lncRNA AL133415.1在SH-SY5Y细胞中对波形蛋白基因表达调控的机制研究

doi:10.3969/j.issn.1003-9198.2026.02.005

摘要/Abstract

摘要： 目的探究长链非编码RNA AL133415.1(lncRNA AL133415.1)对细胞活力、神经元凋亡和氧化应激的影响,并进一步探究其在AD分子机制中的作用。方法选择β-淀粉样蛋白(Aβ)_1-42诱导SH-SY5Y细胞来构建AD细胞模型,采用细胞转染质粒构建技术调控lncRNA AL133415.1基因,采用RT-PCR检测lncRNA AL133415.1、波形蛋白(VIM)基因在细胞中的表达;采用CCK-8方法检测细胞的繁殖速度;采用流式细胞仪检测细胞凋亡;采用DCFH-DA荧光测定法检测SH-SY5Y细胞内活性氧(ROS)、超氧化物歧化酶(SOD)、丙二醛(MDA)水平;采用Western Blot检测VIM在细胞中的表达;采用激光荧光共聚焦法(CLSM法)检测VIM的荧光强度。结果 lncRNA AL133415.1抑制组可以提高SH-SY5Y细胞活性并降低其凋亡率,而lncRNA AL133415.1过表达组显著降低了SH-SY5Y细胞的活性并增加其凋亡率(P均＜0.01)。lncRNA AL133415.1表达下调能够提高细胞内SOD活性,降低MDA、ROS活性,而表达上调则会导致细胞内SOD的活性降低,MDA、ROS的活性增加(P均＜0.05)。抑制lncRNA AL133415.1的表达可以促使VIM基因的表达,而过表达则会抑制VIM基因的表达(P＜0.001)。结论 lncRNA AL133415.1沉默可以促进VIM基因的表达,而过表达则会抑制VIM基因的表达,提示可以通过调控lncRNA AL133415.1间接调控VIM基因的表达,从而减少AD的发病。

关键词: 阿尔茨海默病, 长链非编码RNAAL133415.1, 波形蛋白, 神经炎症

Abstract: Objective To investigate the effects of long non-coding RNA AL133415.1 (lncRNA AL133415.1) on cell viability, neuronal apoptosis and oxidative stress, and further explore its role in the molecular mechanism of Alzheimer’s disease (AD). Methods Amyloid β-protein (Aβ)_1-42-induced SH-SY5Y cells were selected to establish an AD cell model. The lncRNA AL133415.1 gene was regulated by plasmid transfection technology. Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the expression of lncRNA AL133415.1 and vimentin (VIM) gene in cells. Cell Counting Kit-8 (CCK-8) method was used to detect the proliferation rate of cells. Flow cytometry was used to detect cell apoptosis. DCFH-DA fluorescence assay was used to detect the levels of reactive oxygen species (ROS), superoxide dismutase (SOD), and malondialdehyde (MDA) in SH-SY5Y cells. Western Blot was used to detect the expression of VIM protein in the cells. Confocal laser scanning microscopy (CLSM) was used to detect the fluorescence intensity of VIM protein. Results The viability of SH-SY5Y cells was increased and their apoptosis rate was reduced in the lncRNA AL133415.1 inhibition group, while the viability of SH-SY5Y cells was significantly decreased and their apoptosis rate was increased in the lncRNA AL133415.1 overexpression group (all P<0.01). Down-regulation of lncRNA AL133415.1 expression could increase the intracellular SOD activity, while up-regulation would lead to a decrease in intracellular SOD activity; Down-regulation of lncRNA AL133415.1 expression could reduce the intracellular MDA and ROS activities, while up-regulation could increase the intracellular MDA and ROS activities (all P<0.05). Inhibition of lncRNA AL133415.1 expression could promote the expression of VIM gene, while overexpression would inhibit the expression of VIM gene (P<0.001). Conclusions Silencing of lncRNA AL133415.1 can promote the expression of VIM gene, while overexpression can inhibit the expression of VIM gene, which suggests that the expression of VIM gene can be indirectly regulated by regulating lncRNA AL133415.1, thereby reducing the incidence of AD.

Key words: Alzheimer’s disease, long non-coding RNA AL133415.1, vimentin, neuroinflammation

中图分类号:

R 749.16

程毅, 邹婷, 李丽华, 张雷, 周晓辉. lncRNA AL133415.1在SH-SY5Y细胞中对波形蛋白基因表达调控的机制研究[J]. 实用老年医学, 2026, 40(2): 126-131.

CHENG Yi, ZOU Ting, LI Lihua, ZHANG Lei, ZHOU Xiaohui. Study on the mechanism of lncRNA AL133415.1 in regulating vimentin gene expression in SH-SY5Y cells[J]. Practical Geriatrics, 2026, 40(2): 126-131.

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