LncRNA MYL2 Acts as a Sponge for miR-661 to Regulate Postoperative Cognitive Dysfunction

Area of Science:

• Neuroscience
• Molecular Biology
• Gerontology

Background:

• Postoperative cognitive dysfunction (POCD) significantly impacts elderly patients' quality of life, with unclear molecular mechanisms.
• Nearly 50% of the global elderly population is at risk for POCD.

Purpose of the Study:

• To investigate the expression of long non-coding RNA (lncRNA) MYL2 in an aged rat model of POCD.
• To elucidate the effects of MYL2 on cognitive function, neuroinflammation, and oxidative stress in POCD.
• To explore the relationship between MYL2 and microRNA (miRNA) miR-661 as a potential therapeutic target.

Main Methods:

• Established a POCD model in aged rats using osteotomy and sevoflurane anesthesia.
• Assessed cognitive function using the Morris water maze (MWM).
• Measured inflammatory cytokines (TNF-α, IL-6, IL-1β) and oxidative stress markers via ELISA.
• Utilized luciferase reporter assays to confirm the interaction between MYL2 and miR-661.
• Evaluated cell viability and apoptosis using CCK-8 and flow cytometry.

Main Results:

• Sevoflurane treatment upregulated MYL2 expression in the rat hippocampus.
• Overexpression of MYL2 impaired cognitive function, evidenced by increased escape latency and reduced target quadrant entries.
• Elevated levels of pro-inflammatory cytokines and oxidative stress markers were observed with MYL2 overexpression.
• MYL2 acts as a sponge for miR-661, and miR-661 intervention reversed the detrimental effects of MYL2 on POCD.

Conclusions:

• Upregulated lncRNA MYL2 exacerbates neuroinflammation, oxidative damage, and cellular dysfunction in POCD.
• MYL2's interaction with miR-661 presents a novel therapeutic pathway for managing POCD.
• Targeting the MYL2/miR-661 axis may offer a promising strategy for treating POCD in the elderly.