Scholarlink

Background <p>Alzheimer’s disease (AD) is a diverse neurodegenerative disorder that is defined by impairments in cognitive function.</p> Objective <p>This study seeks to examine the apoptotic function of long non-coding RNA linc00968 in amyloid beta 25–35 neurotoxic SH-SY5Y cells.</p> Methods and results <p>Fragments of Aβ25–35 were administered to SH-SY5Y cells in order to simulate the neurotoxicity associated with Alzheimer’s disease. Cell viability was assessed using the MTT test. Using quantitative real-time polymerase chain reaction, the expression levels of linc00968 were examined in treated and untreated (control) cells exposed to Aβ25–35. Subsequently, linc00968 was transfected with siRNA into Aβ25-35-treated SH-SY5Y cells to silence its expression and confirmed by qRT-PCR. The impact of <i>BCL-2</i>,<i> BAX</i>,<i> CYT-C</i>, and the internal control gene <i>GAPDH</i> on apoptotic pathways was examined using quantitative real-time polymerase chain reaction (qRT-PCR). To assess the post-transcriptional effects, the levels of Bcl-2, Bax, Cyt-c, and Beta-actin were analyzed using western blotting. The expression of Linc00968 was observed to be elevated in Aβ 25–35 stimulated SH-SY5Y cells. Aβ25-35-mediated toxicity in SH-SY5Y cells led to a reduction in the expression of the anti-apoptotic gene BCL-2, while the expressions of the pro-apoptotic genes BAX and CYT-C were found to be elevated. Suppression of linc00968 was observed to reverse apoptosis in Aβ25-35-induced SH-SY5Y cells. At the protein level, silencing linc00968 with siRNA resulted in elevated levels of the anti-apoptotic protein Bcl-2 and decreased levels of the pro-apoptotic proteins Bax and Cyt-c.</p> Conclusions <p>Our results show that Aβ25-35-induced SH-SY5Y cells exhibit elevated expression of linc00968. By controlling several apoptosis-related indicators, we proposed that inhibition of linc00968 can shield Aβ25–35 produced neurotoxicity in SH-SY5Y cells.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Can linc00968 Regulate SH-SY5Y Cell Apoptosis Induced by Amyloid beta Neurotoxicity?

  • 期刊论文

  • 发表日期：

    2025年6月6日

查看全文
  • Serap Kurt,
  • Ege Riza Karagur,
  • Deniz Evrim Kavak,
  • Sefa Kizildag

摘要

Background

Alzheimer’s disease (AD) is a diverse neurodegenerative disorder that is defined by impairments in cognitive function.

Objective

This study seeks to examine the apoptotic function of long non-coding RNA linc00968 in amyloid beta 25–35 neurotoxic SH-SY5Y cells.

Methods and results

Fragments of Aβ25–35 were administered to SH-SY5Y cells in order to simulate the neurotoxicity associated with Alzheimer’s disease. Cell viability was assessed using the MTT test. Using quantitative real-time polymerase chain reaction, the expression levels of linc00968 were examined in treated and untreated (control) cells exposed to Aβ25–35. Subsequently, linc00968 was transfected with siRNA into Aβ25-35-treated SH-SY5Y cells to silence its expression and confirmed by qRT-PCR. The impact of BCL-2, BAX, CYT-C, and the internal control gene GAPDH on apoptotic pathways was examined using quantitative real-time polymerase chain reaction (qRT-PCR). To assess the post-transcriptional effects, the levels of Bcl-2, Bax, Cyt-c, and Beta-actin were analyzed using western blotting. The expression of Linc00968 was observed to be elevated in Aβ 25–35 stimulated SH-SY5Y cells. Aβ25-35-mediated toxicity in SH-SY5Y cells led to a reduction in the expression of the anti-apoptotic gene BCL-2, while the expressions of the pro-apoptotic genes BAX and CYT-C were found to be elevated. Suppression of linc00968 was observed to reverse apoptosis in Aβ25-35-induced SH-SY5Y cells. At the protein level, silencing linc00968 with siRNA resulted in elevated levels of the anti-apoptotic protein Bcl-2 and decreased levels of the pro-apoptotic proteins Bax and Cyt-c.

Conclusions

Our results show that Aβ25-35-induced SH-SY5Y cells exhibit elevated expression of linc00968. By controlling several apoptosis-related indicators, we proposed that inhibition of linc00968 can shield Aβ25–35 produced neurotoxicity in SH-SY5Y cells.