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

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。

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

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(P<0.01).Compared with group H/R,the cell activity of LY294002 and PDTC group decreased(P<0.01),the cell activity of LY294002 group decreased(P<0.05) too.Compared with group LY294002,the cell activity of PDTC group decreased(P<0.01).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.