摘要
目的探讨晚期糖基化终产物对人血管内皮细胞核因子κB的激活及作用机制。方法用晚期糖基化终产物修饰的人血清白蛋白与人脐静脉内皮细胞株ECV304体外共同培养。用Westernblot检测核因子κB抑制蛋白水平,凝胶滞留法检测核因子κB的活性。结果晚期糖基化终产物修饰的人血清白蛋白可致ECV304核因子κB抑制蛋白降解及核因子κB激活,并且呈时间、剂量依赖关系,抑制核因子κB抑制蛋白的降解,可抑制核因子κB的激活。结论晚期糖基化终产物修饰的人血清白蛋白通过引起核因子κB抑制蛋白降解,导致核因子κB的激活,这一作用机制可能参与动脉粥样硬化的进程。
Aim To investigate the mechanism of activation of nuclear factor-kB（NF-kB） by advanced glycation end products （AGE） in endothelial cell. Methods Human umbilical vein endothelial cell（ECV304） were stimulated with AGE-human serum albumin（AGE-HAS）, the level of IkBa was mesured by Western blot, and the activation of NF-kB was detected by electrophoretie mobility shift assay（EMSA）. Results The degradation of IkBa and the activation of NF-kB could be induced by AGE-HSA in time and dose dependent way in ECV304. The activation of NF-kB could be blocked by inhibiting the degradation of IkBa. Conclusions AGE-HSA might activate NF-kB in IkBa degradation dependent in ECV304. This pathobiological effect of advanced glycation end products might contribute to the development of atherosclerosis.
出处
《中国动脉硬化杂志》
CAS
CSCD
2005年第3期329-331,共3页
Chinese Journal of Arteriosclerosis
