EZH2 Gene Regulates The Endothelial Inflammation And The Intervention Study Of Salidroside

BackgroundEnhancer Of Zeste 2 Polycomb Repressive Complex 2(EZH2)is the core component of comb inhibition complex 2(Polycomb-group Proteins2,PRC2),which can regulate cell differentiation,proliferation and promote tumor growth.EZH2 promotes the formation and development of atherosclerosis(AS)by regulating the level of lipid metabolism.Although endothelial inflammation plays a decisive role in the process of AS,it is not clear whether EZH2 promotes endothelial inflammation.A large number of studies have shown that salidroside(SAL)has a significant anti-AS effect,but there are few studies on whether EZH2 can inhibit endothelial cell inflammation.Therefore,the purpose of this study is to explore the role of EZH2 in endothelial cell inflammation and the anti-atherosclerotic mechanism of SAL.ObjectiveTo explore the role of EZH2 in promoting endothelial cell inflammation and to provide reference data for the study of whether salidroside interferes with AS through EZH2 anti-inflammation.Methods1.HUVEC inflammation model was successfully constructed: after adding different concentrations of OX-LDL,IL-6 in each group increased in varying degrees,and the secretion was the most significant when 100 μg OX-LDL was added to OX-LDL for 12 h.2.EZH2 has the effect of promoting endothelial cell inflammation: after adenovirus overexpression,the expression of EZH2 gene and EZH2 protein in HUVEC increased.After low expression of GSK126,the expression of EZH2 gene in HUVEC decreased and the expression of EZH2 protein in HUVEC decreased.In the overexpression experiment,the secretion of IL-6 in the experimental group was higher than that in the positive control group.At the same time,the levels of IL-6,TNF-α,e-murine and CRP genes in the experimental group were significantly higher than those in the positive control group.In the low expression experiment,the amount of IL-6 secretion in the experimental group was lower than that in the positive control group,and the levels of IL-6,TNF-α and e Mehry NOSmai 8 genes in the experimental group were lower than those in the positive control group,but the level of CRP gene was not significantly decreased.3.SAL could inhibit the inflammation of endothelial cells: the concentration increased,the expression of IL-6 gene decreased and the expression of IL-6 protein decreased.4.There was no correlation between EZH2 and SAL: there was no correlation between different SAL concentration and EZH2 gene level,suggesting that SAL could not directly regulate EZH2 gene.Results1.HUVEC inflammation model was successfully constructed: after adding different concentrations of OX-LDL,IL-6 in each group increased in varying degrees,and the secretion was the most significant when 100 ug OX-LDL was added to ox-LDL for 12 h.2.EZH2 has the effect of promoting endothelial cell inflammation: after adenovirus overexpression,the expression of EZH2 gene and EZH2 protein in HUVEC increased.After low expression of GSK126,the expression of EZH2 gene in HUVEC decreased and the expression of EZH2 protein in HUVEC decreased.In the overexpression experiment,the secretion of IL-6 in the experimental group was higher than that in the positive control group.At the same time,the levels of IL-6,TNF-α,e-murine and CRP genes in the experimental group were significantly higher than those in the positive control group.In the low expression experiment,the amount of IL-6 secretion in the experimental group was lower than that in the positive control group,and the levels of IL-6,TNF-α and e Mehry NOSmai 8 genes in the experimental group were lower than those in the positive control group,but the level of CRP gene was not significantly decreased.3.SAL inhibit the inflammation of endothelial cells: SAL increased,the expression of IL-6gene decreased and the expression of IL-6 protein decreased.There was no correlation between 4.EZH2 and SAL: there was no correlation between different SAL concentration and EZH2 gene level,suggesting that SAL could not directly regulate EZH2 gene.Conclusion1.EZH2 targets to regulate the levels of inflammatory cytokines IL-6,TNF-α and emurno IL-IL-8,which cause endothelial cell inflammation and promote the formation of AS.2.SAL target can regulate the level of inflammatory factor IL-6,but salidroside is not the upstream regulatory target of EZH2.