ArticleNeural plasticity2022
Dexmedetomidine Mitigates Microglial Activation Associated with Postoperative Cognitive Dysfunction by Modulating the MicroRNA-103a-3p/VAMP1 Axis.
Article in Neural plasticity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Targeting VAMPs in Aging-Related Diseases: From Mechanisms to Pharmacotherapy.Pharmaceutical research · 2026Review
- Serum miR-199a-3p and miR-103a-3p are possible biomarkers for the onset of multiple sclerosis.Scientific reports · 2026Article
- Morin improves postoperative cognitive dysfunction by mediating the miR-138-5p/SIRT1 axis to regulate ferroptosis.Scientific reports · 2026Article
- Esketamine/dexmedetomidine-based opioid-free anesthesia and its association with postoperative bowel and cognitive dysfunction after total laparoscopic hysterectomy.BMC anesthesiology · 2025Observational
- Review
- Dexmedetomidine suppresses microglial activation in postoperative cognitive dysfunction via the mmu-miRNA-125/TRAF6 signaling axis.Open medicine (Warsaw, Poland) · 2025Article
- Bibliometric Analysis of Neuroinflammation and Postoperative Cognitive Dysfunction.Brain and behavior · 2025Article
- 17β-Estradiol Ameliorates Postoperative Cognitive Dysfunction in Aged Mice via miR-138-5p/SIRT1/HMGB1 Pathway.The international journal of neuropsychopharmacology · 2024Article
- Effects of dexmedetomidine on renal function, inflammatory markers, and cognitive functioning in elderly patients undergoing hip replacement surgery.American journal of translational research · 2024Article
- Amelioratory Effect of Melatonin on Cognition Dysfunction Induced by Sevoflurane Anesthesia in Aged Mice.Iranian journal of pharmaceutical research : IJPR · 2022Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Surgery-induced microglial activation is critical in mediating postoperative cognitive dysfunction (POCD) in elderly patients, where the important protective effect of dexmedetomidine has been indicated. However, the mechanisms of action of dexmedetomidine during the neuroinflammatory response that underlies POCD remain largely unknown. We found that lipopolysaccharide (LPS) induced substantial inflammatory responses in primary and BV2 microglial cells. The screening of differentially expressed miRNAs revealed that miR-103a-3p was downregulated in these cell culture models. Overexpression of miR-103a-3p mimics and inhibitors suppressed and enhanced the release of inflammatory factors, respectively. VAMP1 expression was upregulated in LPS-treated primary and BV-2 microglial cells, and it was validated as a downstream target of miR-103-3p. VAMP1-knockdown significantly inhibited the LPS-induced inflammatory response. Dexmedetomidine treatment markedly inhibited LPS-induced inflammation and the expression of VAMP1, and miR-103a-3p expression reversed this inhibition. Moreover, dexmedetomidine mitigated microglial activation and the associated inflammatory response in a rat model of surgical trauma that mimicked POCD. In this model, dexmedetomidine reversed miR-103a-3p and VAMP1 expression; this effect was abolished by miR-103a-3p overexpression. Taken together, the data show that miR-103a-3p/VAMP1 is critical for surgery-induced microglial activation of POCD.
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