右美托咪定通过抑制lncRNA SNHG14/UPF1轴促进HSPB8表达以抑制AD中神经细胞的凋亡：右美托咪定在AD中的作用。

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neurotoxicity Research Pub Date : 2023-10-01 Epub Date: 2023-09-01 DOI:10.1007/s12640-023-00653-4

QingYun Tan, LiLi Liu, Shuo Wang, QingDong Wang, Yu Sun

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引用次数: 0

摘要

据报道，右美托咪定（Dex）在阿尔茨海默病（AD）中具有神经保护作用。然而，具体机制尚不清楚。找出Dex在AD模型中调节神经细胞凋亡的潜在分子机制。用Aβ1处理SH-SY5Y细胞，建立AD模型 - 42在（10μM）下培养24小时。通过RIP分析验证了UPF1、lncRNA SNHG14和HSPB8之间的相互作用。分别用CCK-8法、流式细胞仪、Western blot和qRT-PCR检测细胞活力、细胞凋亡、基因和蛋白质水平。Dex下调lncRNA SNHG14水平并抑制神经细胞凋亡。LncRNA SNHG14过表达逆转了Dex对AD模型中神经细胞凋亡的抑制作用。LncRNA SNHG14通过募集UPF1来减弱HSPB8 mRNA的稳定性。HSPB8过表达抑制AD模型中神经细胞的凋亡。此外，HSPB8敲除逆转了Dex对AD模型中神经细胞凋亡的抑制作用。我们的研究表明，Dex通过抑制lncRNA SNHG14/UPF1轴来抑制AD中的神经细胞凋亡，从而促进HSPB8的表达。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Dexmedetomidine Promoted HSPB8 Expression via Inhibiting the lncRNA SNHG14/UPF1 Axis to Inhibit Apoptosis of Nerve Cells in AD : The Role of Dexmedetomidine in AD.

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Dexmedetomidine Promoted HSPB8 Expression via Inhibiting the lncRNA SNHG14/UPF1 Axis to Inhibit Apoptosis of Nerve Cells in AD : The Role of Dexmedetomidine in AD.

Dexmedetomidine (Dex) is reported to play a neuroprotective role in Alzheimer's disease (AD). However, the specific mechanism remains unclear. Figure out the underlying molecular mechanism of Dex regulating nerve cell apoptosis in the AD model. The AD model in vitro was established after SH-SY5Y cells were treated with Aβ1 - 42 at (10 μM) for 24 h. The interaction among UPF1, lncRNA SNHG14, and HSPB8 was verified by RIP assay. Cell viability, apoptosis, the level of genes, and proteins were detected by CCK-8 assay, flow cytometry, Western blot, and qRT-PCR, respectively. Dex downregulated lncRNA SNHG14 level and inhibited apoptosis of nerve cells. LncRNA SNHG14 overexpression reversed the inhibitory effect of Dex on nerve cell apoptosis in the AD model. LncRNA SNHG14 attenuated HSPB8 mRNA stability by recruiting UPF1. HSPB8 overexpression inhibited apoptosis of nerve cells in the AD model. Moreover, HSPB8 knockdown reversed the inhibitory effect of Dex on nerve cell apoptosis in the AD model. Our study demonstrated that Dex promoted HSPB8 expression via inhibiting the lncRNA SNHG14/UPF1 axis to inhibit nerve cell apoptosis in AD.

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来源期刊

Neurotoxicity Research 医学-神经科学

CiteScore

7.70

自引率

5.40%

发文量

164

审稿时长

6-12 weeks

期刊介绍： Neurotoxicity Research is an international, interdisciplinary broad-based journal for reporting both basic and clinical research on classical neurotoxicity effects and mechanisms associated with neurodegeneration, necrosis, neuronal apoptosis, nerve regeneration, neurotrophin mechanisms, and topics related to these themes. Published papers have focused on: NEURODEGENERATION and INJURY Neuropathologies Neuronal apoptosis Neuronal necrosis Neural death processes (anatomical, histochemical, neurochemical) Neurodegenerative Disorders Neural Effects of Substances of Abuse NERVE REGENERATION and RESPONSES TO INJURY Neural Adaptations Neurotrophin mechanisms and actions NEURO(CYTO)TOXICITY PROCESSES and NEUROPROTECTION Excitatory amino acids Neurotoxins, endogenous and synthetic Reactive oxygen (nitrogen) species Neuroprotection by endogenous and exogenous agents Papers on related themes are welcome.