lncRNA BDNF-AS Attenuates Propofol-Induced Apoptosis in HT22 Cells by Modulating the BDNF/TrkB Pathway

Area of Science:

• Neuroscience
• Molecular Biology
• Pharmacology

Background:

• Propofol, a common anesthetic, can induce neuronal apoptosis.
• Brain-derived neurotrophic factor (BDNF) plays a role in neuronal apoptosis.
• BDNF-AS, a long non-coding RNA, regulates BDNF transcription.

Purpose of the Study:

• To investigate the role of BDNF-AS in propofol-induced apoptosis in HT22 cells.
• To explore the involvement of the BDNF/TrkB pathway in this process.

Main Methods:

• HT22 cells were treated with propofol, and BDNF-AS was silenced using siRNA.
• The TrkB receptor was inhibited using ANA-12.
• Apoptosis, gene, and protein expression were analyzed using flow cytometry, qRT-PCR, and Western blotting.

Main Results:

• Propofol upregulated BDNF-AS and downregulated BDNF in a time- and dose-dependent manner.
• BDNF-AS silencing reduced apoptosis and modulated apoptosis-related proteins (Bcl-2, Bax, caspases).
• TrkB inhibition increased apoptosis and altered apoptosis-related protein expression.

Conclusions:

• BDNF-AS inhibition mitigates propofol-induced apoptosis via the BDNF/TrkB pathway.
• The BDNF-AS-BDNF/TrkB signaling pathway is a potential therapeutic target for propofol neurotoxicity.