山东医药2012，Vol.52Issue(15)：42-45,4.
Mito-KATP对缺氧复氧大鼠心肌微血管内皮细胞凋亡的影响及作用机制
Effects and mechanism of Mito-KATP opening on apoptosis of rat myocardial microvascula endothelial cells undergoing hypoxia-reoxygenation
摘要
Abstract
Objective To investigate the effects and mechanism of Mito-KATP opening on apoptosis of rat myocardial microvascular endothelial cells(MMECs) undergoing hypoxia-reoxygenation. Methods Rat MMECs were cultured and divided into four groups: control group( N group) , modal group( H/R group) , opener group( DZ group) , blocker group(5-HD group). MMECs in DZ group and 5-HD group were pretreated with 100 μmol/L DZ and 100 μmol/L5-HD + 100 μmol/L DZ respectively for 2 h, then MMECs in H/R group, DZ group and 5-HD group were exposed to 2 h hypoxia followed by 2 h reoxygenation. The morphology of apoptosis cells was observed by Hoechst staining method, the apoptosis rate was assayed by Annexin V-FTTC/PI2 h after reoxygenation. The expression of NF-κB, fractalkine( FKN), and p53 mRNA were detected by RT-PCR. Results Compared with N group, a higher apoptosis rate(P<0.01)and an increased expression of NF-κB, FKN and p53 mRNA(P<0.01)were found in H/R group;compared with H/R group, a lower apoptosis rate(P<0.01), an decreased expression of NF-κB, FKN and p53 mRNA were found in DZ group (P<0.01); no significant difference was found between the indexes in 5-HD group and H/R group. Conclusion Opening of mito-KATP can inhibit the apoptosis of MMECs undergoing hypoxia-reoxygenation, the mechanism may be related to the suppressing of NF-κB, FKN and pS3 mRNA expression.关键词
线粒体ATP敏感性钾通道/心肌微血管内皮细胞/缺氧复氧/核因子-κB/趋化因子Fractalkine/抑癌基因p53Key words
mito-KATP/ myocardial microvascular endothelial cells/ hypoxia-reoxygenation/ NF-κB/ chemotactic factor fractalkine/ anti-oncogene p53分类
医药卫生引用本文复制引用
姚菊,曹苏,沈施仁..Mito-KATP对缺氧复氧大鼠心肌微血管内皮细胞凋亡的影响及作用机制[J].山东医药,2012,52(15):42-45,4.基金项目
江苏省卫生厅科技项目(Z201018) （Z201018）
南通大学自然科学项目(10Z048). （10Z048）
