ArticleScientific reports2017
Molecular signaling underlying bulleyaconitine A (BAA)-induced microglial expression of prodynorphin.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Comparison of the efficacy and safety between dezocine injection and morphine injection for persistence of pain in Chinese cancer patients: a meta-analysis.Bioscience reports · 2017Pooled it
- Stress-induced adaptations in nucleus accumbens dopamine D1 receptor-expressing cells correspond to social avoidance behavior in male mice.IBRO neuroscience reports · 2026Article
- Pharmacological, Toxicological, Phytochemical and Ethnobotanical Insights into North AmericanMolecules (Basel, Switzerland) · 2026Review
- Analgesic effects of bulleyaconitine A: new advances in research from ion channel targets to clinical translation.Frontiers in pharmacology · 2025Review
- Inhibition of ADORA3 promotes microglial phagocytosis and alleviates chronic ischemic white matter injury.CNS neuroscience & therapeutics · 2024Article
- Pain-resolving immune mechanisms in neuropathic pain.Nature reviews. Neurology · 2023Review
- CXCR1 participates in bone cancer pain induced by Walker 256 breast cancer cells in female rats.Molecular pain · 2022Article
- Dezocine inhibits cell proliferation, migration, and invasion by targeting CRABP2 in ovarian cancer.Open medicine (Warsaw, Poland) · 2022Article
- Spinal microglial β-endorphin signaling mediates IL-10 and exenatide-induced inhibition of synaptic plasticity in neuropathic pain.CNS neuroscience & therapeutics · 2021Article
- Bulleyaconitine A Inhibits Morphine-Induced Withdrawal Symptoms, Conditioned Place Preference, and Locomotor Sensitization Via Microglial Dynorphin A Expression.Frontiers in pharmacology · 2021Article
- Exercise Reduces Morphine-Induced Hyperalgesia and Antinociceptive Tolerance.BioMed research international · 2021Article
- Microglia mediated neuroinflammation - signaling regulation and therapeutic considerations with special reference to some natural compounds.Histology and histopathology · 2020Review
- Isotalatizidine, a CJournal of neuroinflammation · 2020Article
- Cynandione A Alleviates Neuropathic Pain Through α7-nAChR-Dependent IL-10/β-Endorphin Signaling Complexes.Frontiers in pharmacology · 2020Article
- Activation of GPR40 produces mechanical antiallodynia via the spinal glial interleukin-10/β-endorphin pathway.Journal of neuroinflammation · 2019Article
- Bulleyaconitine A prevents Ti particle-induced osteolysis via suppressing NF-κB signal pathway during osteoclastogenesis and osteoblastogenesis.Journal of cellular physiology · 2018Article
- Lappaconitine, a C18-diterpenoid alkaloid, exhibits antihypersensitivity in chronic pain through stimulation of spinal dynorphin A expression.Psychopharmacology · 2018Article
- Autocrine Interleukin-10 Mediates Glucagon-Like Peptide-1 Receptor-Induced Spinal Microglial β-Endorphin Expression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bulleyaconitine (BAA) has been shown to possess antinociceptive activities by stimulation of dynorphin A release from spinal microglia. This study investigated its underlying signal transduction mechanisms. The data showed that (1) BAA treatment induced phosphorylation of CREB (rather than NF-κB) and prodynorphin expression in cultured primary microglia, and antiallodynia in neuropathy, which were totally inhibited by the CREB inhibitor KG-501; (2) BAA upregulated phosphorylation of p38 (but not ERK or JNK), and the p38 inhibitor SB203580 (but not ERK or JNK inhibitor) and p38β gene silencer siRNA/p38β (but not siRNA/p38α) completely blocked BAA-induced p38 phosphorylation and/or prodynorphin expression, and antiallodynia; (3) BAA stimulated cAMP production and PKA phosphorylation, and the adenylate cyclase inhibitor DDA and PKA inhibitor H-89 entirely antagonized BAA-induced prodynorphin expression and antiallodynia; (4) The Gs-protein inhibitor NF449 completely inhibited BAA-increased cAMP level, prodynorphin expression and antiallodynia, whereas the antagonists of noradrenergic, corticotrophin-releasing factor, A1 adenosine, formyl peptide, D1/D2 dopamine, and glucagon like-peptide-1 receptors failed to block BAA-induced antiallodynia. The data indicate that BAA-induced microglial expression of prodynorphin is mediated by activation of the cAMP-PKA-p38β-CREB signaling pathway, suggesting that its possible target is a Gs-protein-coupled receptor - "aconitine receptor", although the chemical identity is not illustrated.
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