重组腺病毒IκBαM抑制高糖诱导的血管内皮细胞凋亡

Recombinant adenovirus IκBαM inhibit highglucose-mediated apoptosis in vascular endothelial cells

目的 研究NF κB在高浓度葡萄糖 (高糖 )诱导的ECV 30 4血管内皮细胞凋亡中的作用。方法 用携有NF κB抑制物IκBα突变体的IκBαM重组腺病毒 (AdIκBαM)感染ECV 30 4细胞 ,利用WesternBlot、EMSA、电镜、流式细胞仪等检测方法 ,研究NF κB在高糖诱导的血管内皮细胞凋亡中所起的作用 ,以及阻断NF κB活性对血管内皮细胞凋亡及细胞周期改变的影响。结果 高糖能诱导ECV 30 4细胞IκBα的降解和NF κB的激活 ,G0 G1 百分比增加 ,S和G2 M比例下降 ,延缓G0 G1 向S期过渡 ,出现细胞凋亡的形态学改变 ,而感染AdIκBαM的ECV 30 4 IκBαM细胞则能加速G0 G1 向S期过渡 ,未出现细胞凋亡的形态学改变。结论 AdIκBαM能抑制高糖诱导的ECV 30 4细胞NF κB的过度活化及对ECV 30 4细胞的致凋亡作用 ,加速细胞周期转换 ,证实NF

Objective To investigate the role of NF kappaB (NF κB) in highglucose(HG) induced apoptosis and cell cycle of ECV 304 cell, a vascular endothelial cell line.Methods ECV 304 cells were infected with recombinant adenovirus IκBαM. Western Blot, electrophoretic mobility shift assay (EMSA) were applied in this study. Apoptosis and cell cycle were studied with transmission electron microscopy and FACSC assay.Results Highglucose induced IκBα degradation, NF κB activation and apoptosis were found in ECV 304 cells but not in ECV 304/IκBαM cells infected with IκBαM recombinant adenovirus.Conclusion AdIκBαM can efficiently inhibit the excessive activation of NF κB and apoptosis in ECV 304 cells induced by HG. Inhibition of NF κB activation can protect vascular endothelial cells from the cytotoxicity of highglucose.