Function of CoQ10 in Regulation of e NOS in High ox-LDL Induced HUVECs

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[Objectives] To study the function of coenzyme Q10( Co Q 10) in regulation of endothelial nitric oxide synthase( e NOS) in high oxidized low-density lipoprotein( ox-LDL) induced human umbilical vein endothelial cells( HUVECs). [Methods] HUVECs in exponential growth phase were inoculated to 96 orifice plate at the cell density of 1 × 10~4 cells / 100 μL. When cells were fused to 80%,Tween-80 group and Co Q 10 group were randomly divided. After acting 24 hours,cell survival rate was tested by CCK-8 method,to screen cytotoxicity of Tween-80 and Co Q 10. HUVECs were cultured and divided into the control group,model group,Co Q10 low concentration group,Co Q medium concentration group,and Co Q high concentration group. After drug action for 24 hours,except the control group,a1 l groups were given culture solution containing 35 μg / ml ox-LDL to reproduce proliferation model of HUVECs. Changes in expression of e NOS mRNA level were detected by RT-PCR( reverse transcription polymerase chain reaction),and changes in expression of e NOS protein were detected by Western blot.[Results]Tween-80 dilution 10000 times had no cytotoxicity,and the difference was not statistically significant( P > 0. 05); when Co Q 10 concentration was 60 μM,it had cytotoxicity,and the difference was statistically significant( P < 0. 05). Compared with the control group,the e NOS in model group declined in expression of both the mRNA and protein,and the difference was significantly significant( P < 0. 05); compared with the model group,the e NOS mRNA and protein rose in Co Q 10 low concentration,medium concentration and high concentration groups,and the difference was statistically significant( P < 0. 05). [Conclusions]Co Q 10 can mitigate oxidative injury through improving the expression of e NOS in HUVECs. [Objectives] To study the function of coenzyme Q10 (Co Q 10) in regulation of endothelial nitric oxide synthase (e NOS) in high oxidized low-density lipoprotein (ox-LDL) induced human umbilical vein endothelial cells (HUVECs). [Methods ] HUVECs in exponential growth phase were inoculated to 96 orifice plate at the cell density of 1 × 10 4 cells / 100 μL. When acting as 80% Tween-80 group and Co Q 10 group were randomly divided. 24 hours, cell survival rate was tested by CCK-8 method, to screen cytotoxicity of Tween-80 and Co Q 10. HUVECs were cultured and divided into the control group, model group, Co Q10 low concentration group, Co Q medium concentration group , and Co Q high concentration group. After drug action for 24 hours, except the control group, a 11 groups were given culture solution containing 35 μg / ml ox-LDL to reproduce proliferation model of HUVECs. Changes in expression of e NOS mRNA level were detected by RT-PCR (reverse transcription polymerase chain reaction), and changes in expression of eNOS protein were detected by Western blot. [Results] Tween-80 dilution 10000 times had no cytotoxicity, and the difference was not statistically significant (P> 0.05); when Co Q 10 concentration was 60 μM, it had cytotoxicity, and the difference was statistically significant (P <0.05). Compared with the control group, the e NOS in model group declined in expression of both the mRNA and protein, and the difference was significantly significant (P <0.05); compared with the model group, the eNOS mRNA and protein rose in Co Q 10 low concentration, medium concentration and high concentration groups, and the difference was statistically significant (P <0.05). [ Conclusions] Co Q 10 can mitigate oxidative injury through improving the expression of e NOS in HUVECs.
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