右江医学2026，Vol.54Issue(2)：122-130,9.DOI:10.3969/j.issn.1003-1383.2026.02.003
miR-23a-3p通过PTEN/PI3K/AKT通路参与ox-LDL诱导的人脐静脉内皮细胞自噬和凋亡的影响
Effects of miR-23a-3p on autophagy and apoptosis of human umbilical vein endothelial cells induced by ox-LDL via PTEN/PI3K/AKT Pathway
摘要
Abstract
Objective To investigate the effects of miR-23a-3p on autophagy and apoptosis in human umbilical vein en-dothelial cell(HUVEC)induced by oxidized low-density lipoprotein(ox-LDL)via phosphatase and tensin homolog(PTEN)/phosphatidylinositol-3-kinase(PI3K)/protein kinase B(AKT)pathway,and to explore its possible mechanisms,so as to provide theoretical support for the role of miR-23a-3p in atherosclerosis(AS).Methods An in vitro cell model of HUVEC was established by induction with 50 mg/L ox-LDL(ox-LDL HUVEC,abbreviated as ox-LDL).The expression lev-el of miR-23a-3p was detected by quantitative real-time PCR(qRT-PCR).Cell viability was assessed using the CCK8 as-say,and cell apoptosis was measured by flow cytometry.Bioinformatics and dual-luciferase reporter assays were used to veri-fy that miR-23a-3p targeting the gene PTEN.Western blot(WB)was employed to detect the expression levels of the target gene PTEN,autophagy-related proteins LC3Ⅱ/LC3Ⅰ,autophagy substrate protein P62,and proteins related to the PI3K/AKT pathway.Results The dual-luciferase reporter assay results showed that miR-23a-3p could target and regulate PTEN.In HUVEC induced by ox-LDL,the expression of miR-23a-3p decreased(P<0.05).The overexpression of miR-23a-3p in-hibited ox-LDL-induced autophagy in HUVEC,manifested as reduced expression of PTEN and LC3Ⅱ/LC3Ⅰproteins,and increased expression of P62 protein(P<0.05).Simultaneously,it enhanced cell viability and inhibited the apoptosis rate(P<0.05);in contrast,the results in the miR-23a-3p inhibitor group were opposite(P<0.05).The knockdown of PTEN promoted the increase in P-PI3K/PI3K and P-AKT/AKT protein expression in ox-LDL-induced HUVEC(P<0.05),inhibi-ted autophagy(P<0.05),while the overexpression of PTEN had the opposite effects(P<0.05).Conclusion miR-23a-3p inhibits autophagy in ox-LDL-induced HUVEC by targeting PTEN,enhances cell viability,and suppresses cell apoptosis.Its mechanism may be related to the activation of PI3K/AKT pathway protein expression,and miR-23a-3p may serve as a poten-tial therapeutic target for AS.关键词
miR-23a-3p/氧化型低密度脂蛋白/人脐静脉内皮细胞/磷酸酶-张力蛋白同源物/自噬/凋亡/磷脂酰肌醇-3-激酶/蛋白激酶B信号通路/动脉粥样硬化Key words
miR-23a-3p/oxidized low-density lipoprotein(ox-LDL)/human umbilical vein endothelial cell(HUVEC)/phosphatase and tensin homolog(PTEN)/autophagy/apoptosis/phosphatidylinositol-3-kinase(PI3K)/protein kinase B(AKT)signaling pathway/atherosclerosis(AS)分类
医药卫生引用本文复制引用
林金蕊,何则沂,丘金浪,陈娜君..miR-23a-3p通过PTEN/PI3K/AKT通路参与ox-LDL诱导的人脐静脉内皮细胞自噬和凋亡的影响[J].右江医学,2026,54(2):122-130,9.基金项目
福州市卫生健康系统科技计划项目(2022-S-wq19) （2022-S-wq19）
