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首页|期刊导航|解剖学杂志|沉默AK035396表达对脂多糖诱导的人脐静脉血管内皮细胞损伤的作用机制

沉默AK035396表达对脂多糖诱导的人脐静脉血管内皮细胞损伤的作用机制

李红晓 杨阳 刘维 王强

解剖学杂志2025,Vol.48Issue(4):314-318,5.
解剖学杂志2025,Vol.48Issue(4):314-318,5.DOI:10.3969/j.issn.1001-1633.2025.04.008

沉默AK035396表达对脂多糖诱导的人脐静脉血管内皮细胞损伤的作用机制

Effect and mechanism of silencing lncRNAAK035396 on lipopolysaccharide-induced damage to human umbilical vein endothelial cells

李红晓 1杨阳 1刘维 2王强2

作者信息

  • 1. 南阳市中心医院血管外科,南阳 473000
  • 2. 广西中医药大学附属瑞康医院心血管内科,南宁 530011
  • 折叠

摘要

Abstract

Objective:To investigate the effects of long non-coding RNA(lncRNA)AK035396 on lipopolysaccharide-induced vascular endothelial cell injury by regulating the miR-217-5p/chloride intracellular channel protein 4(CLIC4)signaling pathway.Methods:Human umbilical vein endothelial cells(HUVECs)were cultured in vitro.An injury model was established through induction of 1 μg/mL lipopolysaccharide.The HUVECs were divided into the control group(infected with lentivirus lenti-si-NC)and the si-AK035396 group(infected with lentivirus lenti-si-AK035396).Quantitative real-time PCR was used to analyze the expression levels of AK035396,miR-217-5p and CLIC4 mRNA.MTT method and flow cytometry were adopted to detect the viability and apoptosis of HUVECs cells respectively.Dual luciferase assay was utilized to verify the targeting relationship between AK035396 and miR-217-5p.Western blotting was applied to detect the expression levels of CLIC4,Caspase-3,Caspase-9,and Bax proteins.Results:Compared with the control group,the expression of AK035396 in HUVECs cells in the si-AK035396 group was reduced.The viability of HUVECs cells in the si-AK035396 group was significantly higher than that in the control group.The apoptosis rate of cells in the si-AK035396 group was significantly lower than that in the control group.AK035396 can directly target and bind to miR-217-5p.Compared with the control group,the expression of miR-217-5p in HUVECs in the si-AK035396 group was significantly increased,with the expression of CLIC4 mRNA significantly decreased,and the proteins of CLIC4,Caspase-3,Caspase-9,and Bax significantly decreased.Conclusion:AK035396 silencing alleviates lipopolysaccharide-induced vascular endothelial cell injury by regulating the miR-217-5p/CLIC4 signaling pathway.

关键词

人脐静脉血管内皮细胞/脂多糖/长链非编码RNA/miR-217-5p/细胞内氯离子通道蛋白4/凋亡

Key words

human umbilical vein endothelial cells/lipopolysaccharide/long non-coding RNA/miR-217-5p/chloride intracellular channel protein 4/apoptosis

分类

医药卫生

引用本文复制引用

李红晓,杨阳,刘维,王强..沉默AK035396表达对脂多糖诱导的人脐静脉血管内皮细胞损伤的作用机制[J].解剖学杂志,2025,48(4):314-318,5.

基金项目

国家自然科学基金(81960867) (81960867)

解剖学杂志

1001-1633

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