SUR2B/Kir6.1通道开放剂纳他卡林对低氧致大鼠主动脉内皮细胞损伤的保护作用

Protective effects of SUR2B/Kir6.1 potassium channel opener natakalim against RAVECs injuries induced by hypoxia

目的:探讨纳他卡林对低氧引起大鼠主动脉内皮细胞损伤的保护作用及其机制。方法:选取大鼠主动脉内皮细胞作为体外低氧损伤的细胞模型,分为正常对照组、低氧模型组、纳他卡林低、中、高剂量组,利用MTT法测定细胞生存率,硝酸还原酶法检测一氧化氮(NO)释放,RT-PCR法检测细胞间粘附因子-1(ICAM-1)、内皮素-1(ET-1)、血管内皮生长因子(VEGF)mRNA水平。结果:纳他卡林三个剂量组均可逆转低氧所致的血管内皮细胞功能改变,包括提高内皮细胞生存活力和NO的释放水平,显著抑制低氧引发的内皮细胞ICAM-1,ET-1,VEGF mRNA表达量的上调。结论:纳他卡林对低氧诱发的血管内皮细胞分泌功能改变、细胞通透性增加及炎性因子的分泌均具有保护作用。

Objective： To investigate the protective effects of natakalim against rat aortic vascular endothelial cells（RAVECs） injuries induced by hypoxia and its mechanisms. Melhods： Selecting RAVECs as a cell model injured by hypoxia, these RAVECs were divided into 5 groups： i.e. control group, hypoxia group, natakalim low, medium and high group. Rhe cell survival rate was determined by MTF assay, con was measured using Griess Assay, RT-PCR was used to examine the expression of intercellular adhesion molecule-1 （ICAM-1）, vascular endothehal growth factor（VEGF）, endothelin-1 （ET-1） mRNA in RAVEC. Results： Natakalim could reverse hypoxia-induced changes in en- dothelial cell function, including increased endothelial cell survival rate and level of NO concentration, significantly inhibited the hypoxia-in- duced endothehal ICAM-1, ET-1, VEGF mRNA expression levels increased. Condusion： Natakalim have protective effects on hypoxia-in- duced changes in endothelial cell function, increasing of permeation, excess expression of cell adhesion molecules.