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MicroRNA-669f-5p targeting deoxycytidinephosphate deaminase contributes to sevoflurane-induced cognitive impairments
Yuanping Zhong1, Chao Zhang1, Yuan Li2
1Department of Anesthesiology, Affiliated Hospital of Zunyi Medical University, 149 Dalian Road, Huichuan District, Zunyi, Guizhou 563003, PR China.
Background:
Postoperative cognitive dysfunction (POCD) is a common complication associated with sevoflurane anaesthesia in the aged population. MicroRNAs have been implicated in sevoflurane-induced cognitive deficits; however, the role and underlying mechanism of microRNA (miR)-669f-5p remain unclear.
Methods:
Eighteen-month-old mice and mouse hippocampal neurons (HT22) were exposed to sevoflurane. Cognitive function was assessed using the Morris water maze test. Neuroapoptosis and cellular proliferation were evaluated by terminal-deoxynucleotidyl transferase-mediated nick end-labelling staining and Cell Counting Kit-8 assays, respectively. The downstream molecular mechanisms of miR-669f-5p were investigated using bioinformatics analysis, western blotting, quantitative real-time polymerase chain reaction, immunofluorescence and dual-luciferase reporter assays.
Results:
Bioinformatics analysis of the Gene Expression Omnibus database revealed upregulation of miR-669f-5p in hippocampal tissue from mice with POCD. Inhibition of miR-669f-5p substantially improved sevoflurane-induced cognitive impairment in aged mice. Deoxycytidinephosphate deaminase (Dctd) was identified as a direct target of miR-669f-5p. Overexpression of Dctd reversed the effects of miR-669f-5p mimics on apoptosis and proliferation in HT22 cells and suppressed activation of the TLR2/4-MyD88-NF-κB signalling pathway. Moreover, Dctd overexpression ameliorated sevoflurane-induced cognitive impairment in aged mice.
Conclusion:
MicroRNA-669f-5p contributes to sevoflurane-induced cognitive impairment in aged mice by targeting Dctd and activating the TLR2/4-MyD88-NF-κB pathway. These findings provide new insights into potential therapeutic strategies for anaesthesia-related POCD.
Insights
MicroRNA-669f-5p exacerbates sevoflurane-induced cognitive impairment in aged mice by targeting Dctd. Inhibiting this microRNA and targeting the TLR2/4-MyD88-NF-κB pathway may offer therapeutic strategies for postoperative cognitive dysfunction.
Area of Science:
- Neuroscience
- Molecular Biology
- Anesthesiology
Background:
- Postoperative cognitive dysfunction (POCD) is a frequent complication in elderly patients after sevoflurane anesthesia.
- MicroRNAs are implicated in sevoflurane-induced cognitive deficits, but the specific role of microRNA (miR)-669f-5p is not well understood.
Purpose of the Study:
- To investigate the role and mechanism of miR-669f-5p in sevoflurane-induced cognitive impairment in aged mice.
- To identify potential therapeutic targets for preventing POCD.
Main Methods:
- Aged mice and hippocampal neurons were exposed to sevoflurane, with cognitive function assessed via the Morris water maze test.
- Neuroapoptosis, cellular proliferation, and molecular mechanisms involving miR-669f-5p, Dctd, and the TLR2/4-MyD88-NF-κB pathway were analyzed using various molecular and cellular assays.
Main Results:
- Upregulation of miR-669f-5p was observed in the hippocampus of mice with POCD.
- Inhibition of miR-669f-5p improved cognitive function and reduced apoptosis and proliferation.
- Deoxycytidinephosphate deaminase (Dctd) was identified as a direct target of miR-669f-5p; its overexpression reversed miR-669f-5p effects and ameliorated cognitive impairment.
Conclusions:
- miR-669f-5p contributes to sevoflurane-induced cognitive impairment by targeting Dctd and activating the TLR2/4-MyD88-NF-κB pathway.
- These findings highlight miR-669f-5p and the identified pathway as potential therapeutic targets for POCD.
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