The mechanism of Linc01230 antagonizing atherosclerosis through PI3K-AKT-eNOS signaling pathway
Objective To explore the mechanism of linc01230 antagonizing atherosclerosis through PI3K-AKT-eNOS signaling pathway.Methods Human umbilical vein endothelial cells(HUVEC)was induced by 50 μg/ml ox-LDL.Cell counting Kit-8(CCK-8)was used to detect cell viability.Quantitative real-time PCR(qPCR)was employed to measure the mRNA expression levels of PI3K,AKT,and eNOS.Western blot was conducted to assess the protein expression of PI3K,AKT,p-AKT,eNOS,and p-eNOS.Results After induced by ox-LDL,the viability of HUVEC decreased significantly.In Linc01230-311-transfected group,the cell viability was decreased compared to ox-LDL group,while there was increased of cell viability in Linc01230-311-overexpressed group.After induced by ox-LDL,the mRNA and protein expression levels of PI3K,AKT,and eNOS in HUVEC were reduced,in linc01230-311-transfected group,there was a significant decrease of mRNA and protein expression levels of PI3K,AKT,and eNOS compared with NC group,however,overexpression of Linc01230-311 led to an upregulation in the mRNA and protein expression levels of PI3K,AKT,and eNOS,at the same time,the protein expression levels of p-AKT and p-eNOS also had the same trend.Conclusion Linc01230 could improve endothelial cell damage induced by ox-LDL,and the mechanism may be related to the activation of PI3K-AKT-eNOS signaling pathway by Linc01230.
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