Effects of diazoxide pretreatment on the expression of NF-κB mRNA and fractalkine mRNA in rat myocardial microvascular endothelial cells exposed to hypoxia-reoxygenation
10.3760/cma.j.issn.0254-1416.2010.11.034
- VernacularTitle:二氮嗪预先给药对大鼠心肌微血管内皮细胞缺氧复氧时NF-κB mRNA和fractalkine mRNA表达的影响
- Author:
Su CAO
;
Huanju KANG
;
Qiuping CHEN
;
Shiren SHEN
- Publication Type:Journal Article
- Keywords:
Dazoxide;
Heart;
Endothelium,vascular;
Oxygen;
Cell hpoxia;
NF-kappa B;
Chemokine CX3CL1
- From:
Chinese Journal of Anesthesiology
2010;30(11):1394-1396
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of diazoxide pretreatment on the expression of NF-κB mRNA and fractalkine (FKN) mRNA in rat myocardial microvascular endothelial cells exposed to hypoxia-reoxygenation (H/R). Methods The SD rat myocardial microvascular endothelial cells were cultured. The cells were seeded in 96-well plates (100μl/hole) or in 6 cm diameter dishes (2 ml/dish) with the density of 1 × 106/ml and randomly divided into4 groups (n = 24 each): Ⅰ normal control group (group C), Ⅱ H/R group, Ⅲ diazoxide pretreatment group (group DZ), Ⅳ diazoxide pretreatment + mitochondrial ATP-sensitive potassium channel blocker 5-hydroxydecanoate (5-HD) group (group DZ + 5-HD). The cells were exposed to 2 h hypoxia followed by 2 h reoxygenation. Diazoxide 100 μmol/L and diazoxide 100 μmol/L + 5-HD 100μmol/L were added to the cultured medium 2 h before hypoxia in group DZ and DZ + 5-HD respectively. The cell vitality, apoptotic rate and expression of NF-κB mRNA and FKN mRNA were detected at end of reoxygenation. Results Compared with group C, the cell vitality was significantly decreased, apoptotic rate increased and the expression of NF-κB mRNA and FKN mRNA up-regulated in H/R group. Compared with group H/R, the cell vitality was significantly increased,apoptotic rate decreased and the expression of NF-κB mRNA and FKN mRNA down-regulated in group DZ. 5-HD could inhibit diazoxide pretreatment-induced changes mentioned above. Conclusion Diazoxide pretreatment can reduce H/R injury in rat myocardial microvascular endothelial cells through down-regulating the expression of NFκB and FKN, and the mechanism is related to activation of mitochondrial ATP-sensitive potassium channels.
