摘要
目的探讨晚期糖基化终产物对人血管内皮细胞环氧合酶2表达的影响。方法取人脐静脉内皮细胞ECV304与人血清白蛋白修饰的晚期糖基化终产物体外共同培养,然后用Western blot检测环氧合酶2的表达水平。结果内皮细胞环氧合酶2基础表达水平极低,人血清白蛋白修饰的晚期糖基化终产物可诱导环氧合酶2的表达,呈时间与剂量依赖关系;抑制核因子κB的活性可抑制环氧合酶2的表达。结论人血清白蛋白修饰的晚期糖基化终产物可通过激活核因子κB,而引起环氧合酶2的表达。这一作用机制可能参与血管损伤反应。
Aim To elucidate how advanced glycation end products（AGE） effected cyclooxygenase-2 （COX-2） expression in cultured human umbilical vascular endothelial cells （ECV304）. Methods ECV304 were cultured in vitro with AGEhuman serum albumin （AGE-HSA）. The levels of protein COX-2 were measured by Western blot. Results COX-2 expressed little in ECV304, AGE-HSA could induce COX-2 expression, and the expression could be blocked by inhibiting the activation of NF-κB. Conclusion AGE-HSA could induce COX-2 expression by activing NF-κB. This pathobiological effect of AGEs might contribute to vascular lesion.
出处
《中国动脉硬化杂志》
CAS
CSCD
2006年第1期53-54,共2页
Chinese Journal of Arteriosclerosis
