缺氧复氧对大鼠心肌微血管内皮细胞活力的影响及机制研究

The research of effects and mechanism of the proliferation at myocardium microvascular endothelial cells on hypoxia-reoxygen

目的:研究缺氧复氧对大鼠心肌微血管内皮细胞(MMECs)活力的影响及机制。方法:培养大鼠MMECs,制作缺氧复氧模型模拟缺血再灌注损伤。随机分为4组(n=24),正常对照组(N组)不作任何处理、缺氧复氧组(HR组)、LY294002预先给药+缺氧复氧组(LY294002组)、PDTC预先给药+缺氧复氧组(PDTC组),均进行缺氧2 h复氧2 h。复氧2 h时后MTT法测定细胞活力,Hoechst染色观察凋亡细胞显微结构。结果:与N组比较,HR组细胞活力降低(P<0.01);与HR组比较,LY294002组细胞活力降低(P<0.05),PDTC组细胞活力降低(P<0.01);与LY294002组比较,PDTC组组细胞活力降低(P<0.01)。结论:缺氧复氧可导致MMECs活力明显降低;PI3K/Akt/NF-κB信号通路参与了缺氧复氧调控过程,该通路可促进MMECs活力增强。

Objective： To explore the effects and mechanism of the proliferation at myocardium microvascular endothelial cells on hypoxia-reoxygen.Methods： The cultivated rat myocardium microvascular endothelial cells on hypoxia-reoxygen were randomly divided into four groups（n=24）： control group（N）,hypoxia-regoxygen group（H/R）.LY294002＋hypoxia-regoxygen group（LY294002）,PDTC＋ hypoxia-regoxygen group（PDTC＋ H/R）,even hypoxia 2 h regoxygen 2 h each group.Each group was observed the cell activity.Results： Compared with group N,the cell activity dicreased in H/R group（P0.01）.Compared with group H/R,the cell activity of LY294002 and PDTC group decreased（P0.01）,the cell activity of LY294002 group decreased（P0.05） too.Compared with group LY294002,the cell activity of PDTC group decreased（P0.01）.Conclusion： The myocardium microvascular endothelial cells on hypoxia-reoxygen launched damage against injury mechanism,depending on the PI3K/Akt/NF-kB signal pathway to improve the cell activity.