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

Area of Science:

• Neuroscience
• Molecular Biology
• Genetics

Background:

• Alzheimer's disease (AD) is a neurodegenerative disorder characterized by cognitive decline.
• Amyloid beta (Aβ) peptides are implicated in AD pathogenesis.
• SH-SY5Y cells are a common model for studying neuronal toxicity.

Purpose of the Study:

• To investigate the role of long non-coding RNA linc00968 in Aβ25-35-induced neurotoxicity.
• To examine the effect of linc00968 on apoptosis in neuronal cells.

Main Methods:

• SH-SY5Y cells were treated with Aβ25-35 to induce neurotoxicity.
• Cell viability was assessed using MTT assay.
• Linc00968 expression was measured by qRT-PCR.
• Linc00968 was silenced using siRNA.
• Apoptosis-related genes (BCL-2, BAX, CYT-C) and proteins were analyzed by qRT-PCR and Western blotting.

Main Results:

• Aβ25-35 treatment increased linc00968 expression in SH-SY5Y cells.
• Neurotoxicity reduced anti-apoptotic BCL-2 and increased pro-apoptotic BAX and CYT-C.
• Silencing linc00968 reversed Aβ25-35-induced apoptosis.
• Linc00968 inhibition upregulated Bcl-2 and downregulated Bax and Cyt-c protein levels.

Conclusions:

• Linc00968 expression is upregulated in response to Aβ25-35 neurotoxicity.
• Inhibition of linc00968 protects against Aβ25-35-induced neurotoxicity in SH-SY5Y cells.
• Linc00968 plays a role in regulating apoptosis in Alzheimer's disease models.