[Effect of dexmedetomidine pretreatment on hypoxia/reoxygenation-induced injury in human umbilical vein endothelial cells and the possible mechanism].
摘要
OBJECTIVE: To investigate the effect of dexmedetomidine pretreatment on hypoxia/reoxygenation-induced injury in human umbilical vein endothelial cells and the possible mechanism. METHODS: Cultured human umbilical vein endothelial cell-12 (HUVEC-12) were randomly divided into four groups(n = 24): group control (C), group dexmedetomidine (D), group hypoxia/reoxygenation (H/R), group hypoxia/reoxygenation plus dexmedetomidine (H/R+D). In groups D and H/R+D, Dexmedetomidine 50 µmol/L was added to the culture medium and the cells were incubated for 2 h. Then groups C and D were exposed to regular incubator and incubated for 12 h, groups H/R and H/R+D were incubated in an anaerobic chamber for 6 h and then returned to a regular incubator and incubated for 6 h. Cell growth conditions were observed under inverted microscope, the cell viability and apoptosis were measured by methyl thiazolyl tetrazolium (MTT) assay and flow cytometry respectively. Reverse transcriptase polymerase chain reaction (RT-PCR) was used to detect the expression of CHOP mRNA. Western blotting was used to detect the expression of CHOP and cleaved caspase-3 protein. RESULTS: Compared with group C, the cell survival rate was significantly decreased, the expression of CHOP mRNA and CHOP protein, cleaved caspase-3 protein were up-regulated, the apoptotic rate was significantly increased in group H/R and group H/R+D (P < 0.05),No significant difference was found in group D (P > 0.05);compared with group H/R, the cell survival rate was significantly increased, the expression of CHOP mRNA and CHOP protein, cleaved caspase-3 protein were down-regulated, the apoptotic rate was decreased significantly in the group H/R+D (P < 0.05). CONCLUSIONS: Dexmedetomidine pretreatment can effectively attenuate hypoxia/reoxygenation-induced apoptosis to human umbilical vein endothelial cell-12. The mechanism maybe related with down-regulating the expression of CHOP.