Influence of early growth response factor 3 on high lipid induced inflammation and apoptosis of coronary endothelial cells
Objective To observe the changes of early growth response factor 3(Egr3)in coronary endothelial cells injured by high lipid and to investigate the influence of Egr3 on high lipid induced inflammation and apoptosis of coronary endothelial cells.Methods The human coronary artery endothelial cells in logarithmic growth phase were divided into control group(normal culture),high-lipid injury group(oxidized low-density lipoprotein),Egr3 no-load group(siRNA-NC lentivirus transfection+oxidized low-density lipoprotein treatment),and Egr3 knockdown group(siRNA-Egr3 lentivirus transfection+oxidized low-density lipoprotein treatment).After transfection,the relative expression of Egr3 mRNA was detected by real-time fluorescence quantitative PCR,and the relative expressions of Egr3 and caspase-3 proteins were detected by Western blot.The levels of tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6)in the supernatant were detected by ELISA,and the apoptosis rate was detected by CCK-8.Results The relative expressions of Egr3 mRNA,Egr3 protein and caspase-3 protein,the levels of TNF-α and IL-6,and the apoptosis rate were higher in high-lipid injury group[1.56±0.48,1.65±0.35,2.43±0.43,(55.33±4.76)ng/L,(36.34± 1.60)ng/L,(186.08±20.84)％]and Egr3 no-load group[1.53±0.56,1.55±0.45,2.36±0.29,(57.85±2.92)ng/L,(31.69±1.83)ng/L,(174.34±29.98)％]than those in control group[1.04±0.20,0.51± 0.26,1.60±0.22,(46.10±1.52)ng/L,(46.10±1.52)ng/L,(23.35±1.69)ng/L,(100.01±8.64)％]and Egr3 knockdown group[0.16±0.03,0.23±0.07,1.05±0.29,(33.67±3.26)ng/L,(19.75±1.54)ng/L,(12.24± 7.51)％](P＜0.05),were higher in control group than those in Egr3 knockdown group(P＜0.05),and showed no significant differences between high-lipid injury group and Egr3 no-load group(P＞0.05).Conclusion High lipid can induce inflammation and apoptosis of coronary endothelial cells,which may be correlated with the increased expression of Egr3,and to knock down the expression of Egr3 can inhibit the inflammation and apoptosis of coronary endothelial cells.
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