Role of AMPK in HDL-induced antiarterogenic effects in endothelial cells

高密度脂蛋白（HDL）刺激人脐静脉内皮细胞（HUVECs） AMP激酶（AMPK）。HDL通过独立的两条途径激活AMPK。高密度脂蛋白诱导的AMPK活化由鞘氨醇-1磷酸(S1P)/S1P受体途径和清道夫受体(SR-BI)/PDZK-1介导。S1P/S1P受体途径由钙调蛋白介导。在HUVECs中，SR-BI/PDZK-1通路由钙调素和LKB1介导。辛伐他汀、非诺贝特、二甲双胍和AICAR可增强HUVECs中SR-BI和内皮型一氧化氮合酶（eNOS）的蛋白表达。同时预处理辛伐他汀和非诺贝特可增强高密度脂蛋白诱导的huvec中AMPK/Akt的激活。

High density lipoprotein (HDL) stimulated AMP kinase (AMPK) in human umbilical vein endothelial cells (HUVECs). HDL activated AMPK through independent two pathways. HDL-induced AMPK activation was mediated by sphingosine-1 phosphate (S1P)/S1P receptor pathway and scavenger receptor (SR-BI)/PDZK-1. S1P/S1P receptor pathway was mediated by calmodulin. SR-BI/PDZK-1 pathway was mediated by calmodulin and LKB1 in HUVECs. Simvastatin, fenofibrate, metrformin and AICAR enhanced protein expression of SR-BI and endothelial nitric oxide synthase (eNOS) in HUVECs. Simultaneous pretreatment of simvastatin and fenofibrate enhanced HDL-induced AMPK/Akt activation in HUVECs.