Akademik Veri Yönetim Sistemi
Molecular Biology Reports, cilt.52, sa.1, 2025 (SCI-Expanded)
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.