of Western blot showed that OEA up-regulated the protein level of PPAR-α. Conclusion OEA could protect endothelial cell from activation of eytokine through a PPAR-α pathway.