Functional role of lncRNA MEG3 on pyroptosis through interacting with EZH2 and YTHDC1 in postoperative cognitive dysfunction
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View abstract on PubMed
Summary
This summary is machine-generated.Long non-coding RNA MEG3 inhibits neuroinflammation and protects against postoperative cognitive dysfunction (POCD) by suppressing the NLRP3 inflammasome pathway. This discovery offers a potential therapeutic target for POCD treatment.
Area Of Science
- Neuroscience
- Molecular Biology
- Genetics
Background
- Postoperative cognitive dysfunction (POCD) mechanisms are unclear, limiting effective treatments.
- Neuroinflammation-induced NLRP3 pyroptosis pathway contributes to POCD development.
- Long non-coding RNA MEG3's role in neurological injury and pyroptosis requires further investigation.
Purpose Of The Study
- To investigate the molecular mechanisms of lncRNA MEG3 in sevoflurane-induced POCD.
- To elucidate the role of MEG3 in regulating NLRP3 inflammasome and pyroptosis in hippocampal neurons.
- To explore MEG3 as a potential therapeutic target for POCD.
Main Methods
- Sevoflurane-induced in vitro and in vivo POCD models.
- Quantitative real-time PCR (qRT-PCR), Western blot, ELISA, and histological staining for gene and protein expression.
- Cell viability (CCK-8) and injury (LDH) assays, Morris Water Maze (MWM) test for cognitive function.
- RNA immunoprecipitation (RIP) and chromatin immunoprecipitation (ChIP) to validate molecular interactions.
Main Results
- Sevoflurane reduced MEG3 and pyroptosis markers in mice.
- MEG3 overexpression ameliorated sevoflurane-induced cognitive deficits and pyroptosis.
- MEG3 downregulated NLRP3 expression by reducing mRNA stability via EZH2/YTHDC1 interaction.
Conclusions
- MEG3 inhibits NLRP3 inflammasome and hippocampal neuron pyroptosis by recruiting EZH2/YTHDC1.
- MEG3 plays a crucial role in regulating POCD.
- MEG3 presents a promising therapeutic target for treating POCD.
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