ArticleJournal of inflammation research2026
Obacunone Inhibits Microglia-Mediated Neuroinflammation and Ischemic Injury by Targeting Mitogen-Activated Protein Kinase 1.
Article in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Obacunone (OB) possesses anti-inflammatory, antioxidant, and anticancer properties. This study aimed to investigate the neuroprotective effects of OB in ischemic stroke, and to elucidate the underlying mechanisms. Methods: Primary microglia were preincubated with OB for 2 h, followed by lipopolysaccharide (LPS) stimulation for either 3 or 24 h. The levels of inflammatory cytokines in primary microglia were assessed via real-time PCR, enzyme-linked immunosorbent assay (ELISA), and Western blot. The activation of the mitogen-activated protein kinase/nuclear factor kappa B (MAPK/NF-κB) signaling pathway was evaluated via immunofluorescence staining and Western blot. For in vivo experiments, 8-week-old male C57BL/6J mice were randomly assigned to 4 groups: the sham-operated group, the middle cerebral artery occlusion (MCAO) model group and the MCAO group treated with OB (5 mg/kg/day and 10 mg/kg/day), and the sham-operated and MCAO model groups received an equivalent volume of vehicle. The neurological deficits and memory functions were evaluated by a cassette of behavior tests. 2,3,5-Triphenyl tetrazolium chloride (TTC) staining and Evans blue staining were performed to evaluate infarct size and blood-brain barrier permeability. Additionally, network pharmacology and molecular docking predicted mitogen-activated protein kinase 1 (MAPK1) as a potential target of OB, and this interaction was validated via surface plasmon resonance (SPR), cellulase thermal shift assay (CETSA), and drug affinity responsive target stability (DARTS) experiments. Results: OB effectively inhibited the activation of the MAPK/NF-κB pathway and reduced microglia-mediated inflammatory cytokine production both in vitro and in vivo. In addition, OB attenuated ischemic brain injury in MCAO mice and improved memory function 30 days after MCAO. Moreover, OB directly bound to MAPK1, with ARG-146 as the critical binding site. Conclusion: Our findings suggest that OB binds to MAPK1 and alleviates neuroinflammation and ischemic injury, making it a potential therapeutic agent for ischemic stroke.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.