ArticleBMC anesthesiology2019
MiR-34a affects dexmedetomidine-inhibited chronic inflammatory visceral pain by targeting to HDAC2.
Article in BMC anesthesiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- A Novel Opioid-Sparing Analgesia Following Thoracoscopic Surgery: A Non-Inferiority Trial.Drug design, development and therapy · 2023Trial
- Mechanism, Dose, and Administration of Dexmedetomidine in Managing Visceral Pain Associated With Surgery: A Narrative Review.Medical science monitor : international medical journal of experimental and clinical research · 2026Review
- Role of ncRNAs in the Development of Chronic Pain.Non-coding RNA · 2025Review
- Ginger Polyphenols Reverse Molecular Signature of Amygdala Neuroimmune Signaling and Modulate Microbiome in Male Rats with Neuropathic Pain: Evidence for Microbiota-Gut-Brain Axis.Antioxidants (Basel, Switzerland) · 2024Article
- Article
- Dexmedetomidine Co-Administered with Lidocaine Decreases Nociceptive Responses and Trigeminal Fos Expression without Motor Dysfunction and Hypotension in a Murine Orofacial Formalin Model.Life (Basel, Switzerland) · 2022Article
- The emerging power and promise of non-coding RNAs in chronic pain.Frontiers in molecular neuroscience · 2022Review
- Adult zymosan re-exposure exacerbates the molecular alterations in the brainstem rostral ventromedial medulla of rats with early life zymosan-induced cystitis.Neurobiology of pain (Cambridge, Mass.)Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDexmedetomidine (DEX) has been used as an anesthetic for decades. The present investigation aimed to elucidate the analgesic impact of DEX on 2,4,6-Trinitrobenzenesulfonic acid (TNBS)-induced chronic inflammatory visceral pain (CIVP) in rats.
methodsTNBS with or without DEX to Male Sprague-Dawley SD rats were randomly divided into four groups: normal, CIVP, DEX, and vehicle. Pain behaviors were assessed and the abdominal withdrawal reflex, mechanical withdrawal threshold, and thermal withdrawal latency were recorded. Quantitative polymerase chain reaction data showed increased expressions of pro-inflammatory cytokines (IL-6, IL-1β and TNF-α) in the spinal cord tissues of rats.
resultsRNA microarray and quantitative polymerase chain reaction results indicated that miR-34a was downregulated by TNBS induction, but it was upregulated by DEX administration. Further studies showed that transfection of adenovirus-miR-34a inhibitor reversed the effect of DEX on the pain behaviors and spinal-cord pro-inflammatory-cytokine generation in CIVP rats. Additionally, we found that miR-34a targeted the 3'-UTR of the HDAC2 gene, as evinced by the increased HDAC2 expression in the CIVP and DEX + miR-34a inhibitor groups, and decreased HDAC2 signaling in the DEX group. Moreover, knock-down of HDAC2 restored DEX-attenuated pain behaviors and reduced pro-inflammatory cytokine production.
conclusionsDEX thus exhibited an analgesic effect on CIVP rats through the miR-34a-mediated HDAC2 pathway and suppressed visceral hypersensitivity.
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