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目的观察缺氧-复氧(H-R)大鼠心肌微血管内皮细胞(MMECs)NF-κB信号通路中二氮嗪对fractalkine(FKN)表达的作用。方法将培养的大鼠MMECs随机分为正常对照组(C组)、缺氧-复氧组(H-R组,缺氧2h+复氧2h)、二氮嗪+缺氧-复氧组(DZ组,二氮嗪100μmol/L预处理2h+缺氧2h+复氧2h)、NF-κB特异性阻断剂吡咯烷二硫基甲酸盐+二氮嗪+缺氧-复氧组(PDTC组,PDTC 100μmol/L预处理2h+二氮嗪100μmol/L预处理2h+缺氧2h+复氧2h)。Annexin-V-FITC/PI双染法测定细胞凋亡率,MTT法测定细胞活力,RT-PCR法检测FKN mRNA水平。结果与C组比较,H-R组细胞凋亡率升高,增殖率降低,FKN mRNA表达增强(P<0.01);与H-R组比较,DZ组细胞凋亡率降低,增殖率升高,FKN mRNA表达降低(P<0.01);与DZ组比较,PDTC组细胞凋亡率升高,增殖率降低,FKN mRNA表达增强(P<0.01)。结论线粒体ATP敏感性钾通道开放通过NF-κB信号抑制MMECs的H-R损伤和FKN表达。
Objective To observe the effect of diazoxide on the expression of fractalkine (FKN) in NF-κB signaling pathway in hypoxia-reoxygenation (H-R) rat cardiac microvascular endothelial cells (MMECs) Methods The cultured rat MMECs were randomly divided into normal control group (C group), hypoxia-reoxygenation group (HR group, hypoxia 2h + reoxygenation 2h), diazoxide + hypoxia-reoxygenation group Diazoxide 100μmol / L preconditioning 2h + hypoxia 2h + reoxygenation 2h), PDTC group (100μmol / L pretreatment with pyrrolidine dithiocarbamate + diazoxide + hypoxia-reoxygenation group / L pretreatment 2h + diazoxide 100μmol / L pretreatment 2h + hypoxia 2h + reoxygenation 2h). Cell apoptosis rate was determined by Annexin-V-FITC / PI double staining. Cell viability was measured by MTT assay. FKN mRNA level was detected by RT-PCR. Results Compared with group C, the apoptosis rate of HR group increased, the proliferation rate decreased and the expression of FKN mRNA increased (P <0.01). Compared with HR group, the apoptosis rate of DZ group decreased, the proliferation rate increased, FKN mRNA expression (P <0.01). Compared with DZ group, the apoptosis rate of PDTC group increased, the proliferation rate decreased and the expression of FKN mRNA increased (P <0.01). Conclusion Mitochondrial ATP-sensitive potassium channel is open to inhibit H-R injury and FKN expression in MMECs through NF-κB signaling.