ArticleAnnals of translational medicine2020
Dihydromyricetin attenuates neuropathic pain via enhancing the transition from M1 to M2 phenotype polarization by potentially elevating ALDH2 activity
Article in Annals of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 51 citations in OpenAlex.
- Continuous low-intensity ultrasound influences the transcriptomic profile in M1 macrophages by downregulating inflammation and promoting M2-like markers.Scientific reports · 2026Article
- Shared Mechanisms and Integrated Management of Post-Stroke Pain and Depression: A Comprehensive Review.Pain and therapy · 2026Review
- Dihydromyricetin Modulates Neuropathic Pain and Depression: A Correlation with Hippocampal Vascular Endothelial Growth Factor in Mice.Journal of inflammation research · 2026Article
- Microglia Polarization: A Key Regulatory Mechanism of Neuropathic Pain.Journal of pain research · 2026Review
- ALDH2 in autophagy and cell death: molecular mechanisms and implications for diseases.Military Medical Research · 2025Review
- ALDH2 Attenuates Blood-Brain Barrier Injury Induced by Cerebral Ischemia/Reperfusion via Alleviating ROS/NLRP3 Inflammasome Axis.Neurochemical research · 2025Article
- Dihydromyricetin restores lysosomal function in Schwann cells to alleviate bortezomib-induced peripheral neuropathy via ERK/TFEB signaling.Archives of toxicology · 2025Article
- Inhibition of SARM1 Reduces Neuropathic Pain in a Spared Nerve Injury Rodent Model.Muscle & nerve · 2025Article
- Pharmacological mechanisms and potential clinical applications of Dihydromyricetin in neurological disorders.Frontiers in pharmacology · 2025Review
- The role ofFrontiers in neuroscience · 2024Article
- The role of aldehyde dehydrogenase 2 in cardiovascular disease.Nature reviews. Cardiology · 2023Review
- Novel Approach to the Treatment of Neuropathic Pain Using a Combination with Palmitoylethanolamide andInternational journal of molecular sciences · 2023Article
- Spinal cannabinoid receptor 2 activation alleviates neuropathic pain by regulating microglia and suppressing P2X7 receptor.Frontiers in molecular neuroscience · 2023Article
- RNA interference-mediated silencing of DNA methyltransferase 1 attenuates neuropathic pain by accelerating microglia M2 polarization.BMC neurology · 2022Article
- Crotalphine Modulates Microglia M1/M2 Phenotypes and Induces Spinal Analgesia Mediated by Opioid-Cannabinoid Systems.International journal of molecular sciences · 2022Article
- Astrocyte-microglia interaction through C3/C3aR pathway modulates neuropathic pain in rats model of chronic constriction injury.Molecular pain · 2022Article
- Lidocaine ameliorates chronic constriction injury-induced neuropathic pain through regulating M1/M2 microglia polarization.Open medicine (Warsaw, Poland) · 2022Article
- Circular RNA SMEK1 promotes neuropathic pain in rats through targeting microRNA-216a-5p to mediate Thioredoxin Interacting Protein (TXNIP) expression.Bioengineered · 2021Article
Corrections and comments
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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
backgroundTreatment for neuropathic pain as a refractory disease remains unsatisfactory and represents a significant clinical challenge. A highly effective drug is thus urgently needed for neuropathic pain treatment. Dihydromyricetin (DMY) is a flavonoid with a wide range of biological activities. The purpose of this research is to explore the effects of DMY on neuropathic pain and the underlying mechanism of its effect.
methodsThe effect of DMY was investigated in BV-2 cells and lipopolysaccharide (LPS)-induced BV-2 cells. A neuropathic pain model was established via spared nerve injury (SNI) surgery in mice, and the protein expression level was detected via Western blot assay. The percent of M1 and M2 phenotype polarization cells were detected via flow cytometry assay. Immunochemical staining assay was also performed to measure the marker levels of the M1 and M2 phenotype polarization cells and aldehyde dehydrogenase 2 (ALDH2) level, and mechanical pain sensitivity was evaluated via measurement of the mechanical withdrawal threshold.
resultsWe found that DMY promoted the transition from M1 to M2 polarization and upregulated the ALDH2 level
conclusionsOur data demonstrated that DMY alleviated neuropathic pain via enhancing the polarization transition from the M1 to M2 phenotype by potentially elevating ALDH2 activity
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