Practical Geriatrics ›› 2026, Vol. 40 ›› Issue (2): 126-131.doi: 10.3969/j.issn.1003-9198.2026.02.005

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Study on the mechanism of lncRNA AL133415.1 in regulating vimentin gene expression in SH-SY5Y cells

CHENG Yi, ZOU Ting, LI Lihua, ZHANG Lei, ZHOU Xiaohui   

  1. Drug Clinical Institutions (CHENG Yi); Department of Geriatrics (ZOU Ting, ZHANG Lei, ZHOU Xiaohui), the First Affiliated Hospital of Xinjiang Medical University, Urumqi 830013, China;
    Department of Pharmacy, Urumqi Maternal and Child Health Hospital, Urumqi 830011, China (LI Lihua)
  • Received:2025-07-21 Online:2026-02-20 Published:2026-02-27
  • Contact: ZHOU Xiaohui,Email:zhouxiaohui858@sina.com

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

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