Inside the sources
Experiments, reviews and source-screening decisions within the recorded literature window. Each record identifies what was inspected and when. These appraisals do not add a receptor-interaction edge or establish a human benefit.
2020 · Terpenoids Commonly Found in Cannabis sativa Do Not Modulate the Actions of Phytocannabinoids or Endocannabinoids on TRPA1 and TRPV1 Channels.
What this source examined
Seven specified terpenoids were tested in human TRPV1-expressing HEK293 cells, alone and before capsaicin or anandamide challenge.
What this source supports
No significant terpenoid-evoked calcium response or shift of those agonist responses was detected under the tested conditions.
What remains uncertain
This is a bounded cellular negative finding. The named supplier forms were (+)-alpha-pinene,(+)-beta-pinene,(−)-beta-caryophyllene,(±)-linalool,(R)-(+)-limonene,beta-myrcene and alpha-humulene; unspecified or other stereochemical records cannot inherit enantiomer-specific conclusions. Purity and assay context limit interpretation; no consumer combination rule follows.
Study context and methods
HEK293 cells expressing human TRPV1
Seven individually named supplier materials; linalool racemate and R limonene explicitly distinguished
Calcium readout with vehicle, wild-type and agonist controls
- Concentration in the experiment
- 10 µM each terpenoid separately
- Preincubation
- 5 minutes
Results hTRPV1 and Figures 5–7
Reported research conditions, not directions for personal use or a consumer mixture.
Original publication ↗ · Full text ↗
2024 · Evaluation of Cannabimimetic Effects of Selected Minor Cannabinoids and Terpenoids in Mice
What this source examined
Beta-caryophyllene and its oxide were tested for displacement of [3H]CP55,940 in human CB1/CB2-expressing HEK293 cell membranes.
What this source supports
Both terpenes produced limited displacement in this assay, rather than a well-resolved high-affinity competition curve. This differs from reports using other assay systems and must remain attached to the preparation.
What remains uncertain
The table reports an affinity bound, not a measured zero activity or a fitted point estimate. A negative result at a tested concentration cannot establish inactivity at every target or settle findings from different preparations. No clinical or dietary conclusion follows.
Study context and methods
Human CB1 or CB2 in HEK293 membranes; assay BSA concentration for these two terpenes differs from that used for the cannabinoids.
(−)-trans-beta-caryophyllene from Sigma-Aldrich; beta-caryophyllene oxide synthesized at RTI. All compounds reported >95% purity.
Human CB1 or CB2 in HEK293 membranes; assay BSA concentration for these two terpenes differs from that used for the cannabinoids.
- Assay
- Competition radioligand binding
- Tracer
- Approximately 1 nM [3H]CP55,940
- Reported exposure
- 90 minutes
- Temperature
- 30 °C
- Membrane preparation
- 10 µg membrane protein per well; 0.5 mg/mL BSA for these terpenes.
- Replication and uncertainty
- At least three experiments performed in duplicate; footnote displacement estimates use SEM.
- Reported assay bound
- Table 1 lists Ki >10000 nM for both compounds at both receptors; this is retained as a bound, not a fitted affinity.
- Concentration in the experiment
- 31.6 µM highest tested terpene concentration
Table 1 terpene rows and footnotes a–d; Methods §2.4.
Reported research conditions, not directions for personal use or a consumer mixture.
Original publication ↗ · Full text ↗
2024 · β-Caryophyllene Inhibits Monoacylglycerol Lipase Activity and Increases 2-Arachidonoyl Glycerol Levels In Vivo: A New Mechanism of Endocannabinoid-Mediated Analgesia?
What this source examined
Purified MAGL assay and spinal-cord homogenates from rats; accompanying postoperative-pain model. HPLC-MS/MS measurement of arachidonic-acid formation after the original colorimetric assay showed compound interference.
What this source supports
BCP inhibited MAGL-mediated substrate turnover in the biochemical assay. Tissue from treated rats also showed reduced formation of labeled arachidonic acid under the reported conditions.
What remains uncertain
Enzyme inhibition is distinct from direct cannabinoid-receptor activation. The abstract misnames a product that Methods/Results identify as labeled arachidonic acid. Results prose and the figure caption differ on replicate counting; no potency or replicate-based numerical estimate is admitted. These findings do not establish an effect of hemp seed oil or flour.
Study context and methods
Purified MAGL assay and spinal-cord homogenates from rats; accompanying postoperative-pain model.
Beta-caryophyllene; natural 2-AG substrate in vitro and labeled 2-AG substrate in tissue homogenates.
HPLC-MS/MS measurement of arachidonic-acid formation after the original colorimetric assay showed compound interference.
- Research model
- Purified MAGL assay and spinal-cord homogenates from rats; accompanying postoperative-pain model.
- Tested material
- Beta-caryophyllene; natural 2-AG substrate in vitro and labeled 2-AG substrate in tissue homogenates.
- Assay
- HPLC-MS/MS measurement of arachidonic-acid formation after the original colorimetric assay showed compound interference.
- How to read this result
- Experimental evidence classification, not a consumer dose or recipe.
Reported research conditions, not directions for personal use or a consumer mixture.
Original publication ↗ · Full text ↗
2023 · Beta-Caryophyllene Modifies Intracellular Lipid Composition in a Cell Model of Hepatic Steatosis by Acting through CB2 and PPAR Receptors. · PPARα
What this source examined
Human HepG2 cells with experimentally induced steatosis. Lipid measurements, PPAR-alpha/PPAR-gamma and CB2 antagonist comparisons, gene expression and intracellular uptake.
What this source supports
Blocking PPAR-alpha reversed the lipid-reduction response; PPAR-gamma blockade partially reversed it. PPAR-alpha expression increased, while the reported PPAR-gamma mRNA change was not statistically significant.
What remains uncertain
Antagonist sensitivity and gene expression support pathway involvement, not a measured binding affinity or proof of direct receptor agonism. The findings concern cultured cells. These findings do not establish an effect of hemp seed oil or flour.
Study context and methods
Human HepG2 cells with experimentally induced steatosis.
Commercial (E)-beta-caryophyllene.
Lipid measurements, PPAR-alpha/PPAR-gamma and CB2 antagonist comparisons, gene expression and intracellular uptake.
- Research model
- Human HepG2 cells with experimentally induced steatosis.
- Tested material
- Commercial (E)-beta-caryophyllene.
- Assay
- Lipid measurements, PPAR-alpha/PPAR-gamma and CB2 antagonist comparisons, gene expression and intracellular uptake.
- How to read this result
- Experimental evidence classification, not a consumer dose or recipe.
Reported research conditions, not directions for personal use or a consumer mixture.
Original publication ↗ · Full text ↗
2023 · Beta-Caryophyllene Modifies Intracellular Lipid Composition in a Cell Model of Hepatic Steatosis by Acting through CB2 and PPAR Receptors. · PPARγ
What this source examined
Human HepG2 cells with experimentally induced steatosis. Lipid measurements, PPAR-alpha/PPAR-gamma and CB2 antagonist comparisons, gene expression and intracellular uptake.
What this source supports
Blocking PPAR-alpha reversed the lipid-reduction response; PPAR-gamma blockade partially reversed it. PPAR-alpha expression increased, while the reported PPAR-gamma mRNA change was not statistically significant.
What remains uncertain
Antagonist sensitivity and gene expression support pathway involvement, not a measured binding affinity or proof of direct receptor agonism. The findings concern cultured cells. These findings do not establish an effect of hemp seed oil or flour.
Study context and methods
Human HepG2 cells with experimentally induced steatosis.
Commercial (E)-beta-caryophyllene.
Lipid measurements, PPAR-alpha/PPAR-gamma and CB2 antagonist comparisons, gene expression and intracellular uptake.
- Research model
- Human HepG2 cells with experimentally induced steatosis.
- Tested material
- Commercial (E)-beta-caryophyllene.
- Assay
- Lipid measurements, PPAR-alpha/PPAR-gamma and CB2 antagonist comparisons, gene expression and intracellular uptake.
- How to read this result
- Experimental evidence classification, not a consumer dose or recipe.
Reported research conditions, not directions for personal use or a consumer mixture.
Original publication ↗ · Full text ↗
2020 · Beta-caryophyllene inhibits cocaine addiction-related behavior by activation of PPARα and PPARγ: repurposing a FDA-approved food additive for cocaine use disorder. · GPR55
What this source examined
Rats in cocaine self-administration experiments; wild-type and receptor-knockout mice. Behavioral comparisons with PPAR antagonists/agonists and cannabinoid-receptor knockout experiments.
What this source supports
Genetic deletion of GPR55 did not prevent the BCP-associated reduction in cocaine self-administration in this mouse experiment.
What remains uncertain
Behavioral antagonist and knockout results are model-specific mechanism tests, not ligand-binding measurements. They do not establish human addiction treatment, safety, or absence of abuse liability. These findings do not establish an effect of hemp seed oil or flour.
Study context and methods
Rats in cocaine self-administration experiments; wild-type and receptor-knockout mice.
Commercial beta-caryophyllene.
Behavioral comparisons with PPAR antagonists/agonists and cannabinoid-receptor knockout experiments.
- Research model
- Rats in cocaine self-administration experiments; wild-type and receptor-knockout mice.
- Tested material
- Commercial beta-caryophyllene.
- Assay
- Behavioral comparisons with PPAR antagonists/agonists and cannabinoid-receptor knockout experiments.
- How to read this result
- Experimental evidence classification, not a consumer dose or recipe.
Reported research conditions, not directions for personal use or a consumer mixture.
Original publication ↗ · Full text ↗
2020 · Beta-caryophyllene inhibits cocaine addiction-related behavior by activation of PPARα and PPARγ: repurposing a FDA-approved food additive for cocaine use disorder. · PPARα
What this source examined
Rats in cocaine self-administration experiments; wild-type and receptor-knockout mice. Behavioral comparisons with PPAR antagonists/agonists and cannabinoid-receptor knockout experiments.
What this source supports
PPAR-alpha or PPAR-gamma antagonists prevented the BCP-associated reduction in cocaine self-administration. GPR55 deletion did not prevent that response.
What remains uncertain
Behavioral antagonist and knockout results are model-specific mechanism tests, not ligand-binding measurements. They do not establish human addiction treatment, safety, or absence of abuse liability. These findings do not establish an effect of hemp seed oil or flour.
Study context and methods
Rats in cocaine self-administration experiments; wild-type and receptor-knockout mice.
Commercial beta-caryophyllene.
Behavioral comparisons with PPAR antagonists/agonists and cannabinoid-receptor knockout experiments.
- Research model
- Rats in cocaine self-administration experiments; wild-type and receptor-knockout mice.
- Tested material
- Commercial beta-caryophyllene.
- Assay
- Behavioral comparisons with PPAR antagonists/agonists and cannabinoid-receptor knockout experiments.
- How to read this result
- Experimental evidence classification, not a consumer dose or recipe.
Reported research conditions, not directions for personal use or a consumer mixture.
Original publication ↗ · Full text ↗
2020 · Beta-caryophyllene inhibits cocaine addiction-related behavior by activation of PPARα and PPARγ: repurposing a FDA-approved food additive for cocaine use disorder. · PPARγ
What this source examined
Rats in cocaine self-administration experiments; wild-type and receptor-knockout mice. Behavioral comparisons with PPAR antagonists/agonists and cannabinoid-receptor knockout experiments.
What this source supports
PPAR-alpha or PPAR-gamma antagonists prevented the BCP-associated reduction in cocaine self-administration. GPR55 deletion did not prevent that response.
What remains uncertain
Behavioral antagonist and knockout results are model-specific mechanism tests, not ligand-binding measurements. They do not establish human addiction treatment, safety, or absence of abuse liability. These findings do not establish an effect of hemp seed oil or flour.
Study context and methods
Rats in cocaine self-administration experiments; wild-type and receptor-knockout mice.
Commercial beta-caryophyllene.
Behavioral comparisons with PPAR antagonists/agonists and cannabinoid-receptor knockout experiments.
- Research model
- Rats in cocaine self-administration experiments; wild-type and receptor-knockout mice.
- Tested material
- Commercial beta-caryophyllene.
- Assay
- Behavioral comparisons with PPAR antagonists/agonists and cannabinoid-receptor knockout experiments.
- How to read this result
- Experimental evidence classification, not a consumer dose or recipe.
Reported research conditions, not directions for personal use or a consumer mixture.
Original publication ↗ · Full text ↗
2020 · β-Caryophyllene Inhibits Cell Proliferation through a Direct Modulation of CB2 Receptors in Glioblastoma Cells.
What this source examined
Human U373 glioblastoma cells, with additional glioma models described in the study. Cell-viability and apoptosis experiments with immunoblotting of PPAR-gamma and a cannabinoid-receptor antagonist comparison.
What this source supports
BCP treatment increased PPAR-gamma protein alongside changes in inflammatory and apoptosis markers. The antagonist comparison altered these responses.
What remains uncertain
PPAR-gamma protein abundance is not a direct-binding or transactivation assay. The paper inconsistently calls the antagonist AM630 and AM360, including in Methods; that identity ambiguity is retained. No human cancer-treatment inference is made. These findings do not establish an effect of hemp seed oil or flour.
Study context and methods
Human U373 glioblastoma cells, with additional glioma models described in the study.
Commercial beta-caryophyllene dissolved in DMSO.
Cell-viability and apoptosis experiments with immunoblotting of PPAR-gamma and a cannabinoid-receptor antagonist comparison.
- Research model
- Human U373 glioblastoma cells, with additional glioma models described in the study.
- Tested material
- Commercial beta-caryophyllene dissolved in DMSO.
- Assay
- Cell-viability and apoptosis experiments with immunoblotting of PPAR-gamma and a cannabinoid-receptor antagonist comparison.
- How to read this result
- Experimental evidence classification, not a consumer dose or recipe.
Reported research conditions, not directions for personal use or a consumer mixture.
Original publication ↗ · Full text ↗
2019 · β-Caryophyllene Mitigates Collagen Antibody Induced Arthritis (CAIA) in Mice Through a Cross-Talk between CB2 and PPAR-γ Receptors.
What this source examined
Mice with collagen-antibody-induced arthritis and LPS-stimulated human articular chondrocytes. Joint and cell gene/protein expression with a CB2-antagonist comparison in chondrocytes.
What this source supports
BCP restored selected PPAR-gamma and PGC-1-alpha expression measures; AM630 reversed the cultured-cell response.
What remains uncertain
These observations concern expression and downstream CB2-sensitive signaling. They do not directly measure BCP binding to PPAR-gamma or establish benefit in people with arthritis. These findings do not establish an effect of hemp seed oil or flour.
Study context and methods
Mice with collagen-antibody-induced arthritis and LPS-stimulated human articular chondrocytes.
Commercial beta-caryophyllene.
Joint and cell gene/protein expression with a CB2-antagonist comparison in chondrocytes.
- Research model
- Mice with collagen-antibody-induced arthritis and LPS-stimulated human articular chondrocytes.
- Tested material
- Commercial beta-caryophyllene.
- Assay
- Joint and cell gene/protein expression with a CB2-antagonist comparison in chondrocytes.
- How to read this result
- Experimental evidence classification, not a consumer dose or recipe.
Reported research conditions, not directions for personal use or a consumer mixture.
Original publication ↗ · Full text ↗
2020 · β-Caryophyllene Reduces the Inflammatory Phenotype of Periodontal Cells by Targeting CB2 Receptors.
What this source examined
LPS-stimulated human gingival fibroblasts and oral mucosal epithelial cells. Gene-expression, cytokine and cell-viability assays with CB2 antagonist AM630.
What this source supports
BCP increased the PPAR-gamma and PGC-1-alpha messages that LPS had reduced; AM630 reversed these changes.
What remains uncertain
The experiment measured expression rather than PPAR-gamma binding or direct agonism. One viability-method passage says AM360 while the main treatment description says AM630. This is a cell model, not evidence of clinical oral-mucositis treatment. These findings do not establish an effect of hemp seed oil or flour.
Study context and methods
LPS-stimulated human gingival fibroblasts and oral mucosal epithelial cells.
Commercial beta-caryophyllene.
Gene-expression, cytokine and cell-viability assays with CB2 antagonist AM630.
- Research model
- LPS-stimulated human gingival fibroblasts and oral mucosal epithelial cells.
- Tested material
- Commercial beta-caryophyllene.
- Assay
- Gene-expression, cytokine and cell-viability assays with CB2 antagonist AM630.
- How to read this result
- Experimental evidence classification, not a consumer dose or recipe.
Reported research conditions, not directions for personal use or a consumer mixture.
Original publication ↗ · Full text ↗
2022 · Anti-Inflammatory Effect of Beta-Caryophyllene Mediated by the Involvement of TRPV1, BDNF and trkB in the Rat Cerebral Cortex after Hypoperfusion/Reperfusion.
What this source examined
Male rats undergoing transient carotid occlusion/reperfusion or sham surgery. Cortical Western blots and immunohistochemistry.
What this source supports
The direction of TRPV1 protein change depended on surgical condition and brain region: the frontal-cortex response differed between sham and hypoperfusion/reperfusion groups.
What remains uncertain
Protein abundance and immunostaining do not measure channel opening, direct binding or analgesic efficacy. An implausible percentage decrease appears in the source prose; no such percentage is reproduced. These findings do not establish an effect of hemp seed oil or flour.
Study context and methods
Male rats undergoing transient carotid occlusion/reperfusion or sham surgery.
Beta-caryophyllene administered before surgery.
Cortical Western blots and immunohistochemistry.
- Research model
- Male rats undergoing transient carotid occlusion/reperfusion or sham surgery.
- Tested material
- Beta-caryophyllene administered before surgery.
- Assay
- Cortical Western blots and immunohistochemistry.
- How to read this result
- Experimental evidence classification, not a consumer dose or recipe.
Reported research conditions, not directions for personal use or a consumer mixture.
Original publication ↗ · Full text ↗
2018 · Acute administration of beta-caryophyllene prevents endocannabinoid system activation during transient common carotid artery occlusion and reperfusion.
What this source examined
Male Wistar rats undergoing transient carotid occlusion/reperfusion or sham surgery. Cortical Western blotting and lipid measurements, with tissue-region comparisons.
What this source supports
BCP pretreatment was associated with higher frontal-cortex PPAR-alpha protein in the challenged group and changes in selected lipid/inflammation markers.
What remains uncertain
The PPAR-alpha result is protein-expression evidence, not an experimental affinity or agonist measurement. The tissue effect was context-dependent and does not establish human neuroprotection. These findings do not establish an effect of hemp seed oil or flour.
Study context and methods
Male Wistar rats undergoing transient carotid occlusion/reperfusion or sham surgery.
Commercial beta-caryophyllene in sunflower-oil vehicle.
Cortical Western blotting and lipid measurements, with tissue-region comparisons.
- Research model
- Male Wistar rats undergoing transient carotid occlusion/reperfusion or sham surgery.
- Tested material
- Commercial beta-caryophyllene in sunflower-oil vehicle.
- Assay
- Cortical Western blotting and lipid measurements, with tissue-region comparisons.
- How to read this result
- Experimental evidence classification, not a consumer dose or recipe.
Reported research conditions, not directions for personal use or a consumer mixture.
Original publication ↗ · Full text ↗
2011 · β-Caryophyllene inhibits dextran sulfate sodium-induced colitis in mice through CB2 receptor activation and PPARγ pathway.
What this source examined
Mice with dextran-sulfate-sodium-induced colitis; separate cultured-cell experiments. Colitis outcomes and colon gene expression, with PPAR-gamma antagonist GW9662 and CB2 antagonist comparisons.
What this source supports
PPAR-gamma blockade partially reversed the BCP-associated improvement in the colitis model; BCP also partly restored colonic PPAR-gamma mRNA.
What remains uncertain
This supports involvement of the pathway under the tested conditions, not direct BCP binding to PPAR-gamma. The study does not establish treatment efficacy in human inflammatory bowel disease. These findings do not establish an effect of hemp seed oil or flour.
Study context and methods
Mice with dextran-sulfate-sodium-induced colitis; separate cultured-cell experiments.
Commercial beta-caryophyllene.
Colitis outcomes and colon gene expression, with PPAR-gamma antagonist GW9662 and CB2 antagonist comparisons.
- Research model
- Mice with dextran-sulfate-sodium-induced colitis; separate cultured-cell experiments.
- Tested material
- Commercial beta-caryophyllene.
- Assay
- Colitis outcomes and colon gene expression, with PPAR-gamma antagonist GW9662 and CB2 antagonist comparisons.
- How to read this result
- Experimental evidence classification, not a consumer dose or recipe.
Reported research conditions, not directions for personal use or a consumer mixture.
Original publication ↗ · Full text ↗
2017 · β-Caryophyllene protects against alcoholic steatohepatitis by attenuating inflammation and metabolic dysregulation in mice.
What this source examined
Wild-type and CB2-deficient mice in a chronic-plus-binge alcohol liver-injury model. Hepatic protein/mRNA measurements and CB2-knockout comparisons.
What this source supports
BCP preserved PPAR-alpha expression and several related transcripts after ethanol feeding. Selected protective and expression effects were lost in CB2-deficient mice.
What remains uncertain
Expression and knockout dependence are not measurements of direct PPAR-alpha binding. The preparation was not chemically pure. Animal liver-injury outcomes do not establish human treatment or safety. These findings do not establish an effect of hemp seed oil or flour.
Study context and methods
Wild-type and CB2-deficient mice in a chronic-plus-binge alcohol liver-injury model.
(E)-beta-caryophyllene preparation with caryophyllene oxide and alpha-humulene identified as impurities.
Hepatic protein/mRNA measurements and CB2-knockout comparisons.
- Research model
- Wild-type and CB2-deficient mice in a chronic-plus-binge alcohol liver-injury model.
- Tested material
- (E)-beta-caryophyllene preparation with caryophyllene oxide and alpha-humulene identified as impurities.
- Assay
- Hepatic protein/mRNA measurements and CB2-knockout comparisons.
- How to read this result
- Experimental evidence classification, not a consumer dose or recipe.
Reported research conditions, not directions for personal use or a consumer mixture.
Original publication ↗ · Full text ↗
2025 · Effect of β-Caryophyllene on PPAR-γ, NF-κB, and CNR2: Implications for Gut-Brain Axis Communication in a Murine Model of Diet-Induced Obesity.
What this source examined
C57BL/6J mice receiving standard or high-fat diets, with or without BCP. Intestinal Western blot/imaging and brain gene-expression analyses.
What this source supports
PPAR-gamma protein responses differed across intestinal regions and diet groups; the paper reports both decreases and increases in different contexts.
What remains uncertain
The measurements are tissue expression, not direct receptor activation or binding. A uniform PPAR-gamma agonist label would erase the regional differences. This is not a human obesity-treatment trial. These findings do not establish an effect of hemp seed oil or flour.
Study context and methods
C57BL/6J mice receiving standard or high-fat diets, with or without BCP.
Beta-caryophyllene administered by oral gavage in the reported vehicle.
Intestinal Western blot/imaging and brain gene-expression analyses.
- Research model
- C57BL/6J mice receiving standard or high-fat diets, with or without BCP.
- Tested material
- Beta-caryophyllene administered by oral gavage in the reported vehicle.
- Assay
- Intestinal Western blot/imaging and brain gene-expression analyses.
- How to read this result
- Experimental evidence classification, not a consumer dose or recipe.
Reported research conditions, not directions for personal use or a consumer mixture.
Original publication ↗ · Full text ↗
2024 · Beta-Caryophyllene Augments Radiotherapy Efficacy in GBM by Modulating Cell Apoptosis and DNA Damage Repair via PPARγ and NF-κB Pathways.
What this source examined
Human U87MG and mouse GL261 glioma cells; GL261 tumor-bearing mice. Radiation/compound combination experiments, cell survival and Western blotting.
What this source supports
The combination was associated with increased PPAR-gamma protein and apoptosis-related changes in the cell models.
What remains uncertain
PPAR-gamma abundance alone does not demonstrate receptor binding or causal activation. Combination effects in these models do not establish clinical radiosensitization, human safety or a consumer combination. The survival-dataset analysis elsewhere in the paper is not a BCP clinical trial. These findings do not establish an effect of hemp seed oil or flour.
Study context and methods
Human U87MG and mouse GL261 glioma cells; GL261 tumor-bearing mice.
Commercial beta-caryophyllene preparation with limited reported purity.
Radiation/compound combination experiments, cell survival and Western blotting.
- Research model
- Human U87MG and mouse GL261 glioma cells; GL261 tumor-bearing mice.
- Tested material
- Commercial beta-caryophyllene preparation with limited reported purity.
- Assay
- Radiation/compound combination experiments, cell survival and Western blotting.
- How to read this result
- Experimental evidence classification, not a consumer dose or recipe.
Reported research conditions, not directions for personal use or a consumer mixture.
Original publication ↗ · Full text ↗
2024 · Anti-Inflammatory Properties of Cannabidiol and Beta-Caryophyllene Alone or Combined in an In Vitro Inflammation Model.
What this source examined
LPS-stimulated human HaCaT keratinocytes. Inflammatory-protein/gene assays with G3335 used for the CBD arm and AM630 used for the BCP-enriched arm.
What this source supports
The source paired CBD with PPAR-gamma blockade and BCP-enriched extract with CB2 blockade. The selected beta-caryophyllene/ppar-gamma assignment is not supported by those treatment arms.
What remains uncertain
These are different treatment arms. The experiment does not assign the CBD result to CB2 or the BCP result to PPAR-gamma. The BCP material is an enriched extract, not proof of a pure-compound mechanism; no universal synergy or clinical claim follows. These findings do not establish an effect of hemp seed oil or flour.
Study context and methods
LPS-stimulated human HaCaT keratinocytes.
CBD and a beta-caryophyllene-enriched black-pepper extract in a rice-derived carrier, tested separately and together.
Inflammatory-protein/gene assays with G3335 used for the CBD arm and AM630 used for the BCP-enriched arm.
- Research model
- LPS-stimulated human HaCaT keratinocytes.
- Tested material
- CBD and a beta-caryophyllene-enriched black-pepper extract in a rice-derived carrier, tested separately and together.
- Assay
- Inflammatory-protein/gene assays with G3335 used for the CBD arm and AM630 used for the BCP-enriched arm.
- How to read this result
- Experimental evidence classification, not a consumer dose or recipe.
Reported research conditions, not directions for personal use or a consumer mixture.
Original publication ↗ · Full text ↗
2025 · Multi-Target Protective Effects of β-Caryophyllene (BCP) at the Intersection of Neuroinflammation and Neurodegeneration.
What this source examined
Human HMC3 microglial cells challenged with amyloid-beta; separate brain-slice experiments. PPAR-gamma protein and NF-kappaB/BDNF measurements with antagonist comparisons in HMC3 cells.
What this source supports
GW9662 weakened selected BCP-associated NF-kappaB and BDNF responses, and BCP prevented the amyloid-associated decrease in PPAR-gamma protein.
What remains uncertain
The PPAR-gamma assignment is supported by the cultured-cell experiments, not by assuming the same mechanism in every brain-slice outcome. Antagonist sensitivity does not establish direct binding or human Alzheimer disease treatment. These findings do not establish an effect of hemp seed oil or flour.
Study context and methods
Human HMC3 microglial cells challenged with amyloid-beta; separate brain-slice experiments.
Commercial beta-caryophyllene.
PPAR-gamma protein and NF-kappaB/BDNF measurements with antagonist comparisons in HMC3 cells.
- Research model
- Human HMC3 microglial cells challenged with amyloid-beta; separate brain-slice experiments.
- Tested material
- Commercial beta-caryophyllene.
- Assay
- PPAR-gamma protein and NF-kappaB/BDNF measurements with antagonist comparisons in HMC3 cells.
- How to read this result
- Experimental evidence classification, not a consumer dose or recipe.
Reported research conditions, not directions for personal use or a consumer mixture.
Original publication ↗ · Full text ↗
2022 · ViphyllinTM, a Standardized Black Pepper Seed Extract Exerts Antinociceptive Effects in Murine Pain Models via Activation of Cannabinoid Receptor CB2, Peroxisome Proliferator-Activated Receptor-Alpha and TRPV1 Ion Channels. · TRPV1
What this source examined
Male mice in several nociception assays; separate computational docking. Extract/antagonist comparisons in formalin, hot-plate and tail-flick tests, plus BCP docking calculations.
What this source supports
TRPV1 and PPAR-alpha antagonists altered some extract responses in the thermal tests but not the formalin test. A BCP comparator was also tested; docking supplied predicted interactions.
What remains uncertain
The antagonist effects concern the extract and vary by assay. They cannot be reassigned as isolated-BCP receptor binding. Docking scores are predictions, not measured affinity; the BCP comparator does not isolate its contribution to the extract. These findings do not establish an effect of hemp seed oil or flour.
Study context and methods
Male mice in several nociception assays; separate computational docking.
Viphyllin black-pepper extract standardized for BCP; separately tested commercial BCP reference compound.
Extract/antagonist comparisons in formalin, hot-plate and tail-flick tests, plus BCP docking calculations.
- Research model
- Male mice in several nociception assays; separate computational docking.
- Tested material
- Viphyllin black-pepper extract standardized for BCP; separately tested commercial BCP reference compound.
- Assay
- Extract/antagonist comparisons in formalin, hot-plate and tail-flick tests, plus BCP docking calculations.
- How to read this result
- Experimental evidence classification, not a consumer dose or recipe.
Reported research conditions, not directions for personal use or a consumer mixture.
Original publication ↗ · Full text ↗
2022 · ViphyllinTM, a Standardized Black Pepper Seed Extract Exerts Antinociceptive Effects in Murine Pain Models via Activation of Cannabinoid Receptor CB2, Peroxisome Proliferator-Activated Receptor-Alpha and TRPV1 Ion Channels. · PPARα
What this source examined
Male mice in several nociception assays; separate computational docking. Extract/antagonist comparisons in formalin, hot-plate and tail-flick tests, plus BCP docking calculations.
What this source supports
TRPV1 and PPAR-alpha antagonists altered some extract responses in the thermal tests but not the formalin test. A BCP comparator was also tested; docking supplied predicted interactions.
What remains uncertain
The antagonist effects concern the extract and vary by assay. They cannot be reassigned as isolated-BCP receptor binding. Docking scores are predictions, not measured affinity; the BCP comparator does not isolate its contribution to the extract. These findings do not establish an effect of hemp seed oil or flour.
Study context and methods
Male mice in several nociception assays; separate computational docking.
Viphyllin black-pepper extract standardized for BCP; separately tested commercial BCP reference compound.
Extract/antagonist comparisons in formalin, hot-plate and tail-flick tests, plus BCP docking calculations.
- Research model
- Male mice in several nociception assays; separate computational docking.
- Tested material
- Viphyllin black-pepper extract standardized for BCP; separately tested commercial BCP reference compound.
- Assay
- Extract/antagonist comparisons in formalin, hot-plate and tail-flick tests, plus BCP docking calculations.
- How to read this result
- Experimental evidence classification, not a consumer dose or recipe.
Reported research conditions, not directions for personal use or a consumer mixture.
Original publication ↗ · Full text ↗
2024 · Metformin relieves bone cancer pain by reducing TGFβRI-TRPV1 signaling in rats.
What this source examined
Rat bone-cancer-pain model. Pain-behavior, TRPV1-expression and signaling experiments.
What this source supports
The article concerns metformin in bone cancer pain and supplies no beta-caryophyllene treatment evidence.
What remains uncertain
The shared abbreviation BCP produced a false search match. This source is excluded from beta-caryophyllene/TRPV1 pharmacology rather than treated as a negative compound experiment. These findings do not establish an effect of hemp seed oil or flour.
Study context and methods
Rat bone-cancer-pain model.
Metformin and a TGF-beta receptor inhibitor; BCP is the abbreviation for bone cancer pain.
Pain-behavior, TRPV1-expression and signaling experiments.
- Research model
- Rat bone-cancer-pain model.
- Tested material
- Metformin and a TGF-beta receptor inhibitor; BCP is the abbreviation for bone cancer pain.
- Assay
- Pain-behavior, TRPV1-expression and signaling experiments.
- How to read this result
- Experimental evidence classification, not a consumer dose or recipe.
Reported research conditions, not directions for personal use or a consumer mixture.
Original publication ↗ · Full text ↗
CB2: Competitive binding and CB2-related cellular signalling; Human CB2 receptor assays; separate mouse experiments.
CB1: Radioligand binding and CAMYEL cAMP functional assays; Human receptors in cell assays.
CB2: Radioligand binding and CAMYEL cAMP functional assays; Human receptors in cell assays.
CB1: ERK phosphorylation with rimonabant and wild-type CHO controls, Figures 6–7; CHO cells expressing CB1; separate mouse experiments in the paper.
The study reported CB2 binding and agonist activity for (E)-β-caryophyllene.
No supporting direct receptor interaction or functional response was detected under the tested conditions.
A possible weak CB2 binding interaction was noted; no functional terpene effect was detected.
The authors reported a rimonabant-sensitive ERK response in CB1-CHO cells. Some terpenes also activated ERK in cells without engineered CB1, so this readout is not proof of exclusive or direct receptor binding.
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