刘丽丹,徐佳骏,刘文萍,李达丽,彭颜晖.LncRNA SNHG1通过miR-361-3p/Nfat5信号通路
对阿尔茨海默病细胞模型损伤的影响[J].,2024,(22):4221-4223 |
LncRNA SNHG1通过miR-361-3p/Nfat5信号通路
对阿尔茨海默病细胞模型损伤的影响 |
Effect of LncRNA SNHG1 on the Damage of Alzheimer's Disease Cell Models through the miR-361-3p/Nfat5 Signaling Pathway |
投稿时间:2024-05-18 修订日期:2024-06-12 |
DOI:10.13241/j.cnki.pmb.2024.22.004 |
中文关键词: LncRNA SNHG1 miR-361-3p 阿尔茨海默症 凋亡 |
英文关键词: LncRNA SNHG1 miR-361-3p Alzheimer's disease Apoptosis |
基金项目:新疆维吾尔自治区自然科学基金项目(2021D01C456) |
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中文摘要: |
摘要 目的:探讨LncRNA SNHG1表达对AD细胞损伤模型的影响,并研究其作用与miR-361-3p/Nfat5通路的关系。摘要:建立AD细胞模型。向SH-SY5Y细胞转入SNHG1-shRNA以减低SNHG1表达,转入miR-361-3p-mimic以过表达miR-361-3p。检测SNHG1和miR-361表达水平、细胞凋亡、蛋白表达水平,并验证miR-361-3p与SNHG1结合。结果:与空白对照组相比,AD模型组细胞miR-361-3p表达水平降低,而SNHG1表达水平升高,细胞凋亡率升高(P<0.05)。敲低SNHG1表达降低可降低细胞凋亡率(P<0.05)。过表达miR-361-3p降低SNHG1表达水平。AD模型组细胞Nfat5和p-Tau蛋白表达均升高,而Nestin蛋白表达降低(P<0.05);敲低SNHG1降降低AD细胞模型中Nfat5和p-Tau蛋白表达水平,提高Nestin蛋白表达水平。结论:敲低SNHG1可降低Aβ25-35蛋白诱导的AD细胞模型损伤,其机制与激活miR-361-3p/Nfat5通路有关。 |
英文摘要: |
ABSTRACT Objective: To investigate the effect of LncRNA SNHG1 expression on AD cell damage model, and to study its relationship with miR-361-3p/Nfat5 pathway. Methods:Establish an AD cell model. To SH-SY 5 Y cells to SNHG 1-shRNA to reduce SNHG 1 expression and to miR-361-3p-mimic to overexpress miR-361-3p. The expression levels of SNHG 1 and miR-361, apoptosis, and protein expression were examined, and miR-361-3p was bound to SNHG 1. Results: Compared with the blank control group, the AD model group showed decreased miR-361-3p expression, but increased SNHG 1 expression and increased apoptosis rate (P<0.05). Knockdown of reduced SNHG 1 expression decreased the apoptosis rate (P<0.05). Overexpression of miR-361-3p reduces the level of SNHG 1 expression. In the AD model group, Nfat 5 and p-Tau were increased, while Nestin protein decreased (P<0.05); knockdown of SNHG 1 decreased the expression of Nfat 5 and p-Tau and increased the Nestin protein expression. Conclusion: Knockdown of SNHG1 can reduce the damage induced by Aβ25-35 protein in AD cell models, and the mechanism is related to the activation of miR-361-3p/Nfat5 pathway. |
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