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目的研究核转录因子κB(NFκB)在高糖、肿瘤坏死因子(TNFα)、白细胞介素1β(IL1β)诱导ECV304血管内皮细胞损害中的作用。方法以构建含NFκB抑制物IκBα突变体(IκBαM)的重组腺病毒感染ECV304细胞,用Western印迹、凝胶电泳迁移率实验(EMSA)、四甲基偶氮唑盐(MTT)等方法研究NFκB在高糖、TNFα、IL1β介导血管内皮细胞损害中的作用。结果TNFα可诱导ECV304细胞的IκBα降解和NFκB的激活(P<0.01),而对ECV304/IκBαM细胞则无此作用;高糖可导致ECV304细胞NFκB的激活(P<0.05),而对ECV304/IκBαM细胞则无此作用;单独使用高糖、TNFα、IL1β导致ECV304细胞活力的降低(均P<0.01),而ECV304/IκBαM细胞可抵抗这些因素对细胞的损害(均P<0.05)。结论高糖、TNFα、IL1β可致血管内皮细胞活力降低,IκBα能有效抑制上述有害因素导致的ECV304细胞NFκB的过度活化,抵抗内皮细胞的损害。抑制NFκB活性可能有助于保护血管内皮细胞的功能。
Objective To investigate the role of nuclear factor kappa B (NFκB) in the injury induced by high glucose, tumor necrosis factor (TNFα) and interleukin-1β (IL1β) in ECV304 vascular endothelial cells. Methods ECV304 cells were infected with recombinant adenovirus containing IκBα mutant (IκBαM). The expression of NFκB was examined by Western blotting, EMSA and MTT assay The Role of High Glucose, TNFα and IL1β in Vascular Endothelial Cell Injury. Results TNFα induced the degradation of IκBα and activation of NFκB in ECV304 cells (P <0.01), but not in ECV304 / IκBαM cells. High glucose led to the activation of NFκB in ECV304 cells (P <0.05), whereas ECV304 / IκBαM However, ECV304 / IκBαM cells could resist the damage of these cells to the cells (all P <0.05). Conclusion High glucose, TNFα and IL1β can decrease the viability of vascular endothelial cells. IκBα can effectively inhibit the over-activation of NFκB in ECV304 cells induced by these harmful factors and resist the damage of endothelial cells. Inhibition of NFKB activity may help to protect the function of vascular endothelial cells.