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可以linc00968调节SH-SY5Y细胞亡诱导的甲基胺β神经毒性?

Serap Kurt^1,2, Ege Riza Karagur³, Deniz Evrim Kavak⁴

¹Department of Medical Biology and Genetics, Institute of Health Sciences, Dokuz Eylul University, İzmir, Turkey. serapkurt15@gmail.com.

Molecular biology reports

|June 6, 2025

概括

阿尔茨海默病的模型显示增加了linc00968.8. 通过抑制这种长非编码RNA,通过调节亡,可以防止粉样β神经毒性.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
遗传学是一个遗传学.

背景情况:

阿尔茨海默病 (AD) 是一种神经退行性疾病,其特点是认知能力下降.
氨基酸β (Aβ) 都涉及到AD的病变发生.
SH-SY5Y细胞是研究神经元毒性的常见模型.

研究的目的:

调查长非编码RNA linc00968在Aβ25-35诱导的神经毒性的作用.
为了检查linc00968对神经元细胞的亡的影响.

主要方法:

用Aβ25-35治疗SH-SY5Y细胞以诱导神经毒性.
用MTT测定来评估细胞活力.
Linc00968表达是通过qRT-PCR测量的.
Linc00968使用siRNA被安静了.
与亡相关的基因 (BCL-2,BAX,CYT-C) 和蛋白质通过qRT-PCR和西式涂抹进行了分析.

主要成果:

Aβ25-35治疗增加了SH-SY5Y细胞中的linc00968表达.
神经毒性降低了抗亡的BCL-2和增加了亲亡的BAX和CYT-C.
沉默linc00968可以逆转Aβ25-35诱导的亡.
Linc00968抑制调高了Bcl-2和调低了Bax和Cyt-c蛋白水平.

结论:

在对Aβ25-35神经毒性的反应中,Linc00968的表达被上调.
抑制linc00968可以保护SH-SY5Y细胞免受Aβ25-35诱导的神经毒性.
Linc00968在阿尔茨海默氏病模型中调节亡起作用.

关键词:

阿尔茨海默氏症是阿尔茨海默氏症的一种疾病.粉样蛋白β是什么粉样蛋白β是什么细胞灭亡 (apoptosis) 是一种死亡的过程.这是一个LncRNARNA.

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