ArticleNeurochemical research2026
Beta-Caryophyllene Prevents Ouabain-Induced Neurodegeneration and Behavioral Alterations Through PKA/GSK-3β Pathway.
Article in Neurochemical 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
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bipolar disorder (BD) is a severe psychiatric condition characterized by recurrent mood episodes and progressive neurobiological alterations associated with oxidative stress, mitochondrial dysfunction, and neuronal damage. Current pharmacological treatments remain limited by incomplete efficacy and significant adverse effects, highlighting the need for novel therapeutic strategies. The present study investigated the neuroprotective effects of beta-caryophyllene (BCP), a natural sesquiterpene and selective cannabinoid receptor type 2 (CB2R) agonist, in a rat model of mania induced by intracerebroventricular ouabain (OUA) administration. Wistar rats received acute BCP treatment (three doses administered at 8-h intervals) starting one hour after OUA. Behavioral, biochemical, histological, and molecular analyses were performed seven days later. OUA induced manic-like behavioral alterations characterized by hyperactivity, increased risk-taking, and increased reactivity. These behavioral alterations were accompanied by increased lipid peroxidation, alterations in antioxidant enzyme activity, and enhanced neuronal degeneration in hippocampal regions, as indicated by Fluoro-Jade C staining. BCP treatment attenuated behavioral abnormalities, reduced oxidative damage, and prevented OUA-induced neuronal degeneration in the CA1, CA3, and dentate gyrus. Molecular analyses revealed that BCP restored phosphorylation of protein kinase A (PKA) and glycogen synthase kinase-3β (GSK-3β), while reversing the reduction of nuclear factor erythroid-2-related factor 2 (NRF2) expression induced by OUA. Together, these findings support the hypothesis that modulation of redox homeostasis and changes in PKA/GSK-3β/NRF2 signaling may contribute to the neuroprotective and behavioral effects of BCP. These findings provide preclinical evidence supporting further investigation of BCP and the molecular mechanisms that may underlie its effects in experimental models relevant to BD.
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.