ArticleMetabolic brain disease2025
β-Caryophyllene modulates the JAK2/STAT3 signaling pathway to downregulate neutrophil extracellular traps and alleviate cerebral ischemia-reperfusion injury.
Article in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Melissa officinalis extract selectively suppresses STAT1 signaling in oral epithelial cells.Frontiers in immunology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Cerebral ischemia reperfusion injury (CIRI) is a major contributor to mortality and disability in stroke patients. β-Caryophyllene (BCP) had been identified as a promising candidate for the treatment of CIRI. This study aimed to elucidate the mechanisms through which BCP exerts its therapeutic effects in CIRI. A rat model of cerebral ischemia was established by middle cerebral artery occlusion (MCAO) for 2 h followed by reperfusion. Neurological function and cognitive outcome were evaluated using the water maze test and neurobehavioral test. Citrullinated histone H3 (cit-H3) and peptidyl arginine deiminase 4 (PAD4) in brain tissues were detected via Western blot and immunohistochemistry (IHC). The levels of inflammation and oxidative stress factors were evaluated using assay kits. Western blot was applied to examine the expression and activation of JAK2/STAT3 pathway. The results determined that BCP significantly improved neurological functions and promoted cognitive function recovery in CIRI rats. A significant increase of neutrophil extracellular traps (NETs) formation markers of cit-H3, PAD4, cf-DNA and MPO were found in brain tissues of CIRI rats, which were effectively reversed by the treatment of BCP. Moreover, the levels of phosphorylation of JAK2 and STAT3 in the brain tissue of CIRI rats were significantly elevated. In contrast, treatment with BCP significantly reduced the phosphorylation levels of JAK2 and STAT3. Moreover, coumermycin A1(CA1, JAK2 agonist) partially reversed the inhibitory effects of BCP on inflammation, oxidative stress levels, and NETs formation in CIRI rats. The levels of NETs formation in the brain tissues of CIRI rats were significantly elevated. BCP markedly inhibited the formation of NETs, reduced inflammation and oxidative stress levels. BCP facilitated the recovery of cognitive function and neurological functions by modulating the JAK2/STAT3 signaling pathway.
Indexed as
Identifiers
41165931What Socratic 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 Socratic graph.