| 摘要: |
| 目的:观察激活的一磷酸腺苷活化蛋白激酶(AMPK)对软脂酸(PA)诱导的人脐静脉血管内皮细胞(HUVEC)损伤的保护作用,探讨其可能的作用机制.方法:按HUVEC培养液中成分不同,实验分为8组,分别为:空白对照组(常规培养)、PA培养组、5-氨基咪唑-4-甲酰胺核苷酸(AICAR)培养组、PA+AICAR培养组、二甲双胍(Met)培养组、PA+Met培养组、吡格列酮(PGZ)培养组和PA+PGZ培养组.HUVEC在各组培养液中分别培养24、48和72 h,MTT法测定不同时间点各组细胞的存活率,Western印迹法测定培养24 h时各组细胞的磷酸化AMPK蛋白表达水平.结果:与对照组相比,PA组细胞24、48和72 h的存活率明显降低,分别为58.95﹪、36.68﹪和15.09﹪(P＜0.05);培养72 h,AICAR+PA组、Met+PA组和PGZ+PA组细胞的存活率均显著高于PA组(P＜0.05);单独应用AICAR、Met和PGZ培养对细胞的存活率影响不大,与对照组比较无显著差异.与对照组和PA组相比,培养24 h时,AICAR、Met和PGZ刺激HUVEC的磷酸化AMPK表达增加(P＜0.05).结论:AICAR、Met和PGZ可能通过激活AMPK,显著减轻PA诱导的HUVEC的损伤. |
| 关键词: AMP-活化蛋白激酶、5-氨基-4-甲酰胺核苷酸、二甲双胍、吡格列酮 |
| DOI：10.3724/SP.J.1008.2006.00957 |
| 投稿时间：2006-01-09修订日期：2006-07-15 |
| 基金项目: |
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| Protective effect of activated AMP-activated protein kinase on palmatic acid-induced damage of human umbilical vein endothelial cells |
| CHENG Ying,MU Yi-ming,WANG Bao-an,PAN Chang-yu,LU Ju-ming |
| (中国人民解放军成都军区总医院内分泌科,成都,610032;中国人民解放军总医院内分泌科,北京,100853) |
| Abstract: |
| Objective：To investigate the protective effect of activated AMP-activated protein kinase （AMPK） on the human umbilical vein endothelial cell（HUVEC） damage induced by palmatlc acid （PA） and the related mechanism. Methods： HUVEC were divided into 8 groups according to the culture media （cultured for 24 to 72 h）： blank control （conventional culture）, 300 μmol/L PA, 1 mmol/L aminoimidazole-4-carboxamide-l-beta-ribofuranoside （AICAR）, PA＋ AICAR, 2 mmol/L metformin, PAq-metformin, 10 btmol/L pioglitazone, and PAq-pioglitazone groups. Survival rates of HUVEC were determined by MTT at 24, 48 and 72 h after culture. Western blot were performed to detect the expression of phospha-AMPK at 24 h after culture. Results： Compared with blank control group, cell survival rates in PA group were decreased by 58.95M, 36.68% and 15.09M at 24, 48 and 72 h（P〈0.05）, respectively. Seventy-two hours after culture, HUVEC survival rates of AICAR-t-PA group, Metnt-pA group and PGZ＋PA group were obviously higher than that of PA group （P〈0.05） ; AICAR, metformin or pioglita- zone alone had no obvious influence on HUVEC survival rate. Twenty-four hours after culture, Phospha-AMPK expression was increased in AICAR, metforrnin and pioglitazone groups compared with that of control group （P〈0.05）. Conclusion： AICAR, metformin and pioglitazone can decrease the damage of HUVEC induced by PA, possibly through activating AMPK |
| Key words: AMP-activated protein kinase 5-amino-4-imidazolecarboxamide-riboside metformin pioglitazone |
