ArticleJournal of molecular neuroscience : MN2025
LncRNA MYL2 Acts as a Sponge for miR-661 to Regulate Postoperative Cognitive Dysfunction.
Article in Journal of molecular neuroscience : MN, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Postoperative cognitive dysfunction (POCD) has a significant impact on the postoperative life ability of the elderly, and nearly 50% of the elderly are at risk globally, but the molecular mechanism of its pathogenesis is still unclear. The aim of this study was to discuss the expression of lncRNA MYL2 in older rats and its effects to provide possible targets for future treatment. A POCD model of aged rats was established by osteotomy and sevoflurane, cognitive function was measured by the water maze (MWM), and the concentrations of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, and oxidative stress-related factors in the hippocampal tissue of rats were detected by enzyme-linked immunosorbent assay. Luciferase reporter gene analysis was used to detect the target gene of the targeting relationship between MYL2 and miR-661. Cell viability and apoptosis rate were assessed using CCK-8 and flow cytometry. MYL2 was up-regulated by Sev treatment in the rat hippocampus. Overexpression of MYL2 prolonged the escape latency of rats, shortened the time spent in the target quadrant of rats, and reduced the number of platform crossings. At the same time, the concentrations of pro-inflammatory factors and markers of oxidative stress were increased. miR-661 is a miRNA targeting MYL2. miR-661 could reverse the exacerbation effect of MYL2 on POCD. MYL2 serves as a potential sponge of miR-661, and its up-regulation is linked to exacerbated neuroinflammation, oxidative damage, and cellular dysfunction in POCD.
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