ArticleNeurochemical research2025
ANA-12 Targets and Inhibits BDNF/TrkB Signaling to Alleviate Pain Behaviors in Rheumatoid Arthritis Mice.
Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Novel tetrazole annulation on benzopyridodiazepine derivatives as inhibitor of tropomyosin kinase B (TrkB): rational design, synthesis, biological evaluation, SAR, andRSC advances · 2026Article
- Targeted inhibition of the BDNF/AKT/mTOR pathway in the inferior colliculus ameliorates salicylate-induced tinnitus in rats.iScience · 2026Article
- Exerkine-Mediated Regulation of the NLRP3 Inflammasome in Neuroprotection: Mechanistic Insights and the Role of Exercise.Molecular neurobiology · 2026Review
- Article
- Electroacupuncture promotes BDNF-dependent neurogenesis via microglial reprogramming in a chronic stress model.Chinese medicine · 2026Article
- The PANoptotic mosaic of rheumatoid arthritis: epitranscriptomic regulation, systemic relays, and precision death-mode editing.Frontiers in immunology · 2026Review
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4 authors.
Funding
Abstract
Rheumatoid arthritis (RA) is a chronic, systemic, inflammatory disease. Sensitization of central pain pathways by pro-inflammatory mediators has been implicated in RA pain. Locus coeruleus (LC) functions in pain pathways. Brain-derived neurotrophic factor (BDNF) participates in the modulation of nociception and pain. A mouse model of RA immunized with collagen-induced arthritis (CIA) was used for investigating the mechanisms of pain relief by administration of the tropomyosin receptor kinase B (TrkB) receptor antagonist ANA-12. We measured the pain behaviors and locomotor activity and found increased pain sensitivity and locomotor deficit in RA mice; ANA-12 treatment reduced pain behaviors and promoted locomotor function recovery. The glial activation and increased activities of BDNF/TrkB and MAPK signal pathways were found in LC of RA mice. The components of NLRP3 inflammasome were all increased and consequently enhanced the production of pro-inflammatory cytokine interleukin (IL)-1β. Upon ANA-12 treatment, glial cell activation was reduced, BDNF/TrkB and MAPK pathways were suppressed, and the expression levels of the above-mentioned proteins were reduced. Finally, U251 cells were conducted to further confirm the regulatory mechanisms of ANA-12 on inflammation. The results showed the colocalization of BDNF/NLRP3/IL-1β and GFAP. ANA-12 treatment decreased the protein levels of BDNF, TrkB, MAPK, NLRP3, and caspase-1 in IL-1β-induced cells. Besides, ANA-12 treatment decreased NLRC4 and AIM2 inflammasomes both in RA mice and IL-1β-induced cells. These results suggested that ANA-12 alleviates hyperalgesia in RA mice by inhibiting BDNF/TrkB signaling in LC, thereby reducing glial cell activation and inflammatory cytokine release.
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