ArticleBMC anesthesiology2022
Dexmedetomidine pretreatment alleviates ropivacaine-induced neurotoxicity via the miR-10b-5p/BDNF axis.
Article in BMC anesthesiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 12 citations in OpenAlex.
- An evaluation of peripheral nerve damage that may develop following intraneural bupivacaine, dexmedetomidine, and lidocaine injections: multifaceted analysis in an experimental model.BMC anesthesiology · 2026Article
- MiR-134-5p/BDNF/TrkB/CREB signaling pathway involved in the depression-like behaviors in mice following exposure to benzo[a]pyrene.Metabolic brain disease · 2025Article
- Effect of dexmedetomidine on the median effective concentration of ropivacaine for postoperative analgesia in transversus abdominis plane block: an up-down sequential allocation study.Frontiers in medicine · 2025Article
- Inhibition of FOXO3 ameliorates ropivacaine-induced nerve cell damage through the miR-126-5p/TRAF6 axis.In vitro cellular & developmental biology. Animal · 2024Article
- BDNF Modulation by microRNAs: An Update on theCells · 2024Review
- Effects of dexmedetomidine-ropivacaine assisted combined spinal-epidural anesthesia on neutrophil-lymphocyte ratio and postoperative delirium in elderly patients with intertrochanteric femoral fracture.Frontiers in pharmacology · 2024Article
- Enriched Environment Induces Sex-Specific Changes in the Adult Neurogenesis, Cytokine and miRNA Expression in Rat Hippocampus.Biomedicines · 2023Article
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6 authors at 2 institutions in 1 country.
Funding
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Abstract
backgroundRopivacaine is commonly applied for local anesthesia and may cause neurotoxicity. Dexmedetomidine (DEX) exhibits neuroprotective effects on multiple neurological disorders. This study investigated the mechanism of DEX pretreatment in ropivacaine-induced neurotoxicity.
methodsMouse hippocampal neuronal cells (HT22) and human neuroblastoma cells (SH-SY5Y) were treated with 0.5 mM, 1 mM, 2.5 mM, and 5 mM ropivacaine. Then the cells were pretreated with different concentrations of DEX (0.01 μM, 0.1 μM, 1 μM, 10 μM, and 100 μM) before ropivacaine treatment. Proliferative activity of cells, lactate dehydrogenase (LDH) release, and apoptosis rate were measured using CCK-8 assay, LDH detection kit, and flow cytometry, respectively. miR-10b-5p and BDNF expressions were determined using RT-qPCR or Western blot. The binding of miR-10b-5p and BDNF was validated using dual-luciferase assay. Functional rescue experiments were conducted to verify the role of miR-10b-5p and BDNF in the protective mechanism of DEX on ropivacaine-induced neurotoxicity.
resultsTreatment of HT22 or SH-SY5Y cells with ropivacaine led to the increased miR-10b-5p expression (about 1.7 times), decreased BDNF expression (about 2.2 times), reduced cell viability (about 2.5 times), elevated intracellular LDH level (about 2.0-2.5 times), and enhanced apoptosis rate (about 3.0-4.0 times). DEX pretreatment relieved ropivacaine-induced neurotoxicity, as evidenced by enhanced cell viability (about 1.7-2.0 times), reduced LDH release (about 1.7-1.8 times), and suppressed apoptosis rate (about 1.8-1.9 times). DEX pretreatment repressed miR-10b-5p expression (about 2.5 times). miR-10b-5p targeted BDNF. miR-10b-5p overexpression or BDNF silencing reversed the protective effect of DEX pretreatment on ropivacaine-induced neurotoxicity, manifested as reduced cell viability (about 1.3-1.6 times), increased intracellular LDH level (about 1.4-1.7 times), and elevated apoptosis rate (about 1.4-1.6 times).
conclusionsDEX pretreatment elevated BDNF expression by reducing miR-10b-5p expression, thereby alleviating ropivacaine-induced neurotoxicity.
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