PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
30627539-12	2018	Moreover, the finding that the acidic precursor of CBD (cannabidiolic acid, CBDA) is able to inhibit the migration of breast cancer cells and to downregulate the proto-oncogene c-fos and the cyclooxygenase-2 (COX-2) highlights the possibility that CBDA might act on a common pathway of inflammation and cancer mechanisms, which might be responsible for its anticancer activity.	Cannabidiol	51-54	cytochrome c oxidase subunit 2	Cannabis sativa	191-207
30627539-12	2018	Moreover, the finding that the acidic precursor of CBD (cannabidiolic acid, CBDA) is able to inhibit the migration of breast cancer cells and to downregulate the proto-oncogene c-fos and the cyclooxygenase-2 (COX-2) highlights the possibility that CBDA might act on a common pathway of inflammation and cancer mechanisms, which might be responsible for its anticancer activity.	Cannabidiol	51-54	cytochrome c oxidase subunit 2	Cannabis sativa	209-214
30324842-9	2018	Interestingly, cannabidiol at low (5 mg/kg) and intermediate doses (15 mg/kg) successfully blocked the effects induced by acute stress on corticotropin-releasing factor, pro-opiomelanocortin and glucocorticoid receptor gene expression.	Cannabidiol	15-26	corticotropin releasing hormone	Mus musculus	138-168
30324842-9	2018	Interestingly, cannabidiol at low (5 mg/kg) and intermediate doses (15 mg/kg) successfully blocked the effects induced by acute stress on corticotropin-releasing factor, pro-opiomelanocortin and glucocorticoid receptor gene expression.	Cannabidiol	15-26	pro-opiomelanocortin-alpha	Mus musculus	170-190
30324842-9	2018	Interestingly, cannabidiol at low (5 mg/kg) and intermediate doses (15 mg/kg) successfully blocked the effects induced by acute stress on corticotropin-releasing factor, pro-opiomelanocortin and glucocorticoid receptor gene expression.	Cannabidiol	15-26	nuclear receptor subfamily 3, group C, member 1	Mus musculus	195-218
30273593-0	2018	Repeated Cannabidiol treatment reduces cocaine intake and modulates neural proliferation and CB1R expression in the mouse hippocampus.	Cannabidiol	9-20	cannabinoid receptor 1 (brain)	Mus musculus	93-97
30061636-5	2018	Importantly, KPC mice treated with a combination of the GPR55 antagonist Cannabidiol (CBD) and gemcitabine (GEM, one of the most used drugs to treat PDAC), survived nearly three times longer compared to mice treated with vehicle or GEM alone.	Cannabidiol	73-84	G protein-coupled receptor 55	Mus musculus	56-61
30061636-5	2018	Importantly, KPC mice treated with a combination of the GPR55 antagonist Cannabidiol (CBD) and gemcitabine (GEM, one of the most used drugs to treat PDAC), survived nearly three times longer compared to mice treated with vehicle or GEM alone.	Cannabidiol	86-89	G protein-coupled receptor 55	Mus musculus	56-61
30515459-0	2018	Cannabidiol"s Upregulation of N-acyl Ethanolamines in the Central Nervous System Requires N-acyl Phosphatidyl Ethanolamine-Specific Phospholipase D.	Cannabidiol	0-11	N-acyl phosphatidylethanolamine phospholipase D	Mus musculus	90-147
30480157-4	2018	In addition, structure-activity relationship studies were conducted on cannabidiol (CBD), a recently discovered inverse agonist for GPR6.	Cannabidiol	71-82	G protein-coupled receptor 6	Homo sapiens	132-136
30406638-26	2018	The mean CRP in the cannabidiol group was 9.428 mg/L compared to 7.638 mg/L in the placebo group (MD 1.79, 95% CI -5.67 to 9.25; moderate certainty evidence).	Cannabidiol	20-31	C-reactive protein	Homo sapiens	9-12
30194918-0	2018	Cannabidiol skews biased agonism at cannabinoid CB1 and CB2 receptors with smaller effect in CB1-CB2 heteroreceptor complexes.	Cannabidiol	0-11	cannabinoid receptor 1	Homo sapiens	48-51
30194918-0	2018	Cannabidiol skews biased agonism at cannabinoid CB1 and CB2 receptors with smaller effect in CB1-CB2 heteroreceptor complexes.	Cannabidiol	0-11	cannabinoid receptor 2	Homo sapiens	56-59
30194918-0	2018	Cannabidiol skews biased agonism at cannabinoid CB1 and CB2 receptors with smaller effect in CB1-CB2 heteroreceptor complexes.	Cannabidiol	0-11	cannabinoid receptor 1	Homo sapiens	93-96
30194918-0	2018	Cannabidiol skews biased agonism at cannabinoid CB1 and CB2 receptors with smaller effect in CB1-CB2 heteroreceptor complexes.	Cannabidiol	0-11	cannabinoid receptor 2	Homo sapiens	97-100
30217539-0	2018	Cannabidiol prevents haloperidol-induced vacuos chewing movements and inflammatory changes in mice via PPARgamma receptors.	Cannabidiol	0-11	peroxisome proliferator activated receptor gamma	Mus musculus	103-112
30217539-11	2018	On the other hand, the levels of the anti-inflammatory cytokine IL-10 increased in the striatum of animals that received CBD and haloperidol.	Cannabidiol	121-124	interleukin 10	Mus musculus	64-69
30217539-14	2018	The combination of CBD and haloperidol also increased PGC-1alpha mRNA expression, a co-activator of PPARgamma receptors.	Cannabidiol	19-22	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	54-64
30217539-14	2018	The combination of CBD and haloperidol also increased PGC-1alpha mRNA expression, a co-activator of PPARgamma receptors.	Cannabidiol	19-22	peroxisome proliferator activated receptor gamma	Mus musculus	100-109
30217539-15	2018	Pretreatment with the PPARgamma antagonist, GW9662, blocked the behavioural effect of CBD in our TD model.	Cannabidiol	86-89	peroxisome proliferator activated receptor gamma	Mus musculus	22-31
30217539-17	2018	In conclusion, our results suggest that CBD could prevent haloperidol-induced orofacial dyskinesia by activating PPARgamma receptors and attenuating neuroinflammatory changes in the striatum.	Cannabidiol	40-43	peroxisome proliferator activated receptor gamma	Mus musculus	113-122
30480157-4	2018	In addition, structure-activity relationship studies were conducted on cannabidiol (CBD), a recently discovered inverse agonist for GPR6.	Cannabidiol	84-87	G protein-coupled receptor 6	Homo sapiens	132-136
30287853-9	2018	CHP3 bound with high affinity to CBD with an equilibrium dissociation constant (KD) of 56 nM determined by microscale thermophoresis.	Cannabidiol	33-36	tescalcin	Homo sapiens	0-4
30007266-5	2018	CBD-induced apoptosis was accompanied by down-regulation of mTOR, cyclin D1 and up-regulation and localization of PPARgamma protein expression in the nuclei and cytoplasmic of the tested cells.	Cannabidiol	0-3	mechanistic target of rapamycin kinase	Homo sapiens	60-64
30349652-3	2018	This study investigates the effect of cannabidiol (CBD), a non-psychoactive cannabinoid, on HO-1 expression and disease-associated functions of human umbilical artery smooth muscle cells (HUASMC).	Cannabidiol	38-49	heme oxygenase 1	Homo sapiens	92-96
30349652-3	2018	This study investigates the effect of cannabidiol (CBD), a non-psychoactive cannabinoid, on HO-1 expression and disease-associated functions of human umbilical artery smooth muscle cells (HUASMC).	Cannabidiol	51-54	heme oxygenase 1	Homo sapiens	92-96
30349652-10	2018	Collectively, this work provides the first indication of CBD-mediated enhancement of HO-1 in VSMC and potential protective effects against aberrant VSMC proliferation and migration.	Cannabidiol	57-60	heme oxygenase 1	Homo sapiens	85-89
29897289-9	2018	Importantly, cannabidiol treatment preserved psim and reduced cell death and KIM-1 accompanied by restoration of N1 and N2 imbalance and preservation of Treg17 cells while decreasing Th-17 cells.	Cannabidiol	13-24	hepatitis A virus cellular receptor 1	Mus musculus	77-82
30033591-14	2018	CONCLUSIONS AND IMPLICATIONS: VCE-004.3 is a novel semisynthetic cannabidiol derivative that behaves as a dual PPARgamma/CB2 agonist and CB1 receptor modulator that could be considered for the development of novel therapies against different forms of scleroderma.	Cannabidiol	65-76	peroxisome proliferator activated receptor gamma	Homo sapiens	111-120
30033591-14	2018	CONCLUSIONS AND IMPLICATIONS: VCE-004.3 is a novel semisynthetic cannabidiol derivative that behaves as a dual PPARgamma/CB2 agonist and CB1 receptor modulator that could be considered for the development of novel therapies against different forms of scleroderma.	Cannabidiol	65-76	cannabinoid receptor 2	Homo sapiens	121-124
30033591-14	2018	CONCLUSIONS AND IMPLICATIONS: VCE-004.3 is a novel semisynthetic cannabidiol derivative that behaves as a dual PPARgamma/CB2 agonist and CB1 receptor modulator that could be considered for the development of novel therapies against different forms of scleroderma.	Cannabidiol	65-76	cannabinoid receptor 1	Homo sapiens	137-140
30007266-5	2018	CBD-induced apoptosis was accompanied by down-regulation of mTOR, cyclin D1 and up-regulation and localization of PPARgamma protein expression in the nuclei and cytoplasmic of the tested cells.	Cannabidiol	0-3	cyclin D1	Homo sapiens	66-75
30007266-5	2018	CBD-induced apoptosis was accompanied by down-regulation of mTOR, cyclin D1 and up-regulation and localization of PPARgamma protein expression in the nuclei and cytoplasmic of the tested cells.	Cannabidiol	0-3	peroxisome proliferator activated receptor gamma	Homo sapiens	114-123
30006259-0	2018	Open-label use of highly purified CBD (Epidiolex ) in patients with CDKL5 deficiency disorder and Aicardi, Dup15q, and Doose syndromes.	Cannabidiol	34-37	gremlin 1, DAN family BMP antagonist	Homo sapiens	107-113
30235802-7	2018	In cultured HTPCs, application of cannabidiol (CBD), a known TRPV2 agonist, acutely induced a transient increase in intracellular Ca2+ levels.	Cannabidiol	34-45	transient receptor potential cation channel subfamily V member 2	Homo sapiens	61-66
30235802-7	2018	In cultured HTPCs, application of cannabidiol (CBD), a known TRPV2 agonist, acutely induced a transient increase in intracellular Ca2+ levels.	Cannabidiol	34-45	carbonic anhydrase 2	Homo sapiens	130-133
30235802-7	2018	In cultured HTPCs, application of cannabidiol (CBD), a known TRPV2 agonist, acutely induced a transient increase in intracellular Ca2+ levels.	Cannabidiol	47-50	transient receptor potential cation channel subfamily V member 2	Homo sapiens	61-66
30235802-7	2018	In cultured HTPCs, application of cannabidiol (CBD), a known TRPV2 agonist, acutely induced a transient increase in intracellular Ca2+ levels.	Cannabidiol	47-50	carbonic anhydrase 2	Homo sapiens	130-133
30223868-0	2018	Cannabidiol enhances morphine antinociception, diminishes NMDA-mediated seizures and reduces stroke damage via the sigma 1 receptor.	Cannabidiol	0-11	sigma non-opioid intracellular receptor 1	Homo sapiens	115-131
30194563-15	2018	CBD has a clear interaction with clobazam, significantly increasing the levels of its active metabolite N-desmethylclobazam in several studies; this is felt to be due to CBD"s inhibition of CYP2C19.	Cannabidiol	0-3	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	190-197
30109468-10	2018	Furthermore, AM630 (CB2 antagonist) significantly attenuated CBD-mediated neuroprotection, while having no detectable effect on neuroprotection from KLS-13019.	Cannabidiol	61-64	cannabinoid receptor 2	Rattus norvegicus	20-23
30006259-1	2018	OBJECTIVE: We studied our collective open-label, compassionate use experience in using cannabidiol (CBD) to treat epilepsy in patients with CDKL5 deficiency disorder and Aicardi, Doose, and Dup15q syndromes.	Cannabidiol	87-98	gremlin 1, DAN family BMP antagonist	Homo sapiens	190-196
30006259-7	2018	SIGNIFICANCE: This open-label drug trial provides class III evidence for the long-term safety and efficacy of CBD administration in patients with treatment-resistant epilepsy (TRE) associated with CDKL5 deficiency disorder and Aicardi, Dup15q, and Doose syndromes.	Cannabidiol	110-113	gremlin 1, DAN family BMP antagonist	Homo sapiens	236-242
30123217-4	2018	Treatment with CBD caused attenuation of EAE disease paradigms as indicated by a significant reduction in clinical scores of paralysis, decreased T cell infiltration in the central nervous system, and reduced levels of IL-17 and IFNgamma.	Cannabidiol	15-18	interleukin 17A	Mus musculus	219-224
30123217-4	2018	Treatment with CBD caused attenuation of EAE disease paradigms as indicated by a significant reduction in clinical scores of paralysis, decreased T cell infiltration in the central nervous system, and reduced levels of IL-17 and IFNgamma.	Cannabidiol	15-18	interferon gamma	Mus musculus	229-237
29968502-0	2018	Hippocampal mammalian target of rapamycin is implicated in stress-coping behavior induced by cannabidiol in the forced swim test.	Cannabidiol	93-104	mechanistic target of rapamycin kinase	Homo sapiens	12-41
29859012-5	2018	The role of 5-HT1A receptors in the ethanol reduction induced by the administration of CBD + naltrexone was analysed by using the 5-HT1A receptor antagonist WAY100635 (0.3 mg kg-1 , i.p.).	Cannabidiol	87-90	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	12-18
29859012-5	2018	The role of 5-HT1A receptors in the ethanol reduction induced by the administration of CBD + naltrexone was analysed by using the 5-HT1A receptor antagonist WAY100635 (0.3 mg kg-1 , i.p.).	Cannabidiol	87-90	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	12-27
29902416-9	2018	Our results suggest that the effects observed after CBD exposure are intimately related to CB1 receptor that is present in zebrafish since early stages of development.	Cannabidiol	52-55	cannabinoid receptor 1	Danio rerio	91-94
29929108-0	2018	The adult motor phenotype of Dravet syndrome is associated with mutation of the STXBP1 gene and responds well to cannabidiol treatment.	Cannabidiol	113-124	syntaxin binding protein 1	Homo sapiens	80-86
29981580-15	2018	Identifier NCT03024827, Cannabidiol in Children with Refractory Epileptic Encephalopathy: CARE-E; 2017 Jan 19 [cited 2017 Oct]; Available from: http://clinicaltrials.gov/ct2/show/NCT03024827.	Cannabidiol	24-35	plexin A2	Homo sapiens	122-125
29574880-8	2018	These neuroprotective effects of CBD were corroborated by immunohistochemistry experiments that revealed a significant reduction in atrophy and death of PV- and CCK-expressing interneurons after CBD treatment.	Cannabidiol	195-198	parvalbumin	Rattus norvegicus	153-155
29968502-6	2018	BDNF levels were analyzed in the hippocampus of animals treated with cannabidiol (10 mg/kg).	Cannabidiol	69-80	brain derived neurotrophic factor	Mus musculus	0-4
29968502-7	2018	RESULTS: Systemic cannabidiol administration induced antidepressant-like effects and increased BDNF levels in the dorsal hippocampus.	Cannabidiol	18-29	brain derived neurotrophic factor	Mus musculus	95-99
29968502-10	2018	CONCLUSION: Altogether, our data suggest that the hippocampal BDNF-TrkB-mTOR pathway is vital for cannabidiol-induced antidepressant-like effect when the drug is locally administered.	Cannabidiol	98-109	brain derived neurotrophic factor	Mus musculus	62-66
29968502-10	2018	CONCLUSION: Altogether, our data suggest that the hippocampal BDNF-TrkB-mTOR pathway is vital for cannabidiol-induced antidepressant-like effect when the drug is locally administered.	Cannabidiol	98-109	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	67-71
29968502-10	2018	CONCLUSION: Altogether, our data suggest that the hippocampal BDNF-TrkB-mTOR pathway is vital for cannabidiol-induced antidepressant-like effect when the drug is locally administered.	Cannabidiol	98-109	mechanistic target of rapamycin kinase	Mus musculus	72-76
29574880-2	2018	To elucidate the mechanisms by which CBD exerts its anti-seizure effects, we investigated its effects at synaptic connections and on the intrinsic membrane properties of hippocampal CA1 pyramidal cells and two major inhibitory interneurons: fast spiking, parvalbumin (PV)-expressing and adapting, cholecystokinin (CCK)-expressing interneurons.	Cannabidiol	37-40	carbonic anhydrase 1	Rattus norvegicus	182-185
29574880-2	2018	To elucidate the mechanisms by which CBD exerts its anti-seizure effects, we investigated its effects at synaptic connections and on the intrinsic membrane properties of hippocampal CA1 pyramidal cells and two major inhibitory interneurons: fast spiking, parvalbumin (PV)-expressing and adapting, cholecystokinin (CCK)-expressing interneurons.	Cannabidiol	37-40	parvalbumin	Rattus norvegicus	255-266
29574880-2	2018	To elucidate the mechanisms by which CBD exerts its anti-seizure effects, we investigated its effects at synaptic connections and on the intrinsic membrane properties of hippocampal CA1 pyramidal cells and two major inhibitory interneurons: fast spiking, parvalbumin (PV)-expressing and adapting, cholecystokinin (CCK)-expressing interneurons.	Cannabidiol	37-40	parvalbumin	Rattus norvegicus	268-270
29574880-2	2018	To elucidate the mechanisms by which CBD exerts its anti-seizure effects, we investigated its effects at synaptic connections and on the intrinsic membrane properties of hippocampal CA1 pyramidal cells and two major inhibitory interneurons: fast spiking, parvalbumin (PV)-expressing and adapting, cholecystokinin (CCK)-expressing interneurons.	Cannabidiol	37-40	cholecystokinin	Rattus norvegicus	297-312
29574880-2	2018	To elucidate the mechanisms by which CBD exerts its anti-seizure effects, we investigated its effects at synaptic connections and on the intrinsic membrane properties of hippocampal CA1 pyramidal cells and two major inhibitory interneurons: fast spiking, parvalbumin (PV)-expressing and adapting, cholecystokinin (CCK)-expressing interneurons.	Cannabidiol	37-40	cholecystokinin	Rattus norvegicus	314-317
29574880-3	2018	We also investigated whether in vivo treatment with CBD altered the fate of CCK and PV interneurons using immunohistochemistry.	Cannabidiol	52-55	cholecystokinin	Rattus norvegicus	76-79
29574880-3	2018	We also investigated whether in vivo treatment with CBD altered the fate of CCK and PV interneurons using immunohistochemistry.	Cannabidiol	52-55	parvalbumin	Rattus norvegicus	84-86
29574880-8	2018	These neuroprotective effects of CBD were corroborated by immunohistochemistry experiments that revealed a significant reduction in atrophy and death of PV- and CCK-expressing interneurons after CBD treatment.	Cannabidiol	33-36	parvalbumin	Rattus norvegicus	153-155
29574880-8	2018	These neuroprotective effects of CBD were corroborated by immunohistochemistry experiments that revealed a significant reduction in atrophy and death of PV- and CCK-expressing interneurons after CBD treatment.	Cannabidiol	33-36	cholecystokinin	Rattus norvegicus	161-164
29427593-0	2018	Inhibition of aldose reductase activity by Cannabis sativa chemotypes extracts with high content of cannabidiol or cannabigerol.	Cannabidiol	100-111	aldo-keto reductase family 1 member B	Sus scrofa	14-30
29427593-9	2018	The extracts of Cannabis with high content of non-psychotropic cannabinoids CBD/CBDA or CBG/CBGA significantly inhibit aldose reductase activity.	Cannabidiol	76-79	aldo-keto reductase family 1 member B	Sus scrofa	119-135
29510186-3	2018	Here we investigated for the first time if the behavioral and pro-neurogenic effects of CBD administered concomitant the CUS procedure (14 days) are mediated by CB1, CB2 or 5HT1A receptors, as well as CBD effects on dendritic remodeling and on intracellular/synaptic signaling (fatty acid amide hydrolase - FAAH, Akt, GSK3beta and the synaptic proteins Synapsin Ia/b, mGluR1 and PSD95).	Cannabidiol	88-91	cannabinoid receptor 1 (brain)	Mus musculus	161-164
29510186-3	2018	Here we investigated for the first time if the behavioral and pro-neurogenic effects of CBD administered concomitant the CUS procedure (14 days) are mediated by CB1, CB2 or 5HT1A receptors, as well as CBD effects on dendritic remodeling and on intracellular/synaptic signaling (fatty acid amide hydrolase - FAAH, Akt, GSK3beta and the synaptic proteins Synapsin Ia/b, mGluR1 and PSD95).	Cannabidiol	88-91	cannabinoid receptor 2 (macrophage)	Mus musculus	166-169
29510186-3	2018	Here we investigated for the first time if the behavioral and pro-neurogenic effects of CBD administered concomitant the CUS procedure (14 days) are mediated by CB1, CB2 or 5HT1A receptors, as well as CBD effects on dendritic remodeling and on intracellular/synaptic signaling (fatty acid amide hydrolase - FAAH, Akt, GSK3beta and the synaptic proteins Synapsin Ia/b, mGluR1 and PSD95).	Cannabidiol	88-91	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	173-178
29510186-4	2018	After 14 days, CBD injections (30 mg/kg) induced anxiolytic responses in stressed animals in the elevated plus-maze and novelty suppressed feeding tests, that were blocked by pre-treatment with a CB1 (AM251, 0.3 mg/kg) or CB2 (AM630, 0.3 mg/kg), but not by a 5HT1A (WAY100635, 0.05 mg/kg) receptor antagonist.	Cannabidiol	15-18	cannabinoid receptor 1 (brain)	Mus musculus	196-199
29510186-4	2018	After 14 days, CBD injections (30 mg/kg) induced anxiolytic responses in stressed animals in the elevated plus-maze and novelty suppressed feeding tests, that were blocked by pre-treatment with a CB1 (AM251, 0.3 mg/kg) or CB2 (AM630, 0.3 mg/kg), but not by a 5HT1A (WAY100635, 0.05 mg/kg) receptor antagonist.	Cannabidiol	15-18	cannabinoid receptor 2 (macrophage)	Mus musculus	222-225
29510186-4	2018	After 14 days, CBD injections (30 mg/kg) induced anxiolytic responses in stressed animals in the elevated plus-maze and novelty suppressed feeding tests, that were blocked by pre-treatment with a CB1 (AM251, 0.3 mg/kg) or CB2 (AM630, 0.3 mg/kg), but not by a 5HT1A (WAY100635, 0.05 mg/kg) receptor antagonist.	Cannabidiol	15-18	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	259-264
29574880-8	2018	These neuroprotective effects of CBD were corroborated by immunohistochemistry experiments that revealed a significant reduction in atrophy and death of PV- and CCK-expressing interneurons after CBD treatment.	Cannabidiol	195-198	cholecystokinin	Rattus norvegicus	161-164
29441458-9	2018	In Ishikawa cells, contrary to Hec50co, treatment with AEA and CBD resulted in an increase in the levels of activated caspase -3/-7, in cleaved PARP, and in reactive oxygen species generation, confirming that the reduction in cell viability observed in the MTT assay was caused by the activation of the apoptotic pathway.	Cannabidiol	63-66	caspase 3	Homo sapiens	118-131
29441458-9	2018	In Ishikawa cells, contrary to Hec50co, treatment with AEA and CBD resulted in an increase in the levels of activated caspase -3/-7, in cleaved PARP, and in reactive oxygen species generation, confirming that the reduction in cell viability observed in the MTT assay was caused by the activation of the apoptotic pathway.	Cannabidiol	63-66	poly(ADP-ribose) polymerase 1	Homo sapiens	144-148
29561958-8	2018	Maternal use of CBD had a beneficial effect on the intestinal loops of GS with decreased nitrite/nitrate and iNOS expression.	Cannabidiol	16-19	nitric oxide synthase 2	Rattus norvegicus	109-113
29205751-0	2018	LH-21 and abnormal cannabidiol improve beta-cell function in isolated human and mouse islets through GPR55-dependent and -independent signalling.	Cannabidiol	19-30	G protein-coupled receptor 55	Mus musculus	101-106
29495967-5	2018	VCE-004.8, an aminoquinone derivative of cannabidiol (CBD), is a dual PPARgamma and CB2 agonist with potent anti-inflammatory activity.	Cannabidiol	41-52	peroxisome proliferator activated receptor gamma	Mus musculus	70-79
29495967-5	2018	VCE-004.8, an aminoquinone derivative of cannabidiol (CBD), is a dual PPARgamma and CB2 agonist with potent anti-inflammatory activity.	Cannabidiol	41-52	cannabinoid receptor 2 (macrophage)	Mus musculus	84-87
29495967-5	2018	VCE-004.8, an aminoquinone derivative of cannabidiol (CBD), is a dual PPARgamma and CB2 agonist with potent anti-inflammatory activity.	Cannabidiol	54-57	peroxisome proliferator activated receptor gamma	Mus musculus	70-79
29495967-5	2018	VCE-004.8, an aminoquinone derivative of cannabidiol (CBD), is a dual PPARgamma and CB2 agonist with potent anti-inflammatory activity.	Cannabidiol	54-57	cannabinoid receptor 2 (macrophage)	Mus musculus	84-87
29467619-3	2018	We have studied the effects of cannabidiol (CBD) on the ability to produce long term potentiation (LTP) in stratum radiatum of CA1 region of the mouse hippocampus.	Cannabidiol	31-42	carbonic anhydrase 1	Mus musculus	127-130
29467619-3	2018	We have studied the effects of cannabidiol (CBD) on the ability to produce long term potentiation (LTP) in stratum radiatum of CA1 region of the mouse hippocampus.	Cannabidiol	44-47	carbonic anhydrase 1	Mus musculus	127-130
29274332-1	2018	Chronic GPR18 activation by its agonist abnormal cannabidiol (trans-4-[3-methyl-6-(1-methylethenyl)-2-cyclohexen-1-yl]-5-pentyl-1,3-benzenediol; abn-cbd) improves myocardial redox status and function in healthy rats.	Cannabidiol	49-60	G protein-coupled receptor 18	Rattus norvegicus	8-13
29450258-14	2018	The antinociceptive and anti-inflammatory effects of CBD were blocked by the 5-HT1A antagonist WAY100635.	Cannabidiol	53-56	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	77-83
29238589-8	2017	All these effects were significantly and concentration-dependently inhibited by cannabidiol, whose effects were completely abolished in the presence of the cannabinoid receptor type 1 (CB1) antagonist, AM251.	Cannabidiol	80-91	cannabinoid receptor 1	Homo sapiens	185-188
28945920-8	2017	Cannabidiol, an activator of TRPV2 and TRPV4 channels, induced moderate Ca2+ -influxes, inhibited by both tranilast and HC067047, blockers of TRPV2 and TRPV4 channels respectively.	Cannabidiol	0-11	transient receptor potential cation channel subfamily V member 2	Homo sapiens	29-34
28945920-8	2017	Cannabidiol, an activator of TRPV2 and TRPV4 channels, induced moderate Ca2+ -influxes, inhibited by both tranilast and HC067047, blockers of TRPV2 and TRPV4 channels respectively.	Cannabidiol	0-11	transient receptor potential cation channel subfamily V member 4	Homo sapiens	39-44
28945920-8	2017	Cannabidiol, an activator of TRPV2 and TRPV4 channels, induced moderate Ca2+ -influxes, inhibited by both tranilast and HC067047, blockers of TRPV2 and TRPV4 channels respectively.	Cannabidiol	0-11	transient receptor potential cation channel subfamily V member 2	Homo sapiens	142-147
28945920-8	2017	Cannabidiol, an activator of TRPV2 and TRPV4 channels, induced moderate Ca2+ -influxes, inhibited by both tranilast and HC067047, blockers of TRPV2 and TRPV4 channels respectively.	Cannabidiol	0-11	transient receptor potential cation channel subfamily V member 4	Homo sapiens	152-157
29238589-9	2017	Conclusions: Cannabidiol improved Clostridium difficile toxin A-induced damage in Caco-2 cells, by inhibiting the apoptotic process and restoring the intestinal barrier integrity, through the involvement of the CB1 receptor.	Cannabidiol	13-24	cannabinoid receptor 1	Homo sapiens	211-214
28736128-13	2017	The extra augmentation in the absorption of CBD and THC by incorporating piperine into PNL is attributed to the inhibition of Phase I and phase II metabolism by piperine in addition to the Phase I metabolism and P-gp inhibition by PNL.	Cannabidiol	44-47	phosphoglycolate phosphatase	Rattus norvegicus	212-216
28888984-0	2017	Cannabidiol, a novel inverse agonist for GPR12.	Cannabidiol	0-11	G protein-coupled receptor 12	Homo sapiens	41-46
28888984-4	2017	Our data demonstrate that cannabidiol (CBD), a major non-psychoactive phytocannabinoid, acted as an inverse agonist to inhibit cAMP accumulation stimulated by the constitutively active GPR12.	Cannabidiol	26-37	G protein-coupled receptor 12	Homo sapiens	185-190
28888984-4	2017	Our data demonstrate that cannabidiol (CBD), a major non-psychoactive phytocannabinoid, acted as an inverse agonist to inhibit cAMP accumulation stimulated by the constitutively active GPR12.	Cannabidiol	39-42	G protein-coupled receptor 12	Homo sapiens	185-190
28888984-6	2017	The structure-activity relationship studies of CBD indicate that both the free hydroxyl and the pentyl side chain are crucial for the effects of CBD on GPR12.	Cannabidiol	47-50	G protein-coupled receptor 12	Homo sapiens	152-157
28888984-6	2017	The structure-activity relationship studies of CBD indicate that both the free hydroxyl and the pentyl side chain are crucial for the effects of CBD on GPR12.	Cannabidiol	145-148	G protein-coupled receptor 12	Homo sapiens	152-157
28888984-9	2017	Since we have demonstrated that CBD is an inverse agonist for GPR12, this provides novel mechanism of action for CBD, and an initial chemical scaffold upon which highly potent and efficacious agents acting on GPR12 may be developed with the ultimate goal of blocking cancer metastasis.	Cannabidiol	32-35	G protein-coupled receptor 12	Homo sapiens	62-67
28888984-9	2017	Since we have demonstrated that CBD is an inverse agonist for GPR12, this provides novel mechanism of action for CBD, and an initial chemical scaffold upon which highly potent and efficacious agents acting on GPR12 may be developed with the ultimate goal of blocking cancer metastasis.	Cannabidiol	32-35	G protein-coupled receptor 12	Homo sapiens	209-214
29109685-0	2017	Binding and Signaling Studies Disclose a Potential Allosteric Site for Cannabidiol in Cannabinoid CB2 Receptors.	Cannabidiol	71-82	cannabinoid receptor 2	Homo sapiens	98-101
28973916-2	2017	Here we show that cannabidiol (CBD) effectively reduced seizures and autistic-like social deficits in a well-validated mouse genetic model of Dravet syndrome (DS), a severe childhood epilepsy disorder caused by loss-of-function mutations in the brain voltage-gated sodium channel NaV1.1.	Cannabidiol	18-29	sodium channel, voltage-gated, type I, alpha	Mus musculus	280-286
28973916-2	2017	Here we show that cannabidiol (CBD) effectively reduced seizures and autistic-like social deficits in a well-validated mouse genetic model of Dravet syndrome (DS), a severe childhood epilepsy disorder caused by loss-of-function mutations in the brain voltage-gated sodium channel NaV1.1.	Cannabidiol	31-34	sodium channel, voltage-gated, type I, alpha	Mus musculus	280-286
28973916-7	2017	The beneficial effects of CBD on inhibitory neurotransmission were mimicked and occluded by an antagonist of GPR55, suggesting that therapeutic effects of CBD are mediated through this lipid-activated G protein-coupled receptor.	Cannabidiol	26-29	G protein-coupled receptor 55	Mus musculus	109-114
28973916-7	2017	The beneficial effects of CBD on inhibitory neurotransmission were mimicked and occluded by an antagonist of GPR55, suggesting that therapeutic effects of CBD are mediated through this lipid-activated G protein-coupled receptor.	Cannabidiol	155-158	G protein-coupled receptor 55	Mus musculus	109-114
28981597-7	2017	In PC12 cells, Abeta-induced tau protein hyperphosphorylation is inhibited by CBD.	Cannabidiol	78-81	amyloid beta precursor protein	Rattus norvegicus	15-20
28981597-11	2017	CBD suppresses, through activation of PPARgamma, pro-inflammatory signaling and may be a potential new candidate for AD therapy.	Cannabidiol	0-3	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	38-47
28601556-4	2017	The mRNA levels of microphthalmia-associated transcription factor (MITF), tyrosinase, tyrosinase-related protein (TRP) 1, and TRP2 were increased following cannabidiol treatment.	Cannabidiol	156-167	tyrosinase related protein 1	Homo sapiens	86-120
28888984-9	2017	Since we have demonstrated that CBD is an inverse agonist for GPR12, this provides novel mechanism of action for CBD, and an initial chemical scaffold upon which highly potent and efficacious agents acting on GPR12 may be developed with the ultimate goal of blocking cancer metastasis.	Cannabidiol	113-116	G protein-coupled receptor 12	Homo sapiens	62-67
28754373-0	2017	Cannabidiol disrupts the consolidation of specific and generalized fear memories via dorsal hippocampus CB1 and CB2 receptors.	Cannabidiol	0-11	cannabinoid receptor 1	Homo sapiens	104-107
28754373-0	2017	Cannabidiol disrupts the consolidation of specific and generalized fear memories via dorsal hippocampus CB1 and CB2 receptors.	Cannabidiol	0-11	cannabinoid receptor 2	Homo sapiens	112-115
28601556-0	2017	Cannabidiol upregulates melanogenesis through CB1 dependent pathway by activating p38 MAPK and p42/44 MAPK.	Cannabidiol	0-11	cannabinoid receptor 1	Homo sapiens	46-49
28601556-0	2017	Cannabidiol upregulates melanogenesis through CB1 dependent pathway by activating p38 MAPK and p42/44 MAPK.	Cannabidiol	0-11	cyclin dependent kinase 20	Homo sapiens	95-98
28601556-3	2017	We found that cannabidiol increased both melanin content and tyrosinase activity.	Cannabidiol	14-25	tyrosinase	Homo sapiens	61-71
28601556-4	2017	The mRNA levels of microphthalmia-associated transcription factor (MITF), tyrosinase, tyrosinase-related protein (TRP) 1, and TRP2 were increased following cannabidiol treatment.	Cannabidiol	156-167	melanocyte inducing transcription factor	Homo sapiens	19-65
28601556-4	2017	The mRNA levels of microphthalmia-associated transcription factor (MITF), tyrosinase, tyrosinase-related protein (TRP) 1, and TRP2 were increased following cannabidiol treatment.	Cannabidiol	156-167	melanocyte inducing transcription factor	Homo sapiens	67-71
28601556-4	2017	The mRNA levels of microphthalmia-associated transcription factor (MITF), tyrosinase, tyrosinase-related protein (TRP) 1, and TRP2 were increased following cannabidiol treatment.	Cannabidiol	156-167	dopachrome tautomerase	Homo sapiens	126-130
28601556-5	2017	Likewise, cannabidiol increased the protein levels of MITF, TRP 1, TRP 2, and tyrosinase.	Cannabidiol	10-21	melanocyte inducing transcription factor	Homo sapiens	54-58
28601556-5	2017	Likewise, cannabidiol increased the protein levels of MITF, TRP 1, TRP 2, and tyrosinase.	Cannabidiol	10-21	tyrosinase related protein 1	Homo sapiens	60-65
28601556-5	2017	Likewise, cannabidiol increased the protein levels of MITF, TRP 1, TRP 2, and tyrosinase.	Cannabidiol	10-21	dopachrome tautomerase	Homo sapiens	67-72
28601556-4	2017	The mRNA levels of microphthalmia-associated transcription factor (MITF), tyrosinase, tyrosinase-related protein (TRP) 1, and TRP2 were increased following cannabidiol treatment.	Cannabidiol	156-167	tyrosinase	Homo sapiens	74-84
28601556-5	2017	Likewise, cannabidiol increased the protein levels of MITF, TRP 1, TRP 2, and tyrosinase.	Cannabidiol	10-21	tyrosinase	Homo sapiens	78-88
28601556-6	2017	Mechanistically, we found that cannabidiol regulated melanogenesis by upregulating MITF through phosphorylation of p38 mitogen-activated protein kinase (MAPK) and p42/44 MAPK, independent of cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) signaling.	Cannabidiol	31-42	melanocyte inducing transcription factor	Homo sapiens	83-87
28601556-6	2017	Mechanistically, we found that cannabidiol regulated melanogenesis by upregulating MITF through phosphorylation of p38 mitogen-activated protein kinase (MAPK) and p42/44 MAPK, independent of cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) signaling.	Cannabidiol	31-42	mitogen-activated protein kinase 14	Homo sapiens	115-151
28601556-6	2017	Mechanistically, we found that cannabidiol regulated melanogenesis by upregulating MITF through phosphorylation of p38 mitogen-activated protein kinase (MAPK) and p42/44 MAPK, independent of cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) signaling.	Cannabidiol	31-42	cyclin dependent kinase 20	Homo sapiens	163-166
28601556-7	2017	In addition, the melanogenic effect of cannabidiol was found to be mediated by cannabinoid CB1 receptor, not by CB2 receptor.	Cannabidiol	39-50	cannabinoid receptor 1	Homo sapiens	91-94
28601556-8	2017	Taken together, these findings indicate that cannabidiol-induced melanogenesis is cannabinoid CB1 receptor-dependent, and cannabidiol induces melanogenesis through increasing MITF gene expression which is mediated by activation of p38 MAPK and p42/44 MAPK.	Cannabidiol	45-56	cannabinoid receptor 1	Homo sapiens	94-97
28601556-8	2017	Taken together, these findings indicate that cannabidiol-induced melanogenesis is cannabinoid CB1 receptor-dependent, and cannabidiol induces melanogenesis through increasing MITF gene expression which is mediated by activation of p38 MAPK and p42/44 MAPK.	Cannabidiol	122-133	melanocyte inducing transcription factor	Homo sapiens	175-179
28601556-8	2017	Taken together, these findings indicate that cannabidiol-induced melanogenesis is cannabinoid CB1 receptor-dependent, and cannabidiol induces melanogenesis through increasing MITF gene expression which is mediated by activation of p38 MAPK and p42/44 MAPK.	Cannabidiol	122-133	cyclin dependent kinase 20	Homo sapiens	244-247
28087250-5	2017	In contrast to  9-THC, CBD has low affinity for CB1 and CB2 receptors and other targets have been investigated to explain its anticonvulsant properties including TRPV1, voltage gated potassium and sodium channels, and GPR55, among others.	Cannabidiol	23-26	cannabinoid receptor 1	Homo sapiens	48-51
29088769-4	2017	We emphasized three main aspects of signaling mechanisms induced by CBD treatment (alone or in combination with gamma-irradiation) in human GBM that govern cell death: 1) CBD significantly upregulated the active (phosphorylated) JNK1/2 and MAPK p38 levels with the subsequent downregulation of the active phospho-ERK1/2 and phospho-AKT1 levels.	Cannabidiol	68-71	mitogen-activated protein kinase 8	Homo sapiens	229-235
29088769-4	2017	We emphasized three main aspects of signaling mechanisms induced by CBD treatment (alone or in combination with gamma-irradiation) in human GBM that govern cell death: 1) CBD significantly upregulated the active (phosphorylated) JNK1/2 and MAPK p38 levels with the subsequent downregulation of the active phospho-ERK1/2 and phospho-AKT1 levels.	Cannabidiol	68-71	mitogen-activated protein kinase 14	Homo sapiens	245-248
29088769-4	2017	We emphasized three main aspects of signaling mechanisms induced by CBD treatment (alone or in combination with gamma-irradiation) in human GBM that govern cell death: 1) CBD significantly upregulated the active (phosphorylated) JNK1/2 and MAPK p38 levels with the subsequent downregulation of the active phospho-ERK1/2 and phospho-AKT1 levels.	Cannabidiol	68-71	AKT serine/threonine kinase 1	Homo sapiens	332-336
29088769-5	2017	MAPK p38 was one of the main drivers of CBD-induced cell death, while death levels after combined treatment of CBD and radiation were dependent on both MAPK p38 and JNK.	Cannabidiol	40-43	mitogen-activated protein kinase 14	Homo sapiens	5-8
29088769-5	2017	MAPK p38 was one of the main drivers of CBD-induced cell death, while death levels after combined treatment of CBD and radiation were dependent on both MAPK p38 and JNK.	Cannabidiol	111-114	mitogen-activated protein kinase 14	Homo sapiens	157-160
29088769-5	2017	MAPK p38 was one of the main drivers of CBD-induced cell death, while death levels after combined treatment of CBD and radiation were dependent on both MAPK p38 and JNK.	Cannabidiol	111-114	mitogen-activated protein kinase 8	Homo sapiens	165-168
28087250-5	2017	In contrast to  9-THC, CBD has low affinity for CB1 and CB2 receptors and other targets have been investigated to explain its anticonvulsant properties including TRPV1, voltage gated potassium and sodium channels, and GPR55, among others.	Cannabidiol	23-26	cannabinoid receptor 2	Homo sapiens	56-59
28013001-3	2017	In this study, we investigated the impact of three natural compounds, cyclosporine A (CsA), deoxynivalenol (DON) and cannabidiol (CBD) on mitochondrial functions in the THP-1 monocytic cell line.	Cannabidiol	117-128	GLI family zinc finger 2	Homo sapiens	169-174
27889412-4	2017	In addition, ischemic mice treated with CBD exhibited an increase in the hippocampal brain derived neurotrophic factor (BDNF) protein levels.	Cannabidiol	40-43	brain derived neurotrophic factor	Mus musculus	85-118
27889412-4	2017	In addition, ischemic mice treated with CBD exhibited an increase in the hippocampal brain derived neurotrophic factor (BDNF) protein levels.	Cannabidiol	40-43	brain derived neurotrophic factor	Mus musculus	120-124
27471947-6	2017	The phytocannabinoid cannabidiol (CBD) possesses neuroprotective, antioxidant and anti-inflammatory properties and reduces amyloid-beta production and tau hyperphosphorylation in vitro.	Cannabidiol	21-32	amyloid beta precursor protein	Homo sapiens	123-135
27471947-6	2017	The phytocannabinoid cannabidiol (CBD) possesses neuroprotective, antioxidant and anti-inflammatory properties and reduces amyloid-beta production and tau hyperphosphorylation in vitro.	Cannabidiol	21-32	microtubule associated protein tau	Homo sapiens	151-154
27471947-6	2017	The phytocannabinoid cannabidiol (CBD) possesses neuroprotective, antioxidant and anti-inflammatory properties and reduces amyloid-beta production and tau hyperphosphorylation in vitro.	Cannabidiol	34-37	amyloid beta precursor protein	Homo sapiens	123-135
27471947-6	2017	The phytocannabinoid cannabidiol (CBD) possesses neuroprotective, antioxidant and anti-inflammatory properties and reduces amyloid-beta production and tau hyperphosphorylation in vitro.	Cannabidiol	34-37	microtubule associated protein tau	Homo sapiens	151-154
28392768-9	2017	Cannabidiol reduced phosphorylation of mTOR, PKB and S6 pathways related to survival and cell size.	Cannabidiol	0-11	mechanistic target of rapamycin kinase	Homo sapiens	39-43
28392768-9	2017	Cannabidiol reduced phosphorylation of mTOR, PKB and S6 pathways related to survival and cell size.	Cannabidiol	0-11	AKT serine/threonine kinase 1	Homo sapiens	45-48
28539998-13	2017	CONCLUSION: The results of this study indicate that cannabidiol reduced cerebral infarction possibly through diminishing TNFR1/NF-kappaB-induced neurotoxicity in transient focal cerebral ischemia.	Cannabidiol	52-63	TNF receptor superfamily member 1A	Rattus norvegicus	121-126
28490996-0	2017	Cannabidiol in Patients With Intractable Epilepsy Due to TSC: A Possible Medication But Not a Miracle.	Cannabidiol	0-11	TSC complex subunit 1	Homo sapiens	57-60
27865421-6	2017	Most importantly, the Us/o+CBD-induced CD4+CD25+ Tregs robustly suppressed responder T cell proliferation, demonstrating that the mechanism by which CBD is immunosuppressive under low-level T cell stimulation involves induction of functional Tregs.	Cannabidiol	27-30	CD4 antigen	Mus musculus	39-42
27865421-6	2017	Most importantly, the Us/o+CBD-induced CD4+CD25+ Tregs robustly suppressed responder T cell proliferation, demonstrating that the mechanism by which CBD is immunosuppressive under low-level T cell stimulation involves induction of functional Tregs.	Cannabidiol	27-30	interleukin 2 receptor, alpha chain	Mus musculus	43-47
28013001-3	2017	In this study, we investigated the impact of three natural compounds, cyclosporine A (CsA), deoxynivalenol (DON) and cannabidiol (CBD) on mitochondrial functions in the THP-1 monocytic cell line.	Cannabidiol	130-133	GLI family zinc finger 2	Homo sapiens	169-174
27856160-0	2017	Anti-excitotoxic effects of cannabidiol are partly mediated by enhancement of NCX2 and NCX3 expression in animal model of cerebral ischemia.	Cannabidiol	28-39	solute carrier family 8 member A2	Rattus norvegicus	78-82
27856160-0	2017	Anti-excitotoxic effects of cannabidiol are partly mediated by enhancement of NCX2 and NCX3 expression in animal model of cerebral ischemia.	Cannabidiol	28-39	solute carrier family 8 member A3	Rattus norvegicus	87-91
27856160-11	2017	Up-regulation of NCX2 and NCX3 in cannabidiol-received groups was also observed.	Cannabidiol	34-45	solute carrier family 8 member A2	Rattus norvegicus	17-21
27856160-11	2017	Up-regulation of NCX2 and NCX3 in cannabidiol-received groups was also observed.	Cannabidiol	34-45	solute carrier family 8 member A3	Rattus norvegicus	26-30
27677765-1	2016	AIMS/HYPOTHESIS: Abnormal cannabidiol (Abn-CBD) and AS-1269574 are potent selective agonists for GPR55 and GPR119, respectively.	Cannabidiol	26-37	G protein-coupled receptor 55	Mus musculus	97-102
28872345-0	2017	Intra-cerebral cannabidiol infusion-induced neuroprotection is partly associated with the TNF-alpha/TNFR1/NF-kB pathway in transient focal cerebral ischaemia.	Cannabidiol	15-26	tumor necrosis factor	Rattus norvegicus	90-99
28872345-0	2017	Intra-cerebral cannabidiol infusion-induced neuroprotection is partly associated with the TNF-alpha/TNFR1/NF-kB pathway in transient focal cerebral ischaemia.	Cannabidiol	15-26	TNF receptor superfamily member 1A	Rattus norvegicus	100-105
28872345-0	2017	Intra-cerebral cannabidiol infusion-induced neuroprotection is partly associated with the TNF-alpha/TNFR1/NF-kB pathway in transient focal cerebral ischaemia.	Cannabidiol	15-26	nuclear factor kappa B subunit 1	Rattus norvegicus	106-111
28412920-7	2017	CONCLUSION: THC and CBD are metabolized mainly in the liver by cytochrome P-450 isoenzymes (mainly CYP2Cs and CYP3A4).	Cannabidiol	20-23	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	110-116
28412920-8	2017	In vitro studies indicate that THC and CBD both inhibit CYP1A1, 1A2 and 1B1 enzymes, and recent studies have indicated that CBD is also a potent inhibitor of CYP2C19 and CYP3A4.	Cannabidiol	39-42	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	56-62
28412920-8	2017	In vitro studies indicate that THC and CBD both inhibit CYP1A1, 1A2 and 1B1 enzymes, and recent studies have indicated that CBD is also a potent inhibitor of CYP2C19 and CYP3A4.	Cannabidiol	124-127	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	56-62
28412920-8	2017	In vitro studies indicate that THC and CBD both inhibit CYP1A1, 1A2 and 1B1 enzymes, and recent studies have indicated that CBD is also a potent inhibitor of CYP2C19 and CYP3A4.	Cannabidiol	124-127	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	158-165
28412920-8	2017	In vitro studies indicate that THC and CBD both inhibit CYP1A1, 1A2 and 1B1 enzymes, and recent studies have indicated that CBD is also a potent inhibitor of CYP2C19 and CYP3A4.	Cannabidiol	124-127	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	170-176
27890794-0	2017	Target regulation of PI3K/Akt/mTOR pathway by cannabidiol in treatment of experimental multiple sclerosis.	Cannabidiol	46-57	thymoma viral proto-oncogene 1	Mus musculus	26-29
27890794-0	2017	Target regulation of PI3K/Akt/mTOR pathway by cannabidiol in treatment of experimental multiple sclerosis.	Cannabidiol	46-57	mechanistic target of rapamycin kinase	Mus musculus	30-34
27890794-1	2017	This study was aimed to investigate whether treatment with purified cannabidiol (CBD) may counteract the development of experimental multiple sclerosis (MS), by targeting the PI3K/Akt/mTOR pathway.	Cannabidiol	68-79	thymoma viral proto-oncogene 1	Mus musculus	180-183
27890794-1	2017	This study was aimed to investigate whether treatment with purified cannabidiol (CBD) may counteract the development of experimental multiple sclerosis (MS), by targeting the PI3K/Akt/mTOR pathway.	Cannabidiol	68-79	mechanistic target of rapamycin kinase	Mus musculus	184-188
27890794-1	2017	This study was aimed to investigate whether treatment with purified cannabidiol (CBD) may counteract the development of experimental multiple sclerosis (MS), by targeting the PI3K/Akt/mTOR pathway.	Cannabidiol	81-84	thymoma viral proto-oncogene 1	Mus musculus	180-183
27890794-1	2017	This study was aimed to investigate whether treatment with purified cannabidiol (CBD) may counteract the development of experimental multiple sclerosis (MS), by targeting the PI3K/Akt/mTOR pathway.	Cannabidiol	81-84	mechanistic target of rapamycin kinase	Mus musculus	184-188
27890794-8	2017	Also, an increased level of BNDF in CBD-treated mice seems to be involved in the activation of PI3K/Akt/mTOR pathway.	Cannabidiol	36-39	thymoma viral proto-oncogene 1	Mus musculus	100-103
27890794-8	2017	Also, an increased level of BNDF in CBD-treated mice seems to be involved in the activation of PI3K/Akt/mTOR pathway.	Cannabidiol	36-39	mechanistic target of rapamycin kinase	Mus musculus	104-108
27890794-11	2017	These results provide an interesting discovery about the regulation of the PI3K/Akt/mTOR pathway by cannabidiol administration, that could be a new potential therapeutic target for MS management.	Cannabidiol	100-111	thymoma viral proto-oncogene 1	Mus musculus	80-83
27890794-11	2017	These results provide an interesting discovery about the regulation of the PI3K/Akt/mTOR pathway by cannabidiol administration, that could be a new potential therapeutic target for MS management.	Cannabidiol	100-111	mechanistic target of rapamycin kinase	Mus musculus	84-88
27676325-2	2017	In this study, after demonstrating GPR18 expression in the heart, we show that chronic (2 weeks) GPR18 activation with its agonist abnormal cannabidiol (abn-cbd; 100 microg kg d; i.p) produced hypotension, suppressed the cardiac sympathetic dominance, and improved left ventricular (LV) function (increased the contractility index dp/dtmax and reduced LV end-diastolic pressure, LVEDP) in conscious rats.	Cannabidiol	140-151	G protein-coupled receptor 18	Rattus norvegicus	97-102
28025562-5	2016	By comparing the expression profiles between GMSCs treated with CBD (CBD-GMSCs) and control GMSCs (CTR-GMSCs), we found that CBD led to the downregulation of genes linked to AD, including genes coding for the kinases responsible of tau phosphorylation and for the secretases involved in Abeta generation.	Cannabidiol	64-67	microtubule associated protein tau	Homo sapiens	232-235
28025562-6	2016	In parallel, immunocytochemistry analysis has shown that CBD inhibited the expression of GSK3beta, a central player in AD pathogenesis, by promoting PI3K/Akt signalling.	Cannabidiol	57-60	glycogen synthase kinase 3 alpha	Homo sapiens	89-97
28025562-6	2016	In parallel, immunocytochemistry analysis has shown that CBD inhibited the expression of GSK3beta, a central player in AD pathogenesis, by promoting PI3K/Akt signalling.	Cannabidiol	57-60	AKT serine/threonine kinase 1	Homo sapiens	154-157
28025562-8	2016	Here, we have proved that TRPV1 was able to mediate the modulatory effect of CBD on the PI3K/Akt/GSK3beta axis.	Cannabidiol	77-80	transient receptor potential cation channel subfamily V member 1	Homo sapiens	26-31
28025562-8	2016	Here, we have proved that TRPV1 was able to mediate the modulatory effect of CBD on the PI3K/Akt/GSK3beta axis.	Cannabidiol	77-80	AKT serine/threonine kinase 1	Homo sapiens	93-96
28025562-8	2016	Here, we have proved that TRPV1 was able to mediate the modulatory effect of CBD on the PI3K/Akt/GSK3beta axis.	Cannabidiol	77-80	glycogen synthase kinase 3 alpha	Homo sapiens	97-105
28025562-9	2016	In conclusion, we have found that pre-treatment with CBD prevented the expression of proteins potentially involved in tau phosphorylation and Abeta production in GMSCs.	Cannabidiol	53-56	microtubule associated protein tau	Homo sapiens	118-121
27561953-9	2016	In contrast, while the putative endogenous GPR55 agonist lysophosphatidylinositol (LPI, 5 microM) and the GPR55 antagonist cannabidiol (CBD, 1 microM) also elevated [Ca2+ ]i and insulin secretion, these effects were sustained in islets from GPR55 -/- mice.	Cannabidiol	123-134	G protein-coupled receptor 55	Mus musculus	106-111
27561953-9	2016	In contrast, while the putative endogenous GPR55 agonist lysophosphatidylinositol (LPI, 5 microM) and the GPR55 antagonist cannabidiol (CBD, 1 microM) also elevated [Ca2+ ]i and insulin secretion, these effects were sustained in islets from GPR55 -/- mice.	Cannabidiol	123-134	insulin	Homo sapiens	178-185
27561953-9	2016	In contrast, while the putative endogenous GPR55 agonist lysophosphatidylinositol (LPI, 5 microM) and the GPR55 antagonist cannabidiol (CBD, 1 microM) also elevated [Ca2+ ]i and insulin secretion, these effects were sustained in islets from GPR55 -/- mice.	Cannabidiol	123-134	G protein-coupled receptor 55	Mus musculus	106-111
27561953-9	2016	In contrast, while the putative endogenous GPR55 agonist lysophosphatidylinositol (LPI, 5 microM) and the GPR55 antagonist cannabidiol (CBD, 1 microM) also elevated [Ca2+ ]i and insulin secretion, these effects were sustained in islets from GPR55 -/- mice.	Cannabidiol	136-139	G protein-coupled receptor 55	Mus musculus	106-111
27561953-9	2016	In contrast, while the putative endogenous GPR55 agonist lysophosphatidylinositol (LPI, 5 microM) and the GPR55 antagonist cannabidiol (CBD, 1 microM) also elevated [Ca2+ ]i and insulin secretion, these effects were sustained in islets from GPR55 -/- mice.	Cannabidiol	136-139	insulin	Homo sapiens	178-185
27561953-9	2016	In contrast, while the putative endogenous GPR55 agonist lysophosphatidylinositol (LPI, 5 microM) and the GPR55 antagonist cannabidiol (CBD, 1 microM) also elevated [Ca2+ ]i and insulin secretion, these effects were sustained in islets from GPR55 -/- mice.	Cannabidiol	136-139	G protein-coupled receptor 55	Mus musculus	106-111
27677765-1	2016	AIMS/HYPOTHESIS: Abnormal cannabidiol (Abn-CBD) and AS-1269574 are potent selective agonists for GPR55 and GPR119, respectively.	Cannabidiol	26-37	G-protein coupled receptor 119	Mus musculus	107-113
26750641-4	2016	RESULTS: At 30 years, total incremental cost for THC/CBD plus SoC treatment was estimated at $3,836/patient (ICER: $10,891/quality-adjusted life year [QALY]).	Cannabidiol	53-56	cAMP responsive element modulator	Homo sapiens	109-113
27794115-4	2016	RESULTS: 3H-THK5351 was able to bind to tau deposits in the postmortem brain with CBD.	Cannabidiol	82-85	microtubule associated protein tau	Homo sapiens	40-43
27296152-10	2016	Our findings demonstrate a novel NAc VTA circuit responsible for the behavioral and neuronal effects of CBD within the mesolimbic system via functional interactions with serotonergic 5-HT1A receptor signaling.	Cannabidiol	104-107	5-hydroxytryptamine receptor 1A	Rattus norvegicus	183-189
27567873-1	2016	Previous reports have demonstrated that the combination of Delta9-tetrahydrocannabinol (Delta9-THC) and cannabidiol (CBD) botanical extracts, which are the components of an already approved cannabis-based medicine, reduce the Alzheimer-like phenotype of AbetaPP/PS1 transgenic mice when chronically administered during the early symptomatic stage.	Cannabidiol	104-115	presenilin 1	Mus musculus	262-265
27567873-1	2016	Previous reports have demonstrated that the combination of Delta9-tetrahydrocannabinol (Delta9-THC) and cannabidiol (CBD) botanical extracts, which are the components of an already approved cannabis-based medicine, reduce the Alzheimer-like phenotype of AbetaPP/PS1 transgenic mice when chronically administered during the early symptomatic stage.	Cannabidiol	117-120	presenilin 1	Mus musculus	262-265
27567873-4	2016	The positive effects induced by Delta9-THC and CBD in aged AbetaPP/PS1 mice are associated with reduced GluR2/3 and increased levels of GABA-A Ralpha1 in cannabinoid-treated animals when compared with animals treated with vehicle alone.	Cannabidiol	47-50	presenilin 1	Mus musculus	67-70
27567873-4	2016	The positive effects induced by Delta9-THC and CBD in aged AbetaPP/PS1 mice are associated with reduced GluR2/3 and increased levels of GABA-A Ralpha1 in cannabinoid-treated animals when compared with animals treated with vehicle alone.	Cannabidiol	47-50	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	104-109
27567873-4	2016	The positive effects induced by Delta9-THC and CBD in aged AbetaPP/PS1 mice are associated with reduced GluR2/3 and increased levels of GABA-A Ralpha1 in cannabinoid-treated animals when compared with animals treated with vehicle alone.	Cannabidiol	47-50	gamma-aminobutyric acid (GABA) A receptor, subunit alpha 1	Mus musculus	136-150
27430346-9	2016	In addition, cannabidiol reduced caspase-3 gene expression and augmented the Bcl-2 protein expression levels in the nucleus pulposus cells following H2O2 exposure.	Cannabidiol	13-24	caspase 3	Rattus norvegicus	33-42
27430346-9	2016	In addition, cannabidiol reduced caspase-3 gene expression and augmented the Bcl-2 protein expression levels in the nucleus pulposus cells following H2O2 exposure.	Cannabidiol	13-24	BCL2, apoptosis regulator	Rattus norvegicus	77-82
27430346-10	2016	Pre-treatment with cannabidiol suppressed the promotion of COX-2, iNOS, IL-1beta and IL-6 expression in the nucleus pulposus cells following H2O2 exposure.	Cannabidiol	19-30	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	59-64
27430346-10	2016	Pre-treatment with cannabidiol suppressed the promotion of COX-2, iNOS, IL-1beta and IL-6 expression in the nucleus pulposus cells following H2O2 exposure.	Cannabidiol	19-30	nitric oxide synthase 2	Rattus norvegicus	66-70
27430346-10	2016	Pre-treatment with cannabidiol suppressed the promotion of COX-2, iNOS, IL-1beta and IL-6 expression in the nucleus pulposus cells following H2O2 exposure.	Cannabidiol	19-30	interleukin 1 beta	Rattus norvegicus	72-80
27430346-10	2016	Pre-treatment with cannabidiol suppressed the promotion of COX-2, iNOS, IL-1beta and IL-6 expression in the nucleus pulposus cells following H2O2 exposure.	Cannabidiol	19-30	interleukin 6	Rattus norvegicus	85-89
27289270-1	2016	BACKGROUND: Cannabidiol, a therapeutic with potential serotonin (5-hydroxytryptamine; 5-HT) 5-HT1A receptor agonist activity, is the second most prevalent cannabinoid in Cannabis after Delta(9)-THC.	Cannabidiol	12-23	5-hydroxytryptamine receptor 1A	Macaca mulatta	92-98
27131780-0	2016	Cannabidiol attenuates haloperidol-induced catalepsy and c-Fos protein expression in the dorsolateral striatum via 5-HT1A receptors in mice.	Cannabidiol	0-11	FBJ osteosarcoma oncogene	Mus musculus	57-62
27131780-0	2016	Cannabidiol attenuates haloperidol-induced catalepsy and c-Fos protein expression in the dorsolateral striatum via 5-HT1A receptors in mice.	Cannabidiol	0-11	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	115-121
27131780-4	2016	To further investigate this latter effect, we tested whether CBD (15-60mg/kg) would attenuate the catalepsy and c-Fos protein expression in the dorsal striatum induced by haloperidol (0.6mg/kg).	Cannabidiol	61-64	FBJ osteosarcoma oncogene	Mus musculus	112-117
27131780-10	2016	Haloperidol also increased c-Fos protein expression in the dorsolateral striatum, an effect attenuated by previous CBD administration.	Cannabidiol	115-118	FBJ osteosarcoma oncogene	Mus musculus	27-32
27267376-0	2016	Aberrant epilepsy-associated mutant Nav1.6 sodium channel activity can be targeted with cannabidiol.	Cannabidiol	88-99	neuron navigator 1	Homo sapiens	36-40
27267376-9	2016	Interestingly, we found that cannabidiol can preferentially target resurgent sodium currents over peak transient currents generated by wild-type Nav1.6 as well as the aberrant resurgent and persistent current generated by Nav1.6 mutant channels.	Cannabidiol	29-40	neuron navigator 1	Homo sapiens	145-149
27147666-0	2016	Cannabidiol Counteracts Amphetamine-Induced Neuronal and Behavioral Sensitization of the Mesolimbic Dopamine Pathway through a Novel mTOR/p70S6 Kinase Signaling Pathway.	Cannabidiol	0-11	mechanistic target of rapamycin kinase	Rattus norvegicus	133-137
27462203-10	2016	Individually, the hypothermia and the cannabidiol treatments reduced the glutamate/Nacetyl-aspartate ratio, as well as TNFalpha and oxidized protein levels in newborn piglets subjected to hypoxic-ischemic insult.	Cannabidiol	38-49	tumor necrosis factor	Homo sapiens	119-127
27215129-5	2016	Our results show that the cannabidiol (5muM) and moringin (5muM) combination outperformed the single constituents that, at this dosage had only a moderate efficacy on inflammatory (Tumor necrosis factor-alpha, Interleukin-10) and oxidative markers (inducible nitric oxide synthase, nuclear factor erythroid 2-related factor 2, nitrotyrosine).	Cannabidiol	26-37	tumor necrosis factor	Mus musculus	181-208
27215129-5	2016	Our results show that the cannabidiol (5muM) and moringin (5muM) combination outperformed the single constituents that, at this dosage had only a moderate efficacy on inflammatory (Tumor necrosis factor-alpha, Interleukin-10) and oxidative markers (inducible nitric oxide synthase, nuclear factor erythroid 2-related factor 2, nitrotyrosine).	Cannabidiol	26-37	interleukin 10	Mus musculus	210-224
27215129-6	2016	Significant upregulation of Bcl-2 and downregulation of Bax and cleaved caspase-3 was observed in cells treated with cannabidiol-moringin combination.	Cannabidiol	117-128	B cell leukemia/lymphoma 2	Mus musculus	28-33
27215129-6	2016	Significant upregulation of Bcl-2 and downregulation of Bax and cleaved caspase-3 was observed in cells treated with cannabidiol-moringin combination.	Cannabidiol	117-128	BCL2-associated X protein	Mus musculus	56-59
27256343-1	2016	BACKGROUND: Our previous studies showed that the non-psychoactive cannabinoid, cannabidiol (CBD), ameliorates the clinical symptoms in mouse myelin oligodendrocyte glycoprotein (MOG)35-55-induced experimental autoimmune encephalomyelitis model of multiple sclerosis (MS) as well as decreases the memory MOG35-55-specific T cell (TMOG) proliferation and cytokine secretion including IL-17, a key autoimmune factor.	Cannabidiol	79-90	myelin oligodendrocyte glycoprotein	Mus musculus	141-176
27256343-1	2016	BACKGROUND: Our previous studies showed that the non-psychoactive cannabinoid, cannabidiol (CBD), ameliorates the clinical symptoms in mouse myelin oligodendrocyte glycoprotein (MOG)35-55-induced experimental autoimmune encephalomyelitis model of multiple sclerosis (MS) as well as decreases the memory MOG35-55-specific T cell (TMOG) proliferation and cytokine secretion including IL-17, a key autoimmune factor.	Cannabidiol	79-90	myelin oligodendrocyte glycoprotein	Mus musculus	178-181
27256343-1	2016	BACKGROUND: Our previous studies showed that the non-psychoactive cannabinoid, cannabidiol (CBD), ameliorates the clinical symptoms in mouse myelin oligodendrocyte glycoprotein (MOG)35-55-induced experimental autoimmune encephalomyelitis model of multiple sclerosis (MS) as well as decreases the memory MOG35-55-specific T cell (TMOG) proliferation and cytokine secretion including IL-17, a key autoimmune factor.	Cannabidiol	79-90	interleukin 17A	Mus musculus	382-387
27256343-1	2016	BACKGROUND: Our previous studies showed that the non-psychoactive cannabinoid, cannabidiol (CBD), ameliorates the clinical symptoms in mouse myelin oligodendrocyte glycoprotein (MOG)35-55-induced experimental autoimmune encephalomyelitis model of multiple sclerosis (MS) as well as decreases the memory MOG35-55-specific T cell (TMOG) proliferation and cytokine secretion including IL-17, a key autoimmune factor.	Cannabidiol	92-95	myelin oligodendrocyte glycoprotein	Mus musculus	141-176
27256343-1	2016	BACKGROUND: Our previous studies showed that the non-psychoactive cannabinoid, cannabidiol (CBD), ameliorates the clinical symptoms in mouse myelin oligodendrocyte glycoprotein (MOG)35-55-induced experimental autoimmune encephalomyelitis model of multiple sclerosis (MS) as well as decreases the memory MOG35-55-specific T cell (TMOG) proliferation and cytokine secretion including IL-17, a key autoimmune factor.	Cannabidiol	92-95	myelin oligodendrocyte glycoprotein	Mus musculus	178-181
27256343-1	2016	BACKGROUND: Our previous studies showed that the non-psychoactive cannabinoid, cannabidiol (CBD), ameliorates the clinical symptoms in mouse myelin oligodendrocyte glycoprotein (MOG)35-55-induced experimental autoimmune encephalomyelitis model of multiple sclerosis (MS) as well as decreases the memory MOG35-55-specific T cell (TMOG) proliferation and cytokine secretion including IL-17, a key autoimmune factor.	Cannabidiol	92-95	interleukin 17A	Mus musculus	382-387
27147666-14	2016	Specifically, we report that CBD can attenuate both behavioral and dopaminergic neuronal correlates of mesolimbic dopaminergic sensitization, via a direct interaction with mTOR/p70S6 kinase signaling within the mesolimbic pathway.	Cannabidiol	29-32	mechanistic target of rapamycin kinase	Rattus norvegicus	172-176
26187374-9	2016	Moreover, repeated CBD administration at a lower dose (3 mg/kg) increased cell proliferation and neurogenesis, as seen by an increased number of Ki-67-, BrdU- and doublecortin (DCX)-positive cells in both in DG and SVZ.	Cannabidiol	19-22	doublecortin	Mus musculus	153-175
30323891-1	2018	Transient receptor potential vanilloid type-2 (TRPV2) is an ion channel that is triggered by agonists like cannabidiol (CBD).	Cannabidiol	107-118	transient receptor potential cation channel subfamily V member 2	Homo sapiens	0-45
30323891-1	2018	Transient receptor potential vanilloid type-2 (TRPV2) is an ion channel that is triggered by agonists like cannabidiol (CBD).	Cannabidiol	107-118	transient receptor potential cation channel subfamily V member 2	Homo sapiens	47-52
30323891-1	2018	Transient receptor potential vanilloid type-2 (TRPV2) is an ion channel that is triggered by agonists like cannabidiol (CBD).	Cannabidiol	120-123	transient receptor potential cation channel subfamily V member 2	Homo sapiens	0-45
30323891-1	2018	Transient receptor potential vanilloid type-2 (TRPV2) is an ion channel that is triggered by agonists like cannabidiol (CBD).	Cannabidiol	120-123	transient receptor potential cation channel subfamily V member 2	Homo sapiens	47-52
26801828-7	2016	Independent CBD-treated groups were pre-treated with WAY100635 (10, 30 nmol/side, 5-HT1A antagonist) or AM251 (10 pmol/side, CB1 antagonist) and submitted to the same tests.	Cannabidiol	12-15	5-hydroxytryptamine receptor 1A	Rattus norvegicus	82-88
26738731-9	2016	Moreover, the amount of Atg7, conjugation of Atg5/12, Atg12, and LC3II/LC3I ratio increased significantly in epileptic rats treated with repeated injections of cannabidiol.	Cannabidiol	160-171	autophagy related 7	Rattus norvegicus	24-28
26738731-9	2016	Moreover, the amount of Atg7, conjugation of Atg5/12, Atg12, and LC3II/LC3I ratio increased significantly in epileptic rats treated with repeated injections of cannabidiol.	Cannabidiol	160-171	autophagy related 5	Rattus norvegicus	45-49
26738731-9	2016	Moreover, the amount of Atg7, conjugation of Atg5/12, Atg12, and LC3II/LC3I ratio increased significantly in epileptic rats treated with repeated injections of cannabidiol.	Cannabidiol	160-171	autophagy related 12	Rattus norvegicus	54-59
26711860-0	2016	Cannabidiol induces rapid-acting antidepressant-like effects and enhances cortical 5-HT/glutamate neurotransmission: role of 5-HT1A receptors.	Cannabidiol	0-11	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	125-131
26711860-4	2016	For this purpose, we conducted behavioural (open field and sucrose preference tests) and neurochemical (microdialysis and autoradiography of 5-HT1A receptor functionality) studies following treatment with CBD.	Cannabidiol	205-208	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	141-156
26497782-0	2016	Cannabidiol protects an in vitro model of the blood-brain barrier from oxygen-glucose deprivation via PPARgamma and 5-HT1A receptors.	Cannabidiol	0-11	peroxisome proliferator activated receptor gamma	Homo sapiens	102-111
26187374-9	2016	Moreover, repeated CBD administration at a lower dose (3 mg/kg) increased cell proliferation and neurogenesis, as seen by an increased number of Ki-67-, BrdU- and doublecortin (DCX)-positive cells in both in DG and SVZ.	Cannabidiol	19-22	doublecortin	Mus musculus	177-180
26377899-3	2016	The aim of this study was to investigate whether CBD modulated the functional effects and c-Fos expression induced by THC, using a 1:1 dose ratio that approximates therapeutic strains of cannabis and nabiximols.	Cannabidiol	49-52	FBJ osteosarcoma oncogene	Mus musculus	90-95
26436760-7	2016	The inhibitory effects of CID16020046 or cannabidiol were averted by GPR55 siRNA knock down in cancer cells.	Cannabidiol	41-52	G protein-coupled receptor 55	Homo sapiens	69-74
26730399-8	2015	Moreover, a single intraocular injection of LPI increased branching in the DTN, whereas treatment with CBD, an antagonist of GPR55, decreased it.	Cannabidiol	103-106	G protein-coupled receptor 55	Mus musculus	125-130
26556726-0	2015	The neuroprotection of cannabidiol against MPP+-induced toxicity in PC12 cells involves trkA receptors, upregulation of axonal and synaptic proteins, neuritogenesis, and might be relevant to Parkinson"s disease.	Cannabidiol	23-34	neurotrophic receptor tyrosine kinase 1	Rattus norvegicus	88-92
26556726-9	2015	This is the first study to report the involvement of neuronal proteins and trkA in the neuroprotection of CBD.	Cannabidiol	106-109	neurotrophic receptor tyrosine kinase 1	Homo sapiens	75-79
26504004-3	2015	Results showed that a large number of genes belonging to the heat shock protein (HSP) super-family were up-regulated following treatment, specifically with CBD.	Cannabidiol	156-159	heat shock protein 90 beta family member 2, pseudogene	Homo sapiens	61-79
26504004-3	2015	Results showed that a large number of genes belonging to the heat shock protein (HSP) super-family were up-regulated following treatment, specifically with CBD.	Cannabidiol	156-159	heat shock protein 90 beta family member 2, pseudogene	Homo sapiens	81-84
26092099-0	2015	Cannabidiol causes endothelium-dependent vasorelaxation of human mesenteric arteries via CB1 activation.	Cannabidiol	0-11	cannabinoid receptor 1	Homo sapiens	89-92
25903924-0	2015	Cannabidiol stimulates Aml-1a-dependent glial differentiation and inhibits glioma stem-like cells proliferation by inducing autophagy in a TRPV2-dependent manner.	Cannabidiol	0-11	transient receptor potential cation channel subfamily V member 2	Homo sapiens	139-144
25903924-4	2015	Herein, we demonstrated that cannabidiol (CBD) by activating transient receptor potential vanilloid-2 (TRPV2) triggers GSCs differentiation activating the autophagic process and inhibits GSCs proliferation and clonogenic capability.	Cannabidiol	29-40	transient receptor potential cation channel subfamily V member 2	Homo sapiens	61-101
25903924-4	2015	Herein, we demonstrated that cannabidiol (CBD) by activating transient receptor potential vanilloid-2 (TRPV2) triggers GSCs differentiation activating the autophagic process and inhibits GSCs proliferation and clonogenic capability.	Cannabidiol	29-40	transient receptor potential cation channel subfamily V member 2	Homo sapiens	103-108
25903924-4	2015	Herein, we demonstrated that cannabidiol (CBD) by activating transient receptor potential vanilloid-2 (TRPV2) triggers GSCs differentiation activating the autophagic process and inhibits GSCs proliferation and clonogenic capability.	Cannabidiol	42-45	transient receptor potential cation channel subfamily V member 2	Homo sapiens	61-101
25903924-4	2015	Herein, we demonstrated that cannabidiol (CBD) by activating transient receptor potential vanilloid-2 (TRPV2) triggers GSCs differentiation activating the autophagic process and inhibits GSCs proliferation and clonogenic capability.	Cannabidiol	42-45	transient receptor potential cation channel subfamily V member 2	Homo sapiens	103-108
26218440-0	2015	Cannabidiol is a negative allosteric modulator of the cannabinoid CB1 receptor.	Cannabidiol	0-11	cannabinoid receptor 1	Homo sapiens	66-69
26218440-1	2015	BACKGROUND AND PURPOSE: Cannabidiol has been reported to act as an antagonist at cannabinoid CB1 receptors.	Cannabidiol	24-35	cannabinoid receptor 1	Homo sapiens	93-96
26218440-2	2015	We hypothesized that cannabidiol would inhibit cannabinoid agonist activity through negative allosteric modulation of CB1 receptors.	Cannabidiol	21-32	cannabinoid receptor 1	Homo sapiens	118-121
26218440-5	2015	KEY RESULTS: Cannabidiol reduced the efficacy and potency of 2-arachidonylglycerol and Delta(9)-tetrahydrocannabinol on PLCbeta3- and ERK1/2-dependent signalling in cells heterologously (HEK 293A) or endogenously (STHdh(Q7/Q7)) expressing CB1 receptors.	Cannabidiol	13-24	phospholipase C beta 3	Homo sapiens	120-128
26218440-5	2015	KEY RESULTS: Cannabidiol reduced the efficacy and potency of 2-arachidonylglycerol and Delta(9)-tetrahydrocannabinol on PLCbeta3- and ERK1/2-dependent signalling in cells heterologously (HEK 293A) or endogenously (STHdh(Q7/Q7)) expressing CB1 receptors.	Cannabidiol	13-24	mitogen-activated protein kinase 3	Homo sapiens	134-140
26218440-5	2015	KEY RESULTS: Cannabidiol reduced the efficacy and potency of 2-arachidonylglycerol and Delta(9)-tetrahydrocannabinol on PLCbeta3- and ERK1/2-dependent signalling in cells heterologously (HEK 293A) or endogenously (STHdh(Q7/Q7)) expressing CB1 receptors.	Cannabidiol	13-24	cannabinoid receptor 1	Homo sapiens	239-242
26218440-6	2015	By reducing arrestin2 recruitment to CB1 receptors, cannabidiol treatment prevented internalization of these receptors.	Cannabidiol	52-63	arrestin beta 1	Homo sapiens	12-21
26218440-6	2015	By reducing arrestin2 recruitment to CB1 receptors, cannabidiol treatment prevented internalization of these receptors.	Cannabidiol	52-63	cannabinoid receptor 1	Homo sapiens	37-40
26218440-7	2015	The allosteric activity of cannabidiol depended upon polar residues being present at positions 98 and 107 in the extracellular amino terminus of the CB1 receptor.	Cannabidiol	27-38	cannabinoid receptor 1	Homo sapiens	149-152
26761477-4	2015	RESULTS: Ischemia/reperfusion increased the IL-1 and TNF levels, and these levels were attenuated by cannabidiol treatment.	Cannabidiol	101-112	interleukin 1 alpha	Homo sapiens	44-48
26761477-4	2015	RESULTS: Ischemia/reperfusion increased the IL-1 and TNF levels, and these levels were attenuated by cannabidiol treatment.	Cannabidiol	101-112	tumor necrosis factor	Homo sapiens	53-56
26187180-1	2015	AIMS: We herein investigated the inducibility of cytochrome P450 1A1 (CYP1A1) by Delta(9)-tetrahydrocannabinol, cannabidiol (CBD), and cannabinol, three major phytocannabinoids, using human hepatoma HepG2 cells.	Cannabidiol	112-123	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	49-68
26108786-10	2015	The release of Ca(2+) induced by hyperosmotic shock was increased by cannabidiol, an activator of TRPV2, and decreased by tranilast, an inhibitor of TRPV2, suggesting a role for the TRPV2 channel itself.	Cannabidiol	69-80	transient receptor potential cation channel subfamily V member 2	Homo sapiens	98-103
26187180-0	2015	Cannabidiol induces expression of human cytochrome P450 1A1 that is possibly mediated through aryl hydrocarbon receptor signaling in HepG2 cells.	Cannabidiol	0-11	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	40-59
26187180-1	2015	AIMS: We herein investigated the inducibility of cytochrome P450 1A1 (CYP1A1) by Delta(9)-tetrahydrocannabinol, cannabidiol (CBD), and cannabinol, three major phytocannabinoids, using human hepatoma HepG2 cells.	Cannabidiol	112-123	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	70-76
26187180-0	2015	Cannabidiol induces expression of human cytochrome P450 1A1 that is possibly mediated through aryl hydrocarbon receptor signaling in HepG2 cells.	Cannabidiol	0-11	aryl hydrocarbon receptor	Homo sapiens	94-119
26187180-1	2015	AIMS: We herein investigated the inducibility of cytochrome P450 1A1 (CYP1A1) by Delta(9)-tetrahydrocannabinol, cannabidiol (CBD), and cannabinol, three major phytocannabinoids, using human hepatoma HepG2 cells.	Cannabidiol	125-128	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	49-68
26187180-1	2015	AIMS: We herein investigated the inducibility of cytochrome P450 1A1 (CYP1A1) by Delta(9)-tetrahydrocannabinol, cannabidiol (CBD), and cannabinol, three major phytocannabinoids, using human hepatoma HepG2 cells.	Cannabidiol	125-128	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	70-76
26187180-7	2015	The upregulation of CYP1A1 by CBD was significantly suppressed by herbimycin A as was the induction by omeprazole but not 3-methylcholanthrene.	Cannabidiol	30-33	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	20-26
26187180-8	2015	The inducibility of CYP1A1 by CBD-related compounds was examined to clarify the structural requirements for CBD-mediated CYP1A1 induction.	Cannabidiol	30-33	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	20-26
26187180-8	2015	The inducibility of CYP1A1 by CBD-related compounds was examined to clarify the structural requirements for CBD-mediated CYP1A1 induction.	Cannabidiol	108-111	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	20-26
26187180-8	2015	The inducibility of CYP1A1 by CBD-related compounds was examined to clarify the structural requirements for CBD-mediated CYP1A1 induction.	Cannabidiol	108-111	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	121-127
26187180-9	2015	Olivetol, which corresponds to the pentylresorcinol moiety of CBD, significantly induced the expression of CYP1A1, whereas d-limonene, CBD-2"-monomethyl ether, and CBD-2",6"-dimethyl ether did not.	Cannabidiol	62-65	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	107-113
26267945-4	2015	Cytochromes P450 (CYP) 2C9 and 3A4 are involved in the metabolism of tetrahydrocannabinol and cannabidiol, which implies possible DDI with CYP450 inhibitor and inducer, such as anticonvulsivants and HIV protease inhibitors, which may be prescribed in patients with neuropathic pain.	Cannabidiol	94-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-26
26283212-0	2015	Cannabidiol, a Cannabis sativa constituent, inhibits cocaine-induced seizures in mice: Possible role of the mTOR pathway and reduction in glutamate release.	Cannabidiol	0-11	mechanistic target of rapamycin kinase	Mus musculus	108-112
25841876-2	2015	The aim of the present work was to investigate the role played by CB1-cannabinoid receptor of GABAergic pathways terminal boutons in the SNpr or of SNpr-endocannabinoid receptor-containing interneurons on the effect of intra-nigral microinjections of cannabidiol in the activity of nigro-tectal inhibitory pathways.	Cannabidiol	251-262	cannabinoid receptor 1	Homo sapiens	66-69
25841876-8	2015	These findings suggest a CB1 mediated endocannabinoid signalling in cannabidiol modulation of panic-like defensive behaviour, but not of innate fear-induced antinociception evoked by GABAA receptor blockade with bicuculline microinjection into the superior colliculus, with a putative activity in nigro-collicular GABAergic pathways.	Cannabidiol	68-79	cannabinoid receptor 1	Homo sapiens	25-28
26309534-9	2015	Thus, CBD administration inhibited the effect of pentylenetetrazole in rats, decreased the astrocytic hyperplasia, decreased neuronal damage in the hippocampus caused by seizures and selectively reduced the expression of the NR1 subunit of NMDA.	Cannabidiol	6-9	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	225-228
25970609-5	2015	Treatment with cannabidiol, a selective antagonist of GPR55, counteracted these pro-atherogenic and proinflammatory O-1602-mediated effects.	Cannabidiol	15-26	G protein-coupled receptor 55	Homo sapiens	54-59
25595882-4	2015	Recent evidence suggests that the cannabinoids Delta(9)-tetrahydrocannabivarin (THCV) and cannabidiol (CBD) improve insulin sensitivity; we aimed at studying their effects on lipid levels.	Cannabidiol	90-101	insulin	Homo sapiens	116-123
25595882-4	2015	Recent evidence suggests that the cannabinoids Delta(9)-tetrahydrocannabivarin (THCV) and cannabidiol (CBD) improve insulin sensitivity; we aimed at studying their effects on lipid levels.	Cannabidiol	103-106	insulin	Homo sapiens	116-123
25917103-3	2015	In this study, we observed that administering CBD into naive mice triggers robust induction of CD11b(+)Gr-1(+) myeloid-derived suppressor cells (MDSC) in the peritoneum, which expressed functional arginase 1, and potently suppressed T cell proliferation ex vivo.	Cannabidiol	46-49	integrin alpha M	Mus musculus	95-100
25917103-3	2015	In this study, we observed that administering CBD into naive mice triggers robust induction of CD11b(+)Gr-1(+) myeloid-derived suppressor cells (MDSC) in the peritoneum, which expressed functional arginase 1, and potently suppressed T cell proliferation ex vivo.	Cannabidiol	46-49	arginase, liver	Mus musculus	197-207
25917103-5	2015	CBD-induced suppressor cells were comprised of CD11b(+)Ly6-G(+)Ly6-C(+) granulocytic and CD11b(+)Ly6-G(-)Ly6-C(+) monocytic subtypes, with monocytic MDSC exhibiting higher T cell-suppressive function.	Cannabidiol	0-3	integrin alpha M	Mus musculus	47-52
25917103-5	2015	CBD-induced suppressor cells were comprised of CD11b(+)Ly6-G(+)Ly6-C(+) granulocytic and CD11b(+)Ly6-G(-)Ly6-C(+) monocytic subtypes, with monocytic MDSC exhibiting higher T cell-suppressive function.	Cannabidiol	0-3	lymphocyte antigen 6 complex, locus G	Mus musculus	55-60
25917103-5	2015	CBD-induced suppressor cells were comprised of CD11b(+)Ly6-G(+)Ly6-C(+) granulocytic and CD11b(+)Ly6-G(-)Ly6-C(+) monocytic subtypes, with monocytic MDSC exhibiting higher T cell-suppressive function.	Cannabidiol	0-3	lymphocyte antigen 6 complex, locus C1	Mus musculus	63-68
25917103-5	2015	CBD-induced suppressor cells were comprised of CD11b(+)Ly6-G(+)Ly6-C(+) granulocytic and CD11b(+)Ly6-G(-)Ly6-C(+) monocytic subtypes, with monocytic MDSC exhibiting higher T cell-suppressive function.	Cannabidiol	0-3	integrin alpha M	Mus musculus	89-94
25917103-5	2015	CBD-induced suppressor cells were comprised of CD11b(+)Ly6-G(+)Ly6-C(+) granulocytic and CD11b(+)Ly6-G(-)Ly6-C(+) monocytic subtypes, with monocytic MDSC exhibiting higher T cell-suppressive function.	Cannabidiol	0-3	lymphocyte antigen 6 complex, locus G	Mus musculus	97-102
25917103-5	2015	CBD-induced suppressor cells were comprised of CD11b(+)Ly6-G(+)Ly6-C(+) granulocytic and CD11b(+)Ly6-G(-)Ly6-C(+) monocytic subtypes, with monocytic MDSC exhibiting higher T cell-suppressive function.	Cannabidiol	0-3	lymphocyte antigen 6 complex, locus C1	Mus musculus	105-110
25917103-9	2015	CBD administration in mice induced G-CSF, CXCL1, and M-CSF, but not GM-CSF.	Cannabidiol	0-3	peripheral blood stem cell response to granulocyte colony stimulating factor 1	Mus musculus	35-40
25917103-9	2015	CBD administration in mice induced G-CSF, CXCL1, and M-CSF, but not GM-CSF.	Cannabidiol	0-3	chemokine (C-X-C motif) ligand 1	Mus musculus	42-47
25917103-9	2015	CBD administration in mice induced G-CSF, CXCL1, and M-CSF, but not GM-CSF.	Cannabidiol	0-3	colony stimulating factor 1 (macrophage)	Mus musculus	53-58
25344934-7	2015	These over-stimulatory effects of GPR55 were antagonized by its selective antagonist cannabidiol.	Cannabidiol	85-96	G protein-coupled receptor 55	Homo sapiens	34-39
25666611-7	2015	Using computational molecular docking and site-directed mutagenesis we identify key residues within the active site of FAAH that confer the species-specific sensitivity to inhibition by CBD.	Cannabidiol	186-189	fatty acid amide hydrolase	Homo sapiens	119-123
25637488-10	2015	However, there is an antagonistic interaction between CBD and PEA in protection against MOG-induced disease.	Cannabidiol	54-57	myelin oligodendrocyte glycoprotein	Mus musculus	88-91
25660577-0	2015	Modulation of the tumor microenvironment and inhibition of EGF/EGFR pathway: novel anti-tumor mechanisms of Cannabidiol in breast cancer.	Cannabidiol	108-119	epidermal growth factor receptor	Mus musculus	63-67
25595981-11	2015	CBD treatment resulted in an increase in BDNF expression in the hippocampus and decreased levels of proinflammatory cytokines in the hippocampus (TNF-alpha) and prefrontal cortex (IL-6).	Cannabidiol	0-3	brain derived neurotrophic factor	Mus musculus	41-45
25595981-11	2015	CBD treatment resulted in an increase in BDNF expression in the hippocampus and decreased levels of proinflammatory cytokines in the hippocampus (TNF-alpha) and prefrontal cortex (IL-6).	Cannabidiol	0-3	tumor necrosis factor	Mus musculus	146-155
25595981-11	2015	CBD treatment resulted in an increase in BDNF expression in the hippocampus and decreased levels of proinflammatory cytokines in the hippocampus (TNF-alpha) and prefrontal cortex (IL-6).	Cannabidiol	0-3	interleukin 6	Mus musculus	180-184
25586398-2	2015	Cannabis containing high levels of the partial cannabinoid receptor subtype 1 (CB1) agonist tetrahydrocannabinol (THC) is associated with the induction of psychosis in susceptible subjects and with the development of schizophrenia, whereas the use of cannabis variants with relatively high levels of cannabidiol (CBD) is associated with fewer psychotic experiences.	Cannabidiol	313-316	cannabinoid receptor 1	Homo sapiens	79-82
25586398-2	2015	Cannabis containing high levels of the partial cannabinoid receptor subtype 1 (CB1) agonist tetrahydrocannabinol (THC) is associated with the induction of psychosis in susceptible subjects and with the development of schizophrenia, whereas the use of cannabis variants with relatively high levels of cannabidiol (CBD) is associated with fewer psychotic experiences.	Cannabidiol	300-311	cannabinoid receptor 1	Homo sapiens	79-82
25689051-5	2015	In comparison with the other monocyte subpopulations, CD14dimCD16+ cells were at decreased frequency in PBMCs of both BeS-NS and CBD and showed higher HLA-DR expression, compared to HS.	Cannabidiol	129-132	CD14 molecule	Homo sapiens	54-65
25356537-0	2015	Cannabidiol improves lung function and inflammation in mice submitted to LPS-induced acute lung injury.	Cannabidiol	0-11	toll-like receptor 4	Mus musculus	73-76
25880134-0	2015	Cannabidiol, a non-psychoactive cannabinoid, leads to EGR2-dependent anergy in activated encephalitogenic T cells.	Cannabidiol	0-11	early growth response 2	Mus musculus	54-58
25880134-1	2015	BACKGROUND: Cannabidiol (CBD), the main non-psychoactive cannabinoid, has been previously shown by us to ameliorate clinical symptoms and to decrease inflammation in myelin oligodendrocyte glycoprotein (MOG)35-55-induced mouse experimental autoimmune encephalomyelitis model of multiple sclerosis as well as to decrease MOG35-55-induced T cell proliferation and IL-17 secretion.	Cannabidiol	12-23	myelin oligodendrocyte glycoprotein	Mus musculus	166-201
25880134-1	2015	BACKGROUND: Cannabidiol (CBD), the main non-psychoactive cannabinoid, has been previously shown by us to ameliorate clinical symptoms and to decrease inflammation in myelin oligodendrocyte glycoprotein (MOG)35-55-induced mouse experimental autoimmune encephalomyelitis model of multiple sclerosis as well as to decrease MOG35-55-induced T cell proliferation and IL-17 secretion.	Cannabidiol	12-23	myelin oligodendrocyte glycoprotein	Mus musculus	203-206
25880134-1	2015	BACKGROUND: Cannabidiol (CBD), the main non-psychoactive cannabinoid, has been previously shown by us to ameliorate clinical symptoms and to decrease inflammation in myelin oligodendrocyte glycoprotein (MOG)35-55-induced mouse experimental autoimmune encephalomyelitis model of multiple sclerosis as well as to decrease MOG35-55-induced T cell proliferation and IL-17 secretion.	Cannabidiol	12-23	interleukin 17A	Mus musculus	362-367
25880134-1	2015	BACKGROUND: Cannabidiol (CBD), the main non-psychoactive cannabinoid, has been previously shown by us to ameliorate clinical symptoms and to decrease inflammation in myelin oligodendrocyte glycoprotein (MOG)35-55-induced mouse experimental autoimmune encephalomyelitis model of multiple sclerosis as well as to decrease MOG35-55-induced T cell proliferation and IL-17 secretion.	Cannabidiol	25-28	myelin oligodendrocyte glycoprotein	Mus musculus	166-201
25880134-1	2015	BACKGROUND: Cannabidiol (CBD), the main non-psychoactive cannabinoid, has been previously shown by us to ameliorate clinical symptoms and to decrease inflammation in myelin oligodendrocyte glycoprotein (MOG)35-55-induced mouse experimental autoimmune encephalomyelitis model of multiple sclerosis as well as to decrease MOG35-55-induced T cell proliferation and IL-17 secretion.	Cannabidiol	25-28	myelin oligodendrocyte glycoprotein	Mus musculus	203-206
25880134-1	2015	BACKGROUND: Cannabidiol (CBD), the main non-psychoactive cannabinoid, has been previously shown by us to ameliorate clinical symptoms and to decrease inflammation in myelin oligodendrocyte glycoprotein (MOG)35-55-induced mouse experimental autoimmune encephalomyelitis model of multiple sclerosis as well as to decrease MOG35-55-induced T cell proliferation and IL-17 secretion.	Cannabidiol	25-28	interleukin 17A	Mus musculus	362-367
25880134-12	2015	In parallel, we observed decreased levels of major histocompatibility complex class II (MHCII), CD25, and CD69 on CD19(+) B cells following CBD treatment, showing diminished antigen presenting capabilities of B cells and reduction in their pro-inflammatory functions.	Cannabidiol	140-143	interleukin 2 receptor, alpha chain	Mus musculus	96-100
25880134-12	2015	In parallel, we observed decreased levels of major histocompatibility complex class II (MHCII), CD25, and CD69 on CD19(+) B cells following CBD treatment, showing diminished antigen presenting capabilities of B cells and reduction in their pro-inflammatory functions.	Cannabidiol	140-143	CD69 antigen	Mus musculus	106-110
25880134-12	2015	In parallel, we observed decreased levels of major histocompatibility complex class II (MHCII), CD25, and CD69 on CD19(+) B cells following CBD treatment, showing diminished antigen presenting capabilities of B cells and reduction in their pro-inflammatory functions.	Cannabidiol	140-143	CD19 antigen	Mus musculus	114-118
25356537-2	2015	In this work we analyzed the effects of the therapeutic treatment with CBD in mice subjected to the model of lipopolysaccharide (LPS)-induced ALI on pulmonary mechanics and inflammation.	Cannabidiol	71-74	toll-like receptor 4	Mus musculus	129-132
25356537-7	2015	Thus, we conclude that CBD administered therapeutically, i.e. during an ongoing inflammatory process, has a potent anti-inflammatory effect and also improves the lung function in mice submitted to LPS-induced ALI.	Cannabidiol	23-26	toll-like receptor 4	Mus musculus	197-200
25125475-3	2015	Moreover, THC + CBD reduced learning impairment in AbetaPP/PS1 mice.	Cannabidiol	16-19	amyloid beta (A4) precursor protein	Mus musculus	51-58
25125475-3	2015	Moreover, THC + CBD reduced learning impairment in AbetaPP/PS1 mice.	Cannabidiol	16-19	presenilin 1	Mus musculus	59-62
25125475-4	2015	A significant decrease in soluble Abeta42 peptide levels and a change in plaques composition were also observed in THC + CBD-treated AbetaPP/PS1 mice, suggesting a cannabinoid-induced reduction in the harmful effect of the most toxic form of the Abeta peptide.	Cannabidiol	121-124	amyloid beta (A4) precursor protein	Mus musculus	133-140
25125475-4	2015	A significant decrease in soluble Abeta42 peptide levels and a change in plaques composition were also observed in THC + CBD-treated AbetaPP/PS1 mice, suggesting a cannabinoid-induced reduction in the harmful effect of the most toxic form of the Abeta peptide.	Cannabidiol	121-124	presenilin 1	Mus musculus	141-144
25029033-0	2014	Nonpsychotropic plant cannabinoids, cannabidivarin (CBDV) and cannabidiol (CBD), activate and desensitize transient receptor potential vanilloid 1 (TRPV1) channels in vitro: potential for the treatment of neuronal hyperexcitability.	Cannabidiol	62-73	transient receptor potential cation channel subfamily V member 1	Homo sapiens	106-146
25125475-6	2015	Here we observed reduced astrogliosis, microgliosis, and inflammatory-related molecules in treated AbetaPP/PS1 mice, which were more marked after treatment with THC + CBD than with either THC or CBD.	Cannabidiol	167-170	amyloid beta (A4) precursor protein	Mus musculus	99-106
25125475-6	2015	Here we observed reduced astrogliosis, microgliosis, and inflammatory-related molecules in treated AbetaPP/PS1 mice, which were more marked after treatment with THC + CBD than with either THC or CBD.	Cannabidiol	167-170	presenilin 1	Mus musculus	107-110
25125475-6	2015	Here we observed reduced astrogliosis, microgliosis, and inflammatory-related molecules in treated AbetaPP/PS1 mice, which were more marked after treatment with THC + CBD than with either THC or CBD.	Cannabidiol	195-198	amyloid beta (A4) precursor protein	Mus musculus	99-106
25125475-6	2015	Here we observed reduced astrogliosis, microgliosis, and inflammatory-related molecules in treated AbetaPP/PS1 mice, which were more marked after treatment with THC + CBD than with either THC or CBD.	Cannabidiol	195-198	presenilin 1	Mus musculus	107-110
25125475-8	2015	Thus, we have identified the redox protein thioredoxin 2 and the signaling protein Wnt16 as significant substrates for the THC + CBD-induced effects in our AD model.	Cannabidiol	129-132	thioredoxin 2	Mus musculus	43-56
25125475-8	2015	Thus, we have identified the redox protein thioredoxin 2 and the signaling protein Wnt16 as significant substrates for the THC + CBD-induced effects in our AD model.	Cannabidiol	129-132	wingless-type MMTV integration site family, member 16	Mus musculus	83-88
26485425-3	2015	Recent single photon emission tomography (SPECT) studies have reported normal striatal dopamine transporter (DAT) binding in individual patients with CBD.	Cannabidiol	150-153	solute carrier family 6 member 3	Homo sapiens	87-107
26485425-3	2015	Recent single photon emission tomography (SPECT) studies have reported normal striatal dopamine transporter (DAT) binding in individual patients with CBD.	Cannabidiol	150-153	solute carrier family 6 member 3	Homo sapiens	109-112
25029033-0	2014	Nonpsychotropic plant cannabinoids, cannabidivarin (CBDV) and cannabidiol (CBD), activate and desensitize transient receptor potential vanilloid 1 (TRPV1) channels in vitro: potential for the treatment of neuronal hyperexcitability.	Cannabidiol	62-73	transient receptor potential cation channel subfamily V member 1	Homo sapiens	148-153
25029033-0	2014	Nonpsychotropic plant cannabinoids, cannabidivarin (CBDV) and cannabidiol (CBD), activate and desensitize transient receptor potential vanilloid 1 (TRPV1) channels in vitro: potential for the treatment of neuronal hyperexcitability.	Cannabidiol	52-55	transient receptor potential cation channel subfamily V member 1	Homo sapiens	106-146
25029033-0	2014	Nonpsychotropic plant cannabinoids, cannabidivarin (CBDV) and cannabidiol (CBD), activate and desensitize transient receptor potential vanilloid 1 (TRPV1) channels in vitro: potential for the treatment of neuronal hyperexcitability.	Cannabidiol	52-55	transient receptor potential cation channel subfamily V member 1	Homo sapiens	148-153
25029033-3	2014	Since the two nonpsychotropic cannabinoids cannabidivarin (CBDV) and cannabidiol (CBD) exert anticonvulsant activity in vivo and produce TRPV1-mediated intracellular calcium elevation in vitro, we evaluated the effects of these two compounds on TRPV1 channel activation and desensitization and in an in vitro model of epileptiform activity.	Cannabidiol	69-80	transient receptor potential cation channel subfamily V member 1	Homo sapiens	137-142
25029033-3	2014	Since the two nonpsychotropic cannabinoids cannabidivarin (CBDV) and cannabidiol (CBD) exert anticonvulsant activity in vivo and produce TRPV1-mediated intracellular calcium elevation in vitro, we evaluated the effects of these two compounds on TRPV1 channel activation and desensitization and in an in vitro model of epileptiform activity.	Cannabidiol	69-80	transient receptor potential cation channel subfamily V member 1	Homo sapiens	245-250
25029033-3	2014	Since the two nonpsychotropic cannabinoids cannabidivarin (CBDV) and cannabidiol (CBD) exert anticonvulsant activity in vivo and produce TRPV1-mediated intracellular calcium elevation in vitro, we evaluated the effects of these two compounds on TRPV1 channel activation and desensitization and in an in vitro model of epileptiform activity.	Cannabidiol	59-62	transient receptor potential cation channel subfamily V member 1	Homo sapiens	137-142
25029033-3	2014	Since the two nonpsychotropic cannabinoids cannabidivarin (CBDV) and cannabidiol (CBD) exert anticonvulsant activity in vivo and produce TRPV1-mediated intracellular calcium elevation in vitro, we evaluated the effects of these two compounds on TRPV1 channel activation and desensitization and in an in vitro model of epileptiform activity.	Cannabidiol	59-62	transient receptor potential cation channel subfamily V member 1	Homo sapiens	245-250
25069049-3	2014	Cannabidiol (CBD), a non-psychoactive cannabinoid, enhanced the susceptibility of cancer cells to adhere to and subsequently be lysed by LAK cells, with both effects being reversed by a neutralizing ICAM-1 antibody.	Cannabidiol	0-11	intercellular adhesion molecule 1	Homo sapiens	199-205
25069049-3	2014	Cannabidiol (CBD), a non-psychoactive cannabinoid, enhanced the susceptibility of cancer cells to adhere to and subsequently be lysed by LAK cells, with both effects being reversed by a neutralizing ICAM-1 antibody.	Cannabidiol	13-16	intercellular adhesion molecule 1	Homo sapiens	199-205
25069049-4	2014	Increased cancer cell lysis by CBD was likewise abrogated when CBD-induced ICAM-1 expression was blocked by specific siRNA or by antagonists to cannabinoid receptors (CB1, CB2) and to transient receptor potential vanilloid 1.	Cannabidiol	31-34	intercellular adhesion molecule 1	Homo sapiens	75-81
25069049-4	2014	Increased cancer cell lysis by CBD was likewise abrogated when CBD-induced ICAM-1 expression was blocked by specific siRNA or by antagonists to cannabinoid receptors (CB1, CB2) and to transient receptor potential vanilloid 1.	Cannabidiol	31-34	cannabinoid receptor 1	Homo sapiens	167-170
25069049-4	2014	Increased cancer cell lysis by CBD was likewise abrogated when CBD-induced ICAM-1 expression was blocked by specific siRNA or by antagonists to cannabinoid receptors (CB1, CB2) and to transient receptor potential vanilloid 1.	Cannabidiol	31-34	cannabinoid receptor 2	Homo sapiens	172-175
25069049-5	2014	In addition, enhanced killing of CBD-treated cancer cells was reversed by preincubation of LAK cells with an antibody to lymphocyte function associated antigen-1 (LFA-1) suggesting intercellular ICAM-1/LFA-1 crosslink as crucial event within this process.	Cannabidiol	33-36	integrin subunit alpha L	Homo sapiens	121-161
25069049-5	2014	In addition, enhanced killing of CBD-treated cancer cells was reversed by preincubation of LAK cells with an antibody to lymphocyte function associated antigen-1 (LFA-1) suggesting intercellular ICAM-1/LFA-1 crosslink as crucial event within this process.	Cannabidiol	33-36	integrin subunit alpha L	Homo sapiens	163-168
25069049-5	2014	In addition, enhanced killing of CBD-treated cancer cells was reversed by preincubation of LAK cells with an antibody to lymphocyte function associated antigen-1 (LFA-1) suggesting intercellular ICAM-1/LFA-1 crosslink as crucial event within this process.	Cannabidiol	33-36	intercellular adhesion molecule 1	Homo sapiens	195-201
25069049-5	2014	In addition, enhanced killing of CBD-treated cancer cells was reversed by preincubation of LAK cells with an antibody to lymphocyte function associated antigen-1 (LFA-1) suggesting intercellular ICAM-1/LFA-1 crosslink as crucial event within this process.	Cannabidiol	33-36	integrin subunit alpha L	Homo sapiens	202-207
25618402-21	2014	CONCLUSIONS: These results indicate that repeated treatment with CBD, similar to clozapine, reverses the psychotomimetic-like effects and attenuates molecular changes observed after chronic administration of an NMDAR antagonist.	Cannabidiol	65-68	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	211-216
24642454-6	2014	CBD and CBG effects on veratridine-stimulated human recombinant NaV1.1, 1.2 or 1.5 channels were assessed using a membrane potential-sensitive fluorescent dye high-throughput assay.	Cannabidiol	0-3	sodium voltage-gated channel alpha subunit 1	Homo sapiens	64-70
24532152-8	2014	GFAP immunoreactivity was also decreased in ischemic mice treated with CBD (30 mg/kg).	Cannabidiol	71-74	glial fibrillary acidic protein	Mus musculus	0-4
25100751-5	2014	Prior GPR18 blockade with O-1918 (1,3-dimethoxy-5-methyl-2-[(1R,6R)-3-methyl-6-(1-methylethenyl)-2-cyclohexen-1-yl]benzene) produced the opposite effects and abrogated Abn CBD-evoked neurochemical and BP responses.	Cannabidiol	172-175	G protein-coupled receptor 18	Rattus norvegicus	6-11
25253989-3	2014	Cannabidiol protects retinal neurons by preserving glutamine synthetase activity in diabetes.	Cannabidiol	0-11	glutamate-ammonia ligase	Homo sapiens	51-71
24762058-6	2014	KEY RESULTS: Concentration-dependent increases in intracellular calcium and ERK1/2 phosphorylation were observed in the presence of NAGly, abnormal cannabidiol (AbnCBD), O-1602, O-1918 and Delta(9)-tetrahydrocannabinol (Delta(9)-THC) in HEK293/GPR18 cells.	Cannabidiol	148-159	mitogen-activated protein kinase 3	Homo sapiens	76-82
24577515-4	2014	CBD also reverses Abeta-induced spatial memory deficits in rodents.	Cannabidiol	0-3	amyloid beta (A4) precursor protein	Mus musculus	18-23
24751709-4	2014	Results showed that abnormal cannabidiol (Abn-CBD), an agonist at the putative endothelial cannabinoid receptor, CBe, inhibited endothelin 1 (ET-1) induced vasoconstriction in retinal arterioles.	Cannabidiol	29-40	endothelin 1	Rattus norvegicus	128-140
24751709-4	2014	Results showed that abnormal cannabidiol (Abn-CBD), an agonist at the putative endothelial cannabinoid receptor, CBe, inhibited endothelin 1 (ET-1) induced vasoconstriction in retinal arterioles.	Cannabidiol	29-40	endothelin 1	Rattus norvegicus	142-146
24288245-0	2014	Cannabidiol promotes amyloid precursor protein ubiquitination and reduction of beta amyloid expression in SHSY5YAPP+ cells through PPARgamma involvement.	Cannabidiol	0-11	amyloid beta precursor protein	Homo sapiens	21-46
24288245-0	2014	Cannabidiol promotes amyloid precursor protein ubiquitination and reduction of beta amyloid expression in SHSY5YAPP+ cells through PPARgamma involvement.	Cannabidiol	0-11	peroxisome proliferator activated receptor gamma	Homo sapiens	131-140
24288245-4	2014	Cannabidiol (CBD), a Cannabis derivative devoid of psychotropic effects, has attracted much attention because it may beneficially interfere with several Abeta-triggered neurodegenerative pathways, even though the mechanism responsible for such actions remains unknown.	Cannabidiol	0-11	amyloid beta precursor protein	Homo sapiens	153-158
24288245-4	2014	Cannabidiol (CBD), a Cannabis derivative devoid of psychotropic effects, has attracted much attention because it may beneficially interfere with several Abeta-triggered neurodegenerative pathways, even though the mechanism responsible for such actions remains unknown.	Cannabidiol	13-16	amyloid beta precursor protein	Homo sapiens	153-158
24288245-6	2014	In addition, the putative involvement of peroxisome proliferator-activated receptor-gamma (PPARgamma) was explored as a candidate molecular site responsible for CBD actions.	Cannabidiol	161-164	peroxisome proliferator activated receptor gamma	Homo sapiens	41-89
24288245-6	2014	In addition, the putative involvement of peroxisome proliferator-activated receptor-gamma (PPARgamma) was explored as a candidate molecular site responsible for CBD actions.	Cannabidiol	161-164	peroxisome proliferator activated receptor gamma	Homo sapiens	91-100
24288245-9	2014	Obtained results also showed that all, here observed, CBD effects were dependent on the selective activation of PPARgamma.	Cannabidiol	54-57	peroxisome proliferator activated receptor gamma	Homo sapiens	112-121
24667653-0	2014	Characterization of the structural determinants required for potent mechanism-based inhibition of human cytochrome P450 1A1 by cannabidiol.	Cannabidiol	127-138	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	104-123
24667653-1	2014	We previously demonstrated that cannabidiol (CBD) was a potent mechanism-based inhibitor of human cytochrome P450 1A1 (CYP1A1).	Cannabidiol	32-43	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	98-117
24667653-1	2014	We previously demonstrated that cannabidiol (CBD) was a potent mechanism-based inhibitor of human cytochrome P450 1A1 (CYP1A1).	Cannabidiol	32-43	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	119-125
24667653-1	2014	We previously demonstrated that cannabidiol (CBD) was a potent mechanism-based inhibitor of human cytochrome P450 1A1 (CYP1A1).	Cannabidiol	45-48	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	98-117
24667653-1	2014	We previously demonstrated that cannabidiol (CBD) was a potent mechanism-based inhibitor of human cytochrome P450 1A1 (CYP1A1).	Cannabidiol	45-48	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	119-125
24667653-3	2014	Thus, the effects of compounds structurally related to CBD on CYP1A1 activity were examined with recombinant human CYP1A1 in order to characterize the structural requirements for potent inactivation by CBD.	Cannabidiol	55-58	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	62-68
24667653-4	2014	When preincubated in the presence of NADPH for 20min, olivetol, which corresponds to the pentylresorcinol moiety of CBD, enhanced the inhibition of the 7-ethoxyresorufin O-deethylase activity of CYP1A1.	Cannabidiol	116-119	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	195-201
24667653-11	2014	We further confirmed that olivetol, CBDM, CBDD, CBDV, and orcinol, as well as CBD (kinact=0.215min(-1)), inactivated CYP1A1 activity; their kinact values were 0.154, 0.0638, 0.0643, 0.226, and 0.0353min(-1), respectively.	Cannabidiol	36-39	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	117-123
24304686-0	2014	Increase of mesenchymal stem cell migration by cannabidiol via activation of p42/44 MAPK.	Cannabidiol	47-58	cyclin dependent kinase 20	Homo sapiens	77-80
24373545-10	2014	In binding assays, CBD BDS showed greater affinity than pure CBD for both CB1 and CB2 receptors, with pure CBD having very little affinity.	Cannabidiol	19-22	cannabinoid receptor 1	Homo sapiens	74-77
24373545-10	2014	In binding assays, CBD BDS showed greater affinity than pure CBD for both CB1 and CB2 receptors, with pure CBD having very little affinity.	Cannabidiol	19-22	cannabinoid receptor 2	Homo sapiens	82-85
24431468-1	2014	Systemic administration of the G-protein-coupled receptor 18 (GPR18) agonist abnormal cannabidiol (Abn CBD) lowers blood pressure (BP).	Cannabidiol	86-97	G protein-coupled receptor 18	Rattus norvegicus	31-60
24431468-1	2014	Systemic administration of the G-protein-coupled receptor 18 (GPR18) agonist abnormal cannabidiol (Abn CBD) lowers blood pressure (BP).	Cannabidiol	86-97	G protein-coupled receptor 18	Rattus norvegicus	62-67
24398069-4	2014	Cannabidiol can prevent acute alcohol-induced liver steatosis in mice, possibly by preventing the increase in oxidative stress and the activation of the JNK MAPK pathway.	Cannabidiol	0-11	mitogen-activated protein kinase 8	Mus musculus	153-156
24398069-5	2014	Cannabidiol per se can increase autophagy both in CYP2E1-expressing HepG2 cells and in mouse liver.	Cannabidiol	0-11	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	50-56
24398069-7	2014	In conclusion, these results show that cannabidiol protects mouse liver from acute alcohol-induced steatosis through multiple mechanisms including attenuation of alcohol-mediated oxidative stress, prevention of JNK MAPK activation, and increasing autophagy.	Cannabidiol	39-50	mitogen-activated protein kinase 8	Mus musculus	211-214
24304686-5	2014	CBD-induced migration was inhibited by AM-630 (CB2 receptor antagonist) and O-1602 (G protein-coupled receptor 55 [GRP55] agonist).	Cannabidiol	0-3	cannabinoid receptor 2	Homo sapiens	47-50
24304686-5	2014	CBD-induced migration was inhibited by AM-630 (CB2 receptor antagonist) and O-1602 (G protein-coupled receptor 55 [GRP55] agonist).	Cannabidiol	0-3	G protein-coupled receptor 55	Homo sapiens	84-113
24304686-5	2014	CBD-induced migration was inhibited by AM-630 (CB2 receptor antagonist) and O-1602 (G protein-coupled receptor 55 [GRP55] agonist).	Cannabidiol	0-3	G protein-coupled receptor 55	Homo sapiens	115-120
24304686-6	2014	Moreover, the promigratory effect of CBD was antagonized by inhibition of the p42/44 mitogen-activated protein kinase (MAPK) pathway which became activated upon CBD treatment.	Cannabidiol	37-40	cyclin dependent kinase 20	Homo sapiens	78-81
24238999-0	2014	Interleukin 17A evoked mucosal damage is attenuated by cannabidiol and anandamide in a human colonic explant model.	Cannabidiol	55-66	interleukin 17A	Homo sapiens	0-15
24117398-10	2014	CONCLUSIONS AND IMPLICATIONS: Our data suggest that CBD is protective against PAC-induced neurotoxicity mediated in part by the 5-HT(1A) receptor system.	Cannabidiol	52-55	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	128-145
24238999-5	2014	IL-17A incubation caused significant mucosal epithelial and crypt damage which were attenuated following hydrocortisone treatment, and also reduced following anandamide or cannabidiol incubation.	Cannabidiol	172-183	interleukin 17A	Homo sapiens	0-6
23893294-0	2014	Cannabidiol normalizes caspase 3, synaptophysin, and mitochondrial fission protein DNM1L expression levels in rats with brain iron overload: implications for neuroprotection.	Cannabidiol	0-11	caspase 3	Rattus norvegicus	23-32
24160757-5	2014	Clinical pharmacogenetic data further support CYP2C9 as a significant contributor to THC metabolism, and a pharmacokinetic interaction study using ketoconazole with oromucosal cannabis extract further supports CYP3A4 as a significant metabolic pathway for THC and CBD.	Cannabidiol	264-267	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	210-216
24445989-7	2014	The CS/CBD-bFGF group showed more significant improvements in motor than the simply CS-implanted and untreated control group, when evaluated by the 21-point Basso-Beattie-Bresnahan (BBB) score and footprint analysis.	Cannabidiol	7-10	fibroblast growth factor 2	Rattus norvegicus	11-15
24427137-9	2014	Production of Axl, CD40, IGF-I, OPN, and Pro-MMP-9 were significantly altered by NAGly and Delta(9)-THC, and antagonized by CBD.	Cannabidiol	124-127	AXL receptor tyrosine kinase	Homo sapiens	14-17
24427137-9	2014	Production of Axl, CD40, IGF-I, OPN, and Pro-MMP-9 were significantly altered by NAGly and Delta(9)-THC, and antagonized by CBD.	Cannabidiol	124-127	CD40 molecule	Homo sapiens	19-23
24427137-9	2014	Production of Axl, CD40, IGF-I, OPN, and Pro-MMP-9 were significantly altered by NAGly and Delta(9)-THC, and antagonized by CBD.	Cannabidiol	124-127	insulin like growth factor 1	Homo sapiens	25-30
24427137-9	2014	Production of Axl, CD40, IGF-I, OPN, and Pro-MMP-9 were significantly altered by NAGly and Delta(9)-THC, and antagonized by CBD.	Cannabidiol	124-127	secreted phosphoprotein 1	Homo sapiens	32-35
23893294-0	2014	Cannabidiol normalizes caspase 3, synaptophysin, and mitochondrial fission protein DNM1L expression levels in rats with brain iron overload: implications for neuroprotection.	Cannabidiol	0-11	synaptophysin	Rattus norvegicus	34-47
23893294-0	2014	Cannabidiol normalizes caspase 3, synaptophysin, and mitochondrial fission protein DNM1L expression levels in rats with brain iron overload: implications for neuroprotection.	Cannabidiol	0-11	dynamin 1-like	Rattus norvegicus	83-88
24309936-9	2013	The inhibition of VDAC1 by CBD may be responsible for the immunosuppressive and anticancer effects of CBD.	Cannabidiol	27-30	voltage-dependent anion channel 1	Mus musculus	18-23
25024347-6	2014	We found that AbetaPP x PS1 mice developed a social recognition deficit, which was prevented by CBD treatment.	Cannabidiol	96-99	histocompatibility 2, class II antigen A, beta 1	Mus musculus	14-21
25024347-6	2014	We found that AbetaPP x PS1 mice developed a social recognition deficit, which was prevented by CBD treatment.	Cannabidiol	96-99	presenilin 1	Mus musculus	24-27
24309936-0	2013	Direct modulation of the outer mitochondrial membrane channel, voltage-dependent anion channel 1 (VDAC1) by cannabidiol: a novel mechanism for cannabinoid-induced cell death.	Cannabidiol	108-119	voltage-dependent anion channel 1	Mus musculus	63-96
24309936-0	2013	Direct modulation of the outer mitochondrial membrane channel, voltage-dependent anion channel 1 (VDAC1) by cannabidiol: a novel mechanism for cannabinoid-induced cell death.	Cannabidiol	108-119	voltage-dependent anion channel 1	Mus musculus	98-103
23933222-0	2013	Cannabidiol enhances xenobiotic permeability through the human placental barrier by direct inhibition of breast cancer resistance protein: an ex vivo study.	Cannabidiol	0-11	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	105-137
23933222-2	2013	The aim of this study was to examine the influence of short-term (1-2 hours) exposure to cannabidiol, a major phytocannabinoid, on human placental breast cancer resistance protein function.	Cannabidiol	89-100	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	147-179
23892791-6	2013	Pretreatment with CBD also resulted in increased levels of the anti-inflammatory cytokine IL-10.	Cannabidiol	18-21	interleukin 10	Mus musculus	90-95
23926240-9	2013	These findings demonstrate that cannabidiol modulates the defensive behaviors evoked by the presence of threatening stimuli, and the effects of cannabidiol are at least partially dependent on the recruitment of 5-HT1A receptors.	Cannabidiol	144-155	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	211-217
23924692-0	2013	Motor effects of the non-psychotropic phytocannabinoid cannabidiol that are mediated by 5-HT1A receptors.	Cannabidiol	55-66	5-hydroxytryptamine receptor 1A	Rattus norvegicus	88-94
23924692-2	2013	By contrast, cannabidiol (CBD), a phytocannabinoid with a broad therapeutic profile, is generally presented as an example of a cannabinoid compound with no motor effects due to its poor affinity for the CB1 and the CB2 receptor, despite its activity at the TRPV1 receptor.	Cannabidiol	13-24	cannabinoid receptor 1	Rattus norvegicus	203-206
23924692-2	2013	By contrast, cannabidiol (CBD), a phytocannabinoid with a broad therapeutic profile, is generally presented as an example of a cannabinoid compound with no motor effects due to its poor affinity for the CB1 and the CB2 receptor, despite its activity at the TRPV1 receptor.	Cannabidiol	13-24	cannabinoid receptor 2	Rattus norvegicus	215-218
23924692-2	2013	By contrast, cannabidiol (CBD), a phytocannabinoid with a broad therapeutic profile, is generally presented as an example of a cannabinoid compound with no motor effects due to its poor affinity for the CB1 and the CB2 receptor, despite its activity at the TRPV1 receptor.	Cannabidiol	13-24	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	257-262
23924692-2	2013	By contrast, cannabidiol (CBD), a phytocannabinoid with a broad therapeutic profile, is generally presented as an example of a cannabinoid compound with no motor effects due to its poor affinity for the CB1 and the CB2 receptor, despite its activity at the TRPV1 receptor.	Cannabidiol	26-29	cannabinoid receptor 1	Rattus norvegicus	203-206
23924692-2	2013	By contrast, cannabidiol (CBD), a phytocannabinoid with a broad therapeutic profile, is generally presented as an example of a cannabinoid compound with no motor effects due to its poor affinity for the CB1 and the CB2 receptor, despite its activity at the TRPV1 receptor.	Cannabidiol	26-29	cannabinoid receptor 2	Rattus norvegicus	215-218
23924692-2	2013	By contrast, cannabidiol (CBD), a phytocannabinoid with a broad therapeutic profile, is generally presented as an example of a cannabinoid compound with no motor effects due to its poor affinity for the CB1 and the CB2 receptor, despite its activity at the TRPV1 receptor.	Cannabidiol	26-29	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	257-262
23924692-13	2013	Collectively, these results suggest that CBD may influence motor activity, in particular vertical activity, and that this effect seems to be dependent on its ability to target the 5-HT1A receptor, a mechanism of action that has been proposed to account for its anti-emetic, anxiolytic and antidepressant effects.	Cannabidiol	41-44	5-hydroxytryptamine receptor 1A	Rattus norvegicus	180-186
23981015-10	2013	Immunohistochemical analysis (obtained by synaptophysin staining) revealed 30% greater synaptic preservation within the spinal cord in the CBD-treated group.	Cannabidiol	139-142	synaptophysin	Rattus norvegicus	42-55
24309936-9	2013	The inhibition of VDAC1 by CBD may be responsible for the immunosuppressive and anticancer effects of CBD.	Cannabidiol	102-105	voltage-dependent anion channel 1	Mus musculus	18-23
23869687-5	2013	KEY RESULTS: Cannabidiol and cannabigerol significantly reduced the expression of all the genes tested in differentiated HaCaT cells, by increasing DNA methylation of keratin 10 gene, but cannabidivarin was ineffective.	Cannabidiol	13-24	keratin 10	Homo sapiens	167-177
23869687-6	2013	Remarkably, cannabidiol reduced keratin 10 mRNA through a type-1 cannabinoid (CB1 ) receptor-dependent mechanism, whereas cannabigerol did not affect either CB1 or CB2 receptors of HaCaT cells.	Cannabidiol	12-23	keratin 10	Homo sapiens	32-42
23869687-6	2013	Remarkably, cannabidiol reduced keratin 10 mRNA through a type-1 cannabinoid (CB1 ) receptor-dependent mechanism, whereas cannabigerol did not affect either CB1 or CB2 receptors of HaCaT cells.	Cannabidiol	12-23	cannabinoid receptor 1	Homo sapiens	78-81
23869687-7	2013	In addition, cannabidiol, but not cannabigerol, increased global DNA methylation levels by selectively enhancing DNMT1 expression, without affecting DNMT 3a, 3b or 3L.	Cannabidiol	13-24	DNA methyltransferase 1	Homo sapiens	113-118
23993482-7	2013	Immunohistochemical analysis revealed that cannabidiol significantly decreased the cadmium-induced expression of tumor necrosis factor-alpha, cyclooxygenase-2, nuclear factor-kappaB, caspase-3, and caspase-9, and increased the expression of endothelial nitric oxide synthase in liver tissue.	Cannabidiol	43-54	tumor necrosis factor	Rattus norvegicus	113-140
23993482-7	2013	Immunohistochemical analysis revealed that cannabidiol significantly decreased the cadmium-induced expression of tumor necrosis factor-alpha, cyclooxygenase-2, nuclear factor-kappaB, caspase-3, and caspase-9, and increased the expression of endothelial nitric oxide synthase in liver tissue.	Cannabidiol	43-54	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	142-192
23993482-7	2013	Immunohistochemical analysis revealed that cannabidiol significantly decreased the cadmium-induced expression of tumor necrosis factor-alpha, cyclooxygenase-2, nuclear factor-kappaB, caspase-3, and caspase-9, and increased the expression of endothelial nitric oxide synthase in liver tissue.	Cannabidiol	43-54	caspase 9	Rattus norvegicus	198-207
23791616-0	2013	Cannabidiol attenuates catalepsy induced by distinct pharmacological mechanisms via 5-HT1A receptor activation in mice.	Cannabidiol	0-11	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	84-99
23643693-0	2013	Infusion of cannabidiol into infralimbic cortex facilitates fear extinction via CB1 receptors.	Cannabidiol	12-23	cannabinoid receptor 1	Homo sapiens	80-83
24058883-0	2013	Cannabidiol changes P-gp and BCRP expression in trophoblast cell lines.	Cannabidiol	0-11	ATP binding cassette subfamily B member 1	Homo sapiens	20-24
24058883-0	2013	Cannabidiol changes P-gp and BCRP expression in trophoblast cell lines.	Cannabidiol	0-11	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	29-33
24058883-4	2013	We evaluated the impact of cannabidiol (CBD), a major non-psychoactive cannabinoid, on P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP) expression, and P-gp function in a placental model, BeWo and Jar choriocarcinoma cell lines (using P-gp induced MCF7 cells (MCF7/P-gp) for comparison).	Cannabidiol	27-38	ATP binding cassette subfamily B member 1	Homo sapiens	87-101
24058883-4	2013	We evaluated the impact of cannabidiol (CBD), a major non-psychoactive cannabinoid, on P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP) expression, and P-gp function in a placental model, BeWo and Jar choriocarcinoma cell lines (using P-gp induced MCF7 cells (MCF7/P-gp) for comparison).	Cannabidiol	27-38	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	113-145
24058883-4	2013	We evaluated the impact of cannabidiol (CBD), a major non-psychoactive cannabinoid, on P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP) expression, and P-gp function in a placental model, BeWo and Jar choriocarcinoma cell lines (using P-gp induced MCF7 cells (MCF7/P-gp) for comparison).	Cannabidiol	27-38	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	147-151
24058883-4	2013	We evaluated the impact of cannabidiol (CBD), a major non-psychoactive cannabinoid, on P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP) expression, and P-gp function in a placental model, BeWo and Jar choriocarcinoma cell lines (using P-gp induced MCF7 cells (MCF7/P-gp) for comparison).	Cannabidiol	40-43	ATP binding cassette subfamily B member 1	Homo sapiens	87-101
24058883-4	2013	We evaluated the impact of cannabidiol (CBD), a major non-psychoactive cannabinoid, on P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP) expression, and P-gp function in a placental model, BeWo and Jar choriocarcinoma cell lines (using P-gp induced MCF7 cells (MCF7/P-gp) for comparison).	Cannabidiol	40-43	ATP binding cassette subfamily B member 1	Homo sapiens	103-107
24058883-13	2013	P-gp dependent efflux (of calcein, DiOC2(3) and rh123) was inhibited upon short-term exposure to CBD.	Cannabidiol	97-100	ATP binding cassette subfamily B member 1	Homo sapiens	0-4
23721741-5	2013	Cannabidiol significantly reduced the elevations of serum creatine kinase-MB and troponin T, and cardiac malondialdehyde, tumor necrosis factor-alpha, nitric oxide and calcium ion levels, and attenuated the decreases in cardiac reduced glutathione, selenium and zinc ions.	Cannabidiol	0-11	tumor necrosis factor	Rattus norvegicus	122-149
23721741-7	2013	Immunohistochemical analysis revealed that cannabidiol significantly reduced the expression of inducible nitric oxide synthase, nuclear factor-kappaB, Fas ligand and caspase-3, and increased the expression of survivin in cardiac tissue of doxorubicin-treated rats.	Cannabidiol	43-54	Fas ligand	Rattus norvegicus	151-161
23721741-7	2013	Immunohistochemical analysis revealed that cannabidiol significantly reduced the expression of inducible nitric oxide synthase, nuclear factor-kappaB, Fas ligand and caspase-3, and increased the expression of survivin in cardiac tissue of doxorubicin-treated rats.	Cannabidiol	43-54	caspase 3	Rattus norvegicus	166-175
23041353-0	2013	Cannabidiol administration into the bed nucleus of the stria terminalis alters cardiovascular responses induced by acute restraint stress through 5-HT1A receptor.	Cannabidiol	0-11	5-hydroxytryptamine receptor 1A	Homo sapiens	146-161
23041353-1	2013	Systemic administration of cannabidiol (CBD) is able to attenuate cardiovascular responses to acute restraint stress through activation of 5-HT1A receptors.	Cannabidiol	27-38	5-hydroxytryptamine receptor 1A	Homo sapiens	139-145
23041353-1	2013	Systemic administration of cannabidiol (CBD) is able to attenuate cardiovascular responses to acute restraint stress through activation of 5-HT1A receptors.	Cannabidiol	40-43	5-hydroxytryptamine receptor 1A	Homo sapiens	139-145
23811569-0	2013	Structural requirements for potent direct inhibition of human cytochrome P450 1A1 by cannabidiol: role of pentylresorcinol moiety.	Cannabidiol	85-96	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	62-81
23461720-1	2013	BACKGROUND AND PURPOSE: GPR18 is a recently deorphaned lipid receptor that is activated by the endogenous lipid N-arachidonoyl glycine (NAGly) as well the behaviourally inactive atypical cannabinoid, abnormal cannabidiol (Abn-CBD).	Cannabidiol	209-220	G protein-coupled receptor 18	Mus musculus	24-29
23750331-10	2013	Evaluation of the PKs of THC/CBD spray alone and in combination with CYP450 inhibitors/inducers suggests that all analytes are substrates for the isoenzyme CYP3A4, but not CYP2C19.	Cannabidiol	29-32	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	156-162
23750331-11	2013	On the basis of our findings, there is likely to be little impact on other drugs metabolized by CYP enzymes on the PK parameters of THC/CBD spray, but potential effects should be taken into consideration when co-administering THC/CBD spray with compounds which share the CYP3A4 pathway such as rifampicin or ketoconazole.	Cannabidiol	136-139	peptidylprolyl isomerase G	Homo sapiens	96-99
23371366-10	2013	These results suggest that CBD-OPCA is a distinct clinicopathologic variant of CBD with olivopontocerebellar TDP-43 pathology.	Cannabidiol	27-30	TAR DNA binding protein	Homo sapiens	109-115
22862835-0	2013	Cannabidiol inhibits the reward-facilitating effect of morphine: involvement of 5-HT1A receptors in the dorsal raphe nucleus.	Cannabidiol	0-11	5-hydroxytryptamine receptor 1A	Rattus norvegicus	80-86
23243024-8	2013	Furthermore, we show that a nontoxic compound, cannabidiol, significantly downregulates Id-1 gene expression and associated glioma cell invasiveness and self-renewal.	Cannabidiol	47-58	inhibitor of DNA binding 1, HLH protein	Homo sapiens	88-92
23007604-11	2013	CONCLUSIONS: Together, these findings suggest that repeated treatment with CBD induces anti-panic effects by acting on 5-HT1A receptors in DPAG.	Cannabidiol	75-78	5-hydroxytryptamine receptor 1A	Rattus norvegicus	119-125
22625422-6	2013	Within the endocannabinoid system, CBD has been shown to have an inhibitory effect on the inactivation of endocannabinoids (i.e. inhibition of FAAH enzyme), thereby enhancing the action of these endogenous molecules on cannabinoid receptors, which is also noted in certain pathological conditions.	Cannabidiol	35-38	fatty acid amide hydrolase	Homo sapiens	143-147
23811569-1	2013	Our recent work has shown that cannabidiol (CBD) exhibits the most potent direct inhibition of human cytochrome P450 1A1 (CYP1A1) among the CYP enzymes examined.	Cannabidiol	31-42	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	101-120
23811569-1	2013	Our recent work has shown that cannabidiol (CBD) exhibits the most potent direct inhibition of human cytochrome P450 1A1 (CYP1A1) among the CYP enzymes examined.	Cannabidiol	31-42	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	122-128
23811569-1	2013	Our recent work has shown that cannabidiol (CBD) exhibits the most potent direct inhibition of human cytochrome P450 1A1 (CYP1A1) among the CYP enzymes examined.	Cannabidiol	44-47	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	101-120
23811569-1	2013	Our recent work has shown that cannabidiol (CBD) exhibits the most potent direct inhibition of human cytochrome P450 1A1 (CYP1A1) among the CYP enzymes examined.	Cannabidiol	44-47	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	122-128
23811569-4	2013	Olivetol, which corresponds to the pentylresorcinol moiety of CBD, inhibited the 7-ethoxyresorufin O-deethylase activity of CYP1A1; its inhibitory effect (IC50=13.8 microM) was less potent than that of CBD (IC50=0.355 microM).	Cannabidiol	62-65	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	124-130
23811569-4	2013	Olivetol, which corresponds to the pentylresorcinol moiety of CBD, inhibited the 7-ethoxyresorufin O-deethylase activity of CYP1A1; its inhibitory effect (IC50=13.8 microM) was less potent than that of CBD (IC50=0.355 microM).	Cannabidiol	202-205	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	124-130
23811569-5	2013	In contrast, d-limonene, which corresponds to the terpene moiety of CBD, only slightly inhibited CYP1A1 activity.	Cannabidiol	68-71	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	97-103
23811569-6	2013	CBD-2"-monomethyl ether (CBDM) and CBD-2",6"-dimethyl ether inhibited CYP1A1 activity with IC50 values of 4.07 and 23.0 microM, respectively, indicating that their inhibitory effects attenuated depending on the level of methylation on the free phenolic hydroxyl groups in the pentylresorcinol moiety of CBD.	Cannabidiol	0-3	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	70-76
23079154-0	2013	Triggering of the TRPV2 channel by cannabidiol sensitizes glioblastoma cells to cytotoxic chemotherapeutic agents.	Cannabidiol	35-46	transient receptor potential cation channel subfamily V member 2	Homo sapiens	18-23
23079154-5	2013	Herein, we evaluated the involvement of cannabidiol (CBD)-induced TRPV2 activation, in the modulation of glioma cell chemosensitivity to TMZ, BCNU and DOXO.	Cannabidiol	40-51	transient receptor potential cation channel subfamily V member 2	Homo sapiens	66-71
23079154-5	2013	Herein, we evaluated the involvement of cannabidiol (CBD)-induced TRPV2 activation, in the modulation of glioma cell chemosensitivity to TMZ, BCNU and DOXO.	Cannabidiol	53-56	transient receptor potential cation channel subfamily V member 2	Homo sapiens	66-71
23079154-8	2013	Moreover, as the pore region of transient receptor potential (TRP) channels is critical for ion channel permeation, we demonstrated that deletion of TRPV2 poredomain inhibits CBD-induced Ca(2+) influx, drug uptake and cytotoxic effects.	Cannabidiol	175-178	transient receptor potential cation channel subfamily V member 2	Homo sapiens	149-154
23079154-9	2013	Overall, we demonstrated that co-administration of cytotoxic agents together with the TRPV2 agonist CBD increases drug uptake and parallelly potentiates cytotoxic activity in human glioma cells.	Cannabidiol	100-103	transient receptor potential cation channel subfamily V member 2	Homo sapiens	86-91
23318708-0	2013	Cannabidiol is a potent inhibitor of the catalytic activity of cytochrome P450 2C19.	Cannabidiol	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	63-83
23318708-1	2013	The present study investigated the inhibitory effect of cannabidiol (CBD), a major constituent of marijuana, on the catalytic activity of cytochrome P450 2C19 (CYP2C19).	Cannabidiol	56-67	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	138-158
23318708-1	2013	The present study investigated the inhibitory effect of cannabidiol (CBD), a major constituent of marijuana, on the catalytic activity of cytochrome P450 2C19 (CYP2C19).	Cannabidiol	56-67	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	160-167
23318708-1	2013	The present study investigated the inhibitory effect of cannabidiol (CBD), a major constituent of marijuana, on the catalytic activity of cytochrome P450 2C19 (CYP2C19).	Cannabidiol	69-72	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	138-158
23318708-1	2013	The present study investigated the inhibitory effect of cannabidiol (CBD), a major constituent of marijuana, on the catalytic activity of cytochrome P450 2C19 (CYP2C19).	Cannabidiol	69-72	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	160-167
23318708-2	2013	(S)-Mephenytoin 4"-hydroxylase activities of human liver microsomes (HLMs) and recombinant CYP2C19 were inhibited by CBD in a concentration-dependent manner (IC50 = 8.70 and 2.51 microM, respectively).	Cannabidiol	117-120	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	4-30
23318708-2	2013	(S)-Mephenytoin 4"-hydroxylase activities of human liver microsomes (HLMs) and recombinant CYP2C19 were inhibited by CBD in a concentration-dependent manner (IC50 = 8.70 and 2.51 microM, respectively).	Cannabidiol	117-120	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	91-98
23318708-3	2013	Omeprazole 5-hydroxylase and 3-O-methylfluorescein O-demethylase activities in recombinant CYP2C19 were also strongly inhibited by CBD (IC50 = 1.55 and 1.79 microM, respectively).	Cannabidiol	131-134	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	91-98
23318708-4	2013	Kinetic analysis for inhibition revealed that CBD showed a mixed-type inhibition against (S)-mephenytoin 4"-hydroxylation by recombinant CYP2C19.	Cannabidiol	46-49	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	137-144
23318708-5	2013	To clarify the structural requirements for CBD-mediated CYP2C19 inhibition, the effects of CBD-related compounds on CYP2C19 activity were examined.	Cannabidiol	43-46	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	56-63
23318708-7	2013	The inhibitory effect of CBD-2"-monomethyl ether (IC50 = 1.88 microM) on CYP2C19 was comparable to that of CBD, although the inhibitory potency of CBD-2",6"-dimethyl ether (IC50 = 14.8 microM) was lower than that of CBD.	Cannabidiol	25-28	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	73-80
23630418-10	2013	Osteogenesis induced by CBD-BMP4, BMP4, and CBD was also assessed in a bone-defect model.	Cannabidiol	24-27	bone morphogenetic protein 4	Mus musculus	28-32
23630418-13	2013	CBD-BMP4 induced better bone formation than BMP4 did alone, CBD alone, and vehicle after the intramedullary injection into the mouse femur.	Cannabidiol	0-3	bone morphogenetic protein 4	Mus musculus	4-8
23630418-16	2013	CONCLUSION: Altogether, nanocarrier-CBD enhanced the retention of BMP4 in the bone, thereby promoting augmented osteogenic responses in the absence of a scaffold.	Cannabidiol	36-39	bone morphogenetic protein 4	Mus musculus	66-70
23220503-0	2013	COX-2 and PPAR-gamma confer cannabidiol-induced apoptosis of human lung cancer cells.	Cannabidiol	28-39	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	0-5
23220503-0	2013	COX-2 and PPAR-gamma confer cannabidiol-induced apoptosis of human lung cancer cells.	Cannabidiol	28-39	peroxisome proliferator activated receptor gamma	Homo sapiens	10-20
23220503-4	2013	Apoptotic cell death by cannabidiol was suppressed by NS-398 (COX-2 inhibitor), GW9662 (PPAR-gamma antagonist), and siRNA targeting COX-2 and PPAR-gamma.	Cannabidiol	24-35	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	62-67
23220503-4	2013	Apoptotic cell death by cannabidiol was suppressed by NS-398 (COX-2 inhibitor), GW9662 (PPAR-gamma antagonist), and siRNA targeting COX-2 and PPAR-gamma.	Cannabidiol	24-35	peroxisome proliferator activated receptor gamma	Homo sapiens	88-98
23220503-4	2013	Apoptotic cell death by cannabidiol was suppressed by NS-398 (COX-2 inhibitor), GW9662 (PPAR-gamma antagonist), and siRNA targeting COX-2 and PPAR-gamma.	Cannabidiol	24-35	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	132-137
23220503-4	2013	Apoptotic cell death by cannabidiol was suppressed by NS-398 (COX-2 inhibitor), GW9662 (PPAR-gamma antagonist), and siRNA targeting COX-2 and PPAR-gamma.	Cannabidiol	24-35	peroxisome proliferator activated receptor gamma	Homo sapiens	142-152
23220503-5	2013	Cannabidiol-induced apoptosis was paralleled by upregulation of COX-2 and PPAR-gamma mRNA and protein expression with a maximum induction of COX-2 mRNA after 8 hours and continuous increases of PPAR-gamma mRNA when compared with vehicle.	Cannabidiol	0-11	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	64-69
23220503-5	2013	Cannabidiol-induced apoptosis was paralleled by upregulation of COX-2 and PPAR-gamma mRNA and protein expression with a maximum induction of COX-2 mRNA after 8 hours and continuous increases of PPAR-gamma mRNA when compared with vehicle.	Cannabidiol	0-11	peroxisome proliferator activated receptor gamma	Homo sapiens	74-84
23220503-5	2013	Cannabidiol-induced apoptosis was paralleled by upregulation of COX-2 and PPAR-gamma mRNA and protein expression with a maximum induction of COX-2 mRNA after 8 hours and continuous increases of PPAR-gamma mRNA when compared with vehicle.	Cannabidiol	0-11	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	141-146
23220503-5	2013	Cannabidiol-induced apoptosis was paralleled by upregulation of COX-2 and PPAR-gamma mRNA and protein expression with a maximum induction of COX-2 mRNA after 8 hours and continuous increases of PPAR-gamma mRNA when compared with vehicle.	Cannabidiol	0-11	peroxisome proliferator activated receptor gamma	Homo sapiens	194-204
23220503-6	2013	In response to cannabidiol, tumor cell lines exhibited increased levels of COX-2-dependent prostaglandins (PG) among which PGD(2) and 15-deoxy-Delta(12,14)-PGJ(2) (15d-PGJ(2)) caused a translocation of PPAR-gamma to the nucleus and induced a PPAR-gamma-dependent apoptotic cell death.	Cannabidiol	15-26	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	75-80
23220503-6	2013	In response to cannabidiol, tumor cell lines exhibited increased levels of COX-2-dependent prostaglandins (PG) among which PGD(2) and 15-deoxy-Delta(12,14)-PGJ(2) (15d-PGJ(2)) caused a translocation of PPAR-gamma to the nucleus and induced a PPAR-gamma-dependent apoptotic cell death.	Cannabidiol	15-26	peroxisome proliferator activated receptor gamma	Homo sapiens	202-212
23220503-6	2013	In response to cannabidiol, tumor cell lines exhibited increased levels of COX-2-dependent prostaglandins (PG) among which PGD(2) and 15-deoxy-Delta(12,14)-PGJ(2) (15d-PGJ(2)) caused a translocation of PPAR-gamma to the nucleus and induced a PPAR-gamma-dependent apoptotic cell death.	Cannabidiol	15-26	peroxisome proliferator activated receptor gamma	Homo sapiens	242-252
23220503-7	2013	Moreover, in A549-xenografted nude mice, cannabidiol caused upregulation of COX-2 and PPAR-gamma in tumor tissue and tumor regression that was reversible by GW9662.	Cannabidiol	41-52	cytochrome c oxidase II, mitochondrial	Mus musculus	76-81
23220503-7	2013	Moreover, in A549-xenografted nude mice, cannabidiol caused upregulation of COX-2 and PPAR-gamma in tumor tissue and tumor regression that was reversible by GW9662.	Cannabidiol	41-52	peroxisome proliferator activated receptor gamma	Mus musculus	86-96
23220503-8	2013	Together, our data show a novel proapoptotic mechanism of cannabidiol involving initial upregulation of COX-2 and PPAR-gamma and a subsequent nuclear translocation of PPAR-gamma by COX-2-dependent PGs.	Cannabidiol	58-69	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	104-109
23220503-8	2013	Together, our data show a novel proapoptotic mechanism of cannabidiol involving initial upregulation of COX-2 and PPAR-gamma and a subsequent nuclear translocation of PPAR-gamma by COX-2-dependent PGs.	Cannabidiol	58-69	peroxisome proliferator activated receptor gamma	Homo sapiens	114-124
23220503-8	2013	Together, our data show a novel proapoptotic mechanism of cannabidiol involving initial upregulation of COX-2 and PPAR-gamma and a subsequent nuclear translocation of PPAR-gamma by COX-2-dependent PGs.	Cannabidiol	58-69	peroxisome proliferator activated receptor gamma	Homo sapiens	167-177
23220503-8	2013	Together, our data show a novel proapoptotic mechanism of cannabidiol involving initial upregulation of COX-2 and PPAR-gamma and a subsequent nuclear translocation of PPAR-gamma by COX-2-dependent PGs.	Cannabidiol	58-69	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	181-186
22850623-1	2013	OBJECTIVES: The anti-inflammatory effects of O-1602 and cannabidiol (CBD), the ligands of G protein-coupled receptor 55 (GPR55), on experimental acute pancreatitis (AP) were investigated.	Cannabidiol	56-67	G protein-coupled receptor 55	Mus musculus	121-126
22850623-1	2013	OBJECTIVES: The anti-inflammatory effects of O-1602 and cannabidiol (CBD), the ligands of G protein-coupled receptor 55 (GPR55), on experimental acute pancreatitis (AP) were investigated.	Cannabidiol	69-72	G protein-coupled receptor 55	Mus musculus	90-119
22850623-5	2013	RESULTS: Cannabidiol or O-1602 treatment significantly improved the pathological changes of mice with AP and decreased the enzyme activities, IL-6 and tumor necrosis factor alpha; levels, and the myeloperoxidase activities in plasma and in the organ tissues.	Cannabidiol	9-20	interleukin 6	Mus musculus	142-178
22850623-5	2013	RESULTS: Cannabidiol or O-1602 treatment significantly improved the pathological changes of mice with AP and decreased the enzyme activities, IL-6 and tumor necrosis factor alpha; levels, and the myeloperoxidase activities in plasma and in the organ tissues.	Cannabidiol	9-20	myeloperoxidase	Mus musculus	196-211
22850623-6	2013	G protein-coupled receptor 55 mRNA and protein expressed in the pancreatic tissue, and the expressions were decreased in the mice with AP, and either CBD or O-1602 attenuated these changes to a certain extent.	Cannabidiol	150-153	G protein-coupled receptor 55	Mus musculus	0-29
22850623-7	2013	CONCLUSION: Cannabidiol and O-1602 showed anti-inflammatory effects in mice with AP and improved the expression of GPR55 in the pancreatic tissue as well.	Cannabidiol	12-23	G protein-coupled receptor 55	Mus musculus	115-120
23085269-9	2012	The extended administration of cannabidiol at different doses reduced the TNF-alpha level in frontal cortex.	Cannabidiol	31-42	tumor necrosis factor	Rattus norvegicus	74-83
22979992-0	2012	Cannabidiol blocks long-lasting behavioral consequences of predator threat stress: possible involvement of 5HT1A receptors.	Cannabidiol	0-11	5-hydroxytryptamine receptor 1A	Homo sapiens	107-112
22979992-16	2012	Repeated CBD administration prevents the long-lasting anxiogenic effects observed after predator exposure probably by facilitating 5HT1A receptors neurotransmission.	Cannabidiol	9-12	5-hydroxytryptamine receptor 1A	Homo sapiens	131-136
22234957-7	2012	In further testing CBD requirements, we show that MTG binds N-acetylglucosamine (GlcNAc) in a Ca(2+)-dependent manner, and thereby binds HRP-epitope glycans, but that these carbohydrate interactions do not require the CBD.	Cannabidiol	19-22	mind the gap	Drosophila melanogaster	50-53
22899554-6	2012	THC or CBD suppressed or enhanced IFN-gamma and IL-2 production by mouse splenocytes under optimal or suboptimal stimulation, respectively.	Cannabidiol	7-10	interferon gamma	Mus musculus	34-43
22899554-6	2012	THC or CBD suppressed or enhanced IFN-gamma and IL-2 production by mouse splenocytes under optimal or suboptimal stimulation, respectively.	Cannabidiol	7-10	interleukin 2	Mus musculus	48-52
22877651-8	2012	Immunohistochemical analysis revealed that cannabidiol significantly reduced the expression of inducible nitric oxide synthase, tumor necrosis factor-alpha, cyclooxygenase-2, nuclear factor-kappaB, Fas ligand and caspase-3, and increased the expression of survivin in ischemic/reperfused kidney tissue.	Cannabidiol	43-54	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	157-196
22877651-8	2012	Immunohistochemical analysis revealed that cannabidiol significantly reduced the expression of inducible nitric oxide synthase, tumor necrosis factor-alpha, cyclooxygenase-2, nuclear factor-kappaB, Fas ligand and caspase-3, and increased the expression of survivin in ischemic/reperfused kidney tissue.	Cannabidiol	43-54	Fas ligand	Rattus norvegicus	198-208
22877651-8	2012	Immunohistochemical analysis revealed that cannabidiol significantly reduced the expression of inducible nitric oxide synthase, tumor necrosis factor-alpha, cyclooxygenase-2, nuclear factor-kappaB, Fas ligand and caspase-3, and increased the expression of survivin in ischemic/reperfused kidney tissue.	Cannabidiol	43-54	caspase 3	Rattus norvegicus	213-222
22231745-5	2012	Cannabidiol-reduced ACF, polyps and tumours and counteracted AOM-induced phospho-Akt and caspase-3 changes.	Cannabidiol	0-11	thymoma viral proto-oncogene 1	Mus musculus	81-84
22231745-5	2012	Cannabidiol-reduced ACF, polyps and tumours and counteracted AOM-induced phospho-Akt and caspase-3 changes.	Cannabidiol	0-11	caspase 3	Mus musculus	89-98
22231745-6	2012	In colorectal carcinoma cell lines, cannabidiol protected DNA from oxidative damage, increased endocannabinoid levels and reduced cell proliferation in a CB(1)-, TRPV1- and PPARgamma-antagonists sensitive manner.	Cannabidiol	36-47	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	162-167
22231745-6	2012	In colorectal carcinoma cell lines, cannabidiol protected DNA from oxidative damage, increased endocannabinoid levels and reduced cell proliferation in a CB(1)-, TRPV1- and PPARgamma-antagonists sensitive manner.	Cannabidiol	36-47	peroxisome proliferator activated receptor gamma	Mus musculus	173-182
22580290-1	2012	The purpose of this study was to investigate the effects of abnormal-cannabidiol (abn-cbd), a non-psychoactive cannabinoid agonist, on aqueous humor outflow via the trabecular meshwork (TM) of porcine eye, and to examine the involvement of a non-CB1/CB2 cannabinoid receptor and the p42/44 mitogen-activated protein kinase (p42/44 MAPK) pathway.	Cannabidiol	68-80	cannabinoid receptor 1	Homo sapiens	246-249
22535572-4	2012	Treatment of murine primary microglial cultures with CBD resulted in a time- and concentration-dependent induction of apoptosis, as shown by increase in hypodiploid cells and DNA strand breaks, and marked activation of both caspase-8 and -9.	Cannabidiol	53-56	caspase 8	Mus musculus	224-240
22535572-8	2012	Taken together, these results suggest that CBD induces a marked proapoptotic effect in primary microglia through lipid raft coalescence and elevated expression of GM1 ganglioside and caveolin-1.	Cannabidiol	43-46	coenzyme Q10A	Mus musculus	163-166
22535572-8	2012	Taken together, these results suggest that CBD induces a marked proapoptotic effect in primary microglia through lipid raft coalescence and elevated expression of GM1 ganglioside and caveolin-1.	Cannabidiol	43-46	caveolin 1, caveolae protein	Mus musculus	183-193
22580290-1	2012	The purpose of this study was to investigate the effects of abnormal-cannabidiol (abn-cbd), a non-psychoactive cannabinoid agonist, on aqueous humor outflow via the trabecular meshwork (TM) of porcine eye, and to examine the involvement of a non-CB1/CB2 cannabinoid receptor and the p42/44 mitogen-activated protein kinase (p42/44 MAPK) pathway.	Cannabidiol	68-80	cannabinoid receptor 2	Homo sapiens	250-253
22580290-1	2012	The purpose of this study was to investigate the effects of abnormal-cannabidiol (abn-cbd), a non-psychoactive cannabinoid agonist, on aqueous humor outflow via the trabecular meshwork (TM) of porcine eye, and to examine the involvement of a non-CB1/CB2 cannabinoid receptor and the p42/44 mitogen-activated protein kinase (p42/44 MAPK) pathway.	Cannabidiol	68-80	cyclin dependent kinase 20	Homo sapiens	283-286
22580290-1	2012	The purpose of this study was to investigate the effects of abnormal-cannabidiol (abn-cbd), a non-psychoactive cannabinoid agonist, on aqueous humor outflow via the trabecular meshwork (TM) of porcine eye, and to examine the involvement of a non-CB1/CB2 cannabinoid receptor and the p42/44 mitogen-activated protein kinase (p42/44 MAPK) pathway.	Cannabidiol	68-80	cyclin dependent kinase 20	Homo sapiens	324-327
22092062-12	2012	Cannabidiol increased fibronectin production by as much as approximately 100% (p < 0.001).	Cannabidiol	0-11	fibronectin 1	Homo sapiens	22-33
21827451-0	2012	Cannabidiol, a non-psychotropic component of cannabis, attenuates vomiting and nausea-like behaviour via indirect agonism of 5-HT(1A)  somatodendritic autoreceptors in the dorsal raphe nucleus.	Cannabidiol	0-11	5-hydroxytryptamine receptor 1A	Rattus norvegicus	125-132
21827451-1	2012	BACKGROUND AND PURPOSE: To evaluate the hypothesis that activation of somatodendritic 5-HT(1A) autoreceptors in the dorsal raphe nucleus (DRN) produces the anti-emetic/anti-nausea effects of cannabidiol (CBD), a primary non-psychoactive cannabinoid found in cannabis.	Cannabidiol	191-202	5-hydroxytryptamine receptor 1A	Rattus norvegicus	86-93
21827451-2	2012	EXPERIMENTAL APPROACH: The potential of systemic and intra-DRN administration of 5-HT(1A) receptor antagonists, WAY100135 or WAY100635, to prevent the anti-emetic effect of CBD in shrews (Suncus murinus) and the anti-nausea-like effects of CBD (conditioned gaping) in rats were evaluated.	Cannabidiol	173-176	5-hydroxytryptamine receptor 1A	Rattus norvegicus	81-88
21827451-10	2012	CONCLUSIONS AND IMPLICATIONS: These results suggest that CBD produced its anti-emetic/anti-nausea effects by indirect activation of the somatodendritic 5-HT(1A) autoreceptors in the DRN.	Cannabidiol	57-60	5-hydroxytryptamine receptor 1A	Rattus norvegicus	152-159
22198381-0	2012	Cannabidiol inhibits lung cancer cell invasion and metastasis via intercellular adhesion molecule-1.	Cannabidiol	0-11	intercellular adhesion molecule 1	Homo sapiens	66-99
22198381-3	2012	In the lung cancer cell lines A549, H358, and H460, cannabidiol (CBD; 0.001-3 muM) elicited concentration-dependent ICAM-1 up-regulation compared to vehicle via cannabinoid receptors, transient receptor potential vanilloid 1, and p42/44 mitogen-activated protein kinase.	Cannabidiol	52-63	latexin	Homo sapiens	78-81
22198381-3	2012	In the lung cancer cell lines A549, H358, and H460, cannabidiol (CBD; 0.001-3 muM) elicited concentration-dependent ICAM-1 up-regulation compared to vehicle via cannabinoid receptors, transient receptor potential vanilloid 1, and p42/44 mitogen-activated protein kinase.	Cannabidiol	52-63	intercellular adhesion molecule 1	Homo sapiens	116-122
22198381-3	2012	In the lung cancer cell lines A549, H358, and H460, cannabidiol (CBD; 0.001-3 muM) elicited concentration-dependent ICAM-1 up-regulation compared to vehicle via cannabinoid receptors, transient receptor potential vanilloid 1, and p42/44 mitogen-activated protein kinase.	Cannabidiol	52-63	cyclin dependent kinase 20	Homo sapiens	230-233
22198381-3	2012	In the lung cancer cell lines A549, H358, and H460, cannabidiol (CBD; 0.001-3 muM) elicited concentration-dependent ICAM-1 up-regulation compared to vehicle via cannabinoid receptors, transient receptor potential vanilloid 1, and p42/44 mitogen-activated protein kinase.	Cannabidiol	65-68	latexin	Homo sapiens	78-81
22198381-3	2012	In the lung cancer cell lines A549, H358, and H460, cannabidiol (CBD; 0.001-3 muM) elicited concentration-dependent ICAM-1 up-regulation compared to vehicle via cannabinoid receptors, transient receptor potential vanilloid 1, and p42/44 mitogen-activated protein kinase.	Cannabidiol	65-68	intercellular adhesion molecule 1	Homo sapiens	116-122
22198381-3	2012	In the lung cancer cell lines A549, H358, and H460, cannabidiol (CBD; 0.001-3 muM) elicited concentration-dependent ICAM-1 up-regulation compared to vehicle via cannabinoid receptors, transient receptor potential vanilloid 1, and p42/44 mitogen-activated protein kinase.	Cannabidiol	65-68	cyclin dependent kinase 20	Homo sapiens	230-233
22198381-7	2012	In athymic nude mice, CBD elicited a 2.6- and 3.0-fold increase of ICAM-1 and TIMP-1 protein in A549 xenografts, as compared to vehicle-treated animals, and an antimetastatic effect that was fully reversed by a neutralizing antibody against ICAM-1 [% metastatic lung nodules vs. isotype control (100%): 47.7% for CBD + isotype antibody and 106.6% for CBD + ICAM-1 antibody].	Cannabidiol	22-25	intercellular adhesion molecule 1	Mus musculus	67-73
22198381-7	2012	In athymic nude mice, CBD elicited a 2.6- and 3.0-fold increase of ICAM-1 and TIMP-1 protein in A549 xenografts, as compared to vehicle-treated animals, and an antimetastatic effect that was fully reversed by a neutralizing antibody against ICAM-1 [% metastatic lung nodules vs. isotype control (100%): 47.7% for CBD + isotype antibody and 106.6% for CBD + ICAM-1 antibody].	Cannabidiol	22-25	tissue inhibitor of metalloproteinase 1	Mus musculus	78-84
22198381-7	2012	In athymic nude mice, CBD elicited a 2.6- and 3.0-fold increase of ICAM-1 and TIMP-1 protein in A549 xenografts, as compared to vehicle-treated animals, and an antimetastatic effect that was fully reversed by a neutralizing antibody against ICAM-1 [% metastatic lung nodules vs. isotype control (100%): 47.7% for CBD + isotype antibody and 106.6% for CBD + ICAM-1 antibody].	Cannabidiol	22-25	intercellular adhesion molecule 1	Mus musculus	241-247
22198381-7	2012	In athymic nude mice, CBD elicited a 2.6- and 3.0-fold increase of ICAM-1 and TIMP-1 protein in A549 xenografts, as compared to vehicle-treated animals, and an antimetastatic effect that was fully reversed by a neutralizing antibody against ICAM-1 [% metastatic lung nodules vs. isotype control (100%): 47.7% for CBD + isotype antibody and 106.6% for CBD + ICAM-1 antibody].	Cannabidiol	22-25	intercellular adhesion molecule 1	Mus musculus	241-247
22265864-0	2012	Cannabidiol, a non-psychotropic plant-derived cannabinoid, decreases inflammation in a murine model of acute lung injury: role for the adenosine A(2A) receptor.	Cannabidiol	0-11	adenosine A2a receptor	Mus musculus	135-159
22265864-7	2012	Thus, we show that cannabidiol has anti-inflammatory effects in a murine model of acute lung injury and that this effect is most likely associated with an increase in the extracellular adenosine offer and signaling through adenosine A(2A) receptor.	Cannabidiol	19-30	adenosine A2a receptor	Mus musculus	223-247
21726418-1	2012	AIM: Plant cannabinoids, like Delta(9)-tetrahydrocannabinol (THC) and cannabidiol (CBD), activate/desensitize thermosensitive transient receptor potential (TRP) channels of vanilloid type-1 or -2 (TRPV1 or TRPV2).	Cannabidiol	70-81	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	197-202
21726418-1	2012	AIM: Plant cannabinoids, like Delta(9)-tetrahydrocannabinol (THC) and cannabidiol (CBD), activate/desensitize thermosensitive transient receptor potential (TRP) channels of vanilloid type-1 or -2 (TRPV1 or TRPV2).	Cannabidiol	70-81	transient receptor potential cation channel, subfamily V, member 2	Mus musculus	206-211
21726418-1	2012	AIM: Plant cannabinoids, like Delta(9)-tetrahydrocannabinol (THC) and cannabidiol (CBD), activate/desensitize thermosensitive transient receptor potential (TRP) channels of vanilloid type-1 or -2 (TRPV1 or TRPV2).	Cannabidiol	83-86	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	197-202
21726418-1	2012	AIM: Plant cannabinoids, like Delta(9)-tetrahydrocannabinol (THC) and cannabidiol (CBD), activate/desensitize thermosensitive transient receptor potential (TRP) channels of vanilloid type-1 or -2 (TRPV1 or TRPV2).	Cannabidiol	83-86	transient receptor potential cation channel, subfamily V, member 2	Mus musculus	206-211
22414698-8	2012	Intrarectal treatment with CBD also led to a significant improvement of disease parameters and to a decrease in MPO activity while oral treatment, using the same dose as per rectum, had no ameliorating effect on colitis.	Cannabidiol	27-30	myeloperoxidase	Mus musculus	112-115
21148020-0	2012	Cannabidiol injected into the bed nucleus of the stria terminalis reduces the expression of contextual fear conditioning via 5-HT1A receptors.	Cannabidiol	0-11	5-hydroxytryptamine receptor 1A	Rattus norvegicus	125-131
22814029-5	2012	RESULTS: We showed that both cannabidiol (CBD) and Delta(9)-tetrahydrocannabinol (Delta(9)-THC) (10 muM) transiently induced the MDR1 transcript in P-gp overexpressing cells at 4 but not 8 or 48 h incubation durations.	Cannabidiol	29-40	latexin	Homo sapiens	100-103
22814029-5	2012	RESULTS: We showed that both cannabidiol (CBD) and Delta(9)-tetrahydrocannabinol (Delta(9)-THC) (10 muM) transiently induced the MDR1 transcript in P-gp overexpressing cells at 4 but not 8 or 48 h incubation durations.	Cannabidiol	29-40	ATP binding cassette subfamily B member 1	Homo sapiens	129-133
22814029-5	2012	RESULTS: We showed that both cannabidiol (CBD) and Delta(9)-tetrahydrocannabinol (Delta(9)-THC) (10 muM) transiently induced the MDR1 transcript in P-gp overexpressing cells at 4 but not 8 or 48 h incubation durations.	Cannabidiol	29-40	ATP binding cassette subfamily B member 1	Homo sapiens	148-152
22814029-5	2012	RESULTS: We showed that both cannabidiol (CBD) and Delta(9)-tetrahydrocannabinol (Delta(9)-THC) (10 muM) transiently induced the MDR1 transcript in P-gp overexpressing cells at 4 but not 8 or 48 h incubation durations.	Cannabidiol	42-45	ATP binding cassette subfamily B member 1	Homo sapiens	129-133
22814029-5	2012	RESULTS: We showed that both cannabidiol (CBD) and Delta(9)-tetrahydrocannabinol (Delta(9)-THC) (10 muM) transiently induced the MDR1 transcript in P-gp overexpressing cells at 4 but not 8 or 48 h incubation durations.	Cannabidiol	42-45	ATP binding cassette subfamily B member 1	Homo sapiens	148-152
22814029-6	2012	CBD and THC also concomitantly increased P-gp activity as measured by reduced accumulation of the P-gp substrate Rhodamine 123 in these cells with a maximal inhibitory effect observed at 4 h that slowly diminished by 48 h. CEM/VLB(100) cell lines were shown to express CB(2) and TRPV(1) receptors.	Cannabidiol	0-3	ATP binding cassette subfamily B member 1	Homo sapiens	41-45
22814029-6	2012	CBD and THC also concomitantly increased P-gp activity as measured by reduced accumulation of the P-gp substrate Rhodamine 123 in these cells with a maximal inhibitory effect observed at 4 h that slowly diminished by 48 h. CEM/VLB(100) cell lines were shown to express CB(2) and TRPV(1) receptors.	Cannabidiol	0-3	ATP binding cassette subfamily B member 1	Homo sapiens	98-102
22814029-6	2012	CBD and THC also concomitantly increased P-gp activity as measured by reduced accumulation of the P-gp substrate Rhodamine 123 in these cells with a maximal inhibitory effect observed at 4 h that slowly diminished by 48 h. CEM/VLB(100) cell lines were shown to express CB(2) and TRPV(1) receptors.	Cannabidiol	0-3	transient receptor potential cation channel subfamily V member 1	Homo sapiens	279-286
22509273-0	2012	Distinct neurobehavioural effects of cannabidiol in transmembrane domain neuregulin 1 mutant mice.	Cannabidiol	37-48	neuregulin 1	Mus musculus	73-85
23185387-7	2012	The TRPV channel activator cannabidiol (CBD) at 15 microM stimulates intracellular Ca(2+)-rise suggesting that porcine RPE cells express TRPV2 channels.	Cannabidiol	27-38	transient receptor potential cation channel, subfamily V, member 2	Mus musculus	137-142
23185387-7	2012	The TRPV channel activator cannabidiol (CBD) at 15 microM stimulates intracellular Ca(2+)-rise suggesting that porcine RPE cells express TRPV2 channels.	Cannabidiol	40-43	transient receptor potential cation channel, subfamily V, member 2	Mus musculus	137-142
23185387-8	2012	Further evidence supporting the functional expression of TRPV2 channels comes from experiments in which 100 microM SKF96365 (a TRPV channel inhibitor) reduced the cannabidiol-induced Ca(2+)-rise.	Cannabidiol	163-174	transient receptor potential cation channel, subfamily V, member 2	Mus musculus	57-62
22509273-8	2012	However, long-term CBD (50 and 100 mg/kg) selectively enhanced social interaction in Nrg1 TM HET mice.	Cannabidiol	19-22	neuregulin 1	Mus musculus	85-89
22509273-9	2012	Furthermore, acute CBD (100 mg/kg) selectively increased PPI in Nrg1 TM HET mice, although tolerance to this effect was manifest upon repeated CBD administration.	Cannabidiol	19-22	neuregulin 1	Mus musculus	64-68
22509273-10	2012	Long-term CBD (50 mg/kg) also selectively increased GABA(A) receptor binding in the granular retrosplenial cortex in Nrg1 TM HET mice and reduced 5-HT(2A) binding in the substantia nigra in WT mice.	Cannabidiol	10-13	neuregulin 1	Mus musculus	117-121
22509273-11	2012	Nrg1 appears necessary for CBD-induced anxiolysis since only WT mice developed decreased anxiety-related behaviour with repeated CBD treatment.	Cannabidiol	27-30	neuregulin 1	Mus musculus	0-4
22509273-11	2012	Nrg1 appears necessary for CBD-induced anxiolysis since only WT mice developed decreased anxiety-related behaviour with repeated CBD treatment.	Cannabidiol	129-132	neuregulin 1	Mus musculus	0-4
22509273-13	2012	Here we demonstrate that Nrg1 modulates acute and long-term neurobehavioural effects of CBD, which does not reverse the schizophrenia-relevant phenotypes.	Cannabidiol	88-91	neuregulin 1	Mus musculus	25-29
21930120-7	2011	Immunohistochemical analysis revealed that cannabidiol significantly reduced the expression of inducible nitric oxide synthase, cyclooxygenase-2, nuclear factor-kappaB, Fas ligand and caspase-3, and increased the expression of survivin protein in ischemic/reperfused liver tissue.	Cannabidiol	43-54	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	128-167
21930120-7	2011	Immunohistochemical analysis revealed that cannabidiol significantly reduced the expression of inducible nitric oxide synthase, cyclooxygenase-2, nuclear factor-kappaB, Fas ligand and caspase-3, and increased the expression of survivin protein in ischemic/reperfused liver tissue.	Cannabidiol	43-54	Fas ligand	Rattus norvegicus	169-179
21930120-7	2011	Immunohistochemical analysis revealed that cannabidiol significantly reduced the expression of inducible nitric oxide synthase, cyclooxygenase-2, nuclear factor-kappaB, Fas ligand and caspase-3, and increased the expression of survivin protein in ischemic/reperfused liver tissue.	Cannabidiol	43-54	caspase 3	Rattus norvegicus	184-193
22110202-4	2011	RESULTS: CBD and WIN inhibited LNCaP and SW480 cell growth and induced mRNA expression of several phosphatases, and the phosphatase inhibitor sodium orthovanadate significantly inhibited cannabinoid-induced PARP cleavage in both cell lines, whereas only CBD-induced apoptosis was CB1 and CB2 receptor-dependent.	Cannabidiol	9-12	poly(ADP-ribose) polymerase 1	Homo sapiens	207-211
22110202-4	2011	RESULTS: CBD and WIN inhibited LNCaP and SW480 cell growth and induced mRNA expression of several phosphatases, and the phosphatase inhibitor sodium orthovanadate significantly inhibited cannabinoid-induced PARP cleavage in both cell lines, whereas only CBD-induced apoptosis was CB1 and CB2 receptor-dependent.	Cannabidiol	9-12	cannabinoid receptor 1	Homo sapiens	280-283
22110202-4	2011	RESULTS: CBD and WIN inhibited LNCaP and SW480 cell growth and induced mRNA expression of several phosphatases, and the phosphatase inhibitor sodium orthovanadate significantly inhibited cannabinoid-induced PARP cleavage in both cell lines, whereas only CBD-induced apoptosis was CB1 and CB2 receptor-dependent.	Cannabidiol	9-12	cannabinoid receptor 2	Homo sapiens	288-291
21821735-0	2011	Cannabidiol, a major phytocannabinoid, as a potent atypical inhibitor for CYP2D6.	Cannabidiol	0-11	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	74-80
21821735-5	2011	CBD competitively inhibited the CYP2D6 activities with the apparent K(i) values of 1.16 to 2.69 muM.	Cannabidiol	0-3	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	32-38
21821735-6	2011	To clarify the structural requirement for CBD-mediated CYP2D6 inhibition, effects of CBD-related compounds on the AMMC O-demethylase activity of recombinant CYP2D6 were examined.	Cannabidiol	42-45	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	55-61
21821735-6	2011	To clarify the structural requirement for CBD-mediated CYP2D6 inhibition, effects of CBD-related compounds on the AMMC O-demethylase activity of recombinant CYP2D6 were examined.	Cannabidiol	42-45	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	157-163
21887521-3	2011	We suggested that CBD and PPA should be included with frontal lobe dementia as Pick complex.	Cannabidiol	18-21	protein interacting with PRKCA 1	Homo sapiens	79-83
25379896-0	2011	Administration of cannabidiol and imipramine induces antidepressant-like effects in the forced swimming test and increases brain-derived neurotrophic factor levels in the rat amygdala.	Cannabidiol	18-29	brain-derived neurotrophic factor	Rattus norvegicus	123-156
21674569-4	2011	The administration of Delta(9)-THC- and CBD-enriched botanical extracts combined in a ratio of 1:1 as in Sativex attenuated 3NP-induced GABA deficiency, loss of Nissl-stained neurons, down-regulation of CB(1) receptor and IGF-1 expression, and up-regulation of calpain expression, whereas it completely reversed the reduction in superoxide dismutase-1 expression.	Cannabidiol	40-43	insulin-like growth factor 1	Rattus norvegicus	222-227
21674569-5	2011	Similar responses were generally found with other combinations of Delta(9)-THC- and CBD-enriched botanical extracts, suggesting that these effects are probably related to the antioxidant and CB(1) and CB(2) receptor-independent properties of both phytocannabinoids.	Cannabidiol	84-87	cannabinoid receptor 1	Rattus norvegicus	191-196
21674569-5	2011	Similar responses were generally found with other combinations of Delta(9)-THC- and CBD-enriched botanical extracts, suggesting that these effects are probably related to the antioxidant and CB(1) and CB(2) receptor-independent properties of both phytocannabinoids.	Cannabidiol	84-87	cannabinoid receptor 2	Rattus norvegicus	201-215
21683763-0	2011	The abnormal cannabidiol analogue O-1602 reduces nociception in a rat model of acute arthritis via the putative cannabinoid receptor GPR55.	Cannabidiol	13-24	G protein-coupled receptor 55	Rattus norvegicus	133-138
21726355-1	2011	BACKGROUND: This study was to investigate the effects of the novel cannabinoid receptor - G protein-coupled receptor 55 (GPR55) - and its ligands O-1602 and cannabidiol (CBD) on gastrointestinal (GI) motility in rodents.	Cannabidiol	157-168	G protein-coupled receptor 55	Rattus norvegicus	90-119
21726355-1	2011	BACKGROUND: This study was to investigate the effects of the novel cannabinoid receptor - G protein-coupled receptor 55 (GPR55) - and its ligands O-1602 and cannabidiol (CBD) on gastrointestinal (GI) motility in rodents.	Cannabidiol	157-168	G protein-coupled receptor 55	Rattus norvegicus	121-126
21726355-1	2011	BACKGROUND: This study was to investigate the effects of the novel cannabinoid receptor - G protein-coupled receptor 55 (GPR55) - and its ligands O-1602 and cannabidiol (CBD) on gastrointestinal (GI) motility in rodents.	Cannabidiol	170-173	G protein-coupled receptor 55	Rattus norvegicus	90-119
21726355-1	2011	BACKGROUND: This study was to investigate the effects of the novel cannabinoid receptor - G protein-coupled receptor 55 (GPR55) - and its ligands O-1602 and cannabidiol (CBD) on gastrointestinal (GI) motility in rodents.	Cannabidiol	170-173	G protein-coupled receptor 55	Rattus norvegicus	121-126
21175579-4	2011	KEY RESULTS: CBD, CBG, CBGV and THCV stimulated and desensitized human TRPV1.	Cannabidiol	13-16	transient receptor potential cation channel subfamily V member 1	Homo sapiens	71-76
21175579-10	2011	CBD was the only compound to inhibit FAAH, whereas the BDS of CBC > CBG > CBGV inhibited NAAA.	Cannabidiol	0-3	fatty-acid amide hydrolase-like	Rattus norvegicus	37-41
20859676-5	2011	We previously reported that cannabidiol (CBD), a cannabinoid with a low toxicity profile, down-regulated Id-1 gene expression in aggressive human breast cancer cells in culture.	Cannabidiol	28-39	inhibitor of DNA binding 1, HLH protein	Homo sapiens	105-109
20859676-5	2011	We previously reported that cannabidiol (CBD), a cannabinoid with a low toxicity profile, down-regulated Id-1 gene expression in aggressive human breast cancer cells in culture.	Cannabidiol	41-44	inhibitor of DNA binding 1, HLH protein	Homo sapiens	105-109
21533611-8	2011	Moreover, we found that pretreatment of the cells with the cholesterol chelating agent, methyl-beta-cyclodextrin (MBCD), reversed the CBD-induced increase in Soat2 mRNA but not in Plin2 mRNA.	Cannabidiol	134-137	sterol O-acyltransferase 2	Homo sapiens	158-163
21533611-8	2011	Moreover, we found that pretreatment of the cells with the cholesterol chelating agent, methyl-beta-cyclodextrin (MBCD), reversed the CBD-induced increase in Soat2 mRNA but not in Plin2 mRNA.	Cannabidiol	134-137	perilipin 2	Homo sapiens	180-185
21683763-2	2011	One such receptor is GPR55 which is activated by the abnormal cannabidiol analogue O-1602.	Cannabidiol	62-73	G protein-coupled receptor 55	Rattus norvegicus	21-26
21566064-6	2011	We showed that CBD induces endoplasmic reticulum stress and, subsequently, inhibits AKT and mTOR signaling as shown by decreased levels of phosphorylated mTOR and 4EBP1, and cyclin D1.	Cannabidiol	15-18	AKT serine/threonine kinase 1	Homo sapiens	84-87
21704641-0	2011	Identification of cytochrome P450 enzymes responsible for metabolism of cannabidiol by human liver microsomes.	Cannabidiol	72-83	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	18-33
21704641-3	2011	In this study, we examined in vitro metabolism of CBD with human liver microsomes (HLMs) to clarify cytochrome P450 (CYP) isoforms involved in the CBD oxidations.	Cannabidiol	50-53	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	100-115
21704641-3	2011	In this study, we examined in vitro metabolism of CBD with human liver microsomes (HLMs) to clarify cytochrome P450 (CYP) isoforms involved in the CBD oxidations.	Cannabidiol	50-53	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	117-120
21704641-7	2011	Seven of 14 recombinant human CYP enzymes examined (CYP1A1, CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5) were capable of metabolizing CBD.	Cannabidiol	142-145	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	30-33
21704641-7	2011	Seven of 14 recombinant human CYP enzymes examined (CYP1A1, CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5) were capable of metabolizing CBD.	Cannabidiol	142-145	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	52-58
21704641-7	2011	Seven of 14 recombinant human CYP enzymes examined (CYP1A1, CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5) were capable of metabolizing CBD.	Cannabidiol	142-145	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	60-66
21704641-7	2011	Seven of 14 recombinant human CYP enzymes examined (CYP1A1, CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5) were capable of metabolizing CBD.	Cannabidiol	142-145	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
21704641-7	2011	Seven of 14 recombinant human CYP enzymes examined (CYP1A1, CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5) were capable of metabolizing CBD.	Cannabidiol	142-145	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	76-83
21704641-7	2011	Seven of 14 recombinant human CYP enzymes examined (CYP1A1, CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5) were capable of metabolizing CBD.	Cannabidiol	142-145	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	85-91
21704641-7	2011	Seven of 14 recombinant human CYP enzymes examined (CYP1A1, CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5) were capable of metabolizing CBD.	Cannabidiol	142-145	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	93-99
21704641-7	2011	Seven of 14 recombinant human CYP enzymes examined (CYP1A1, CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5) were capable of metabolizing CBD.	Cannabidiol	142-145	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	105-111
21566064-6	2011	We showed that CBD induces endoplasmic reticulum stress and, subsequently, inhibits AKT and mTOR signaling as shown by decreased levels of phosphorylated mTOR and 4EBP1, and cyclin D1.	Cannabidiol	15-18	mechanistic target of rapamycin kinase	Homo sapiens	92-96
21566064-6	2011	We showed that CBD induces endoplasmic reticulum stress and, subsequently, inhibits AKT and mTOR signaling as shown by decreased levels of phosphorylated mTOR and 4EBP1, and cyclin D1.	Cannabidiol	15-18	tortured	Mus musculus	154-168
21566064-6	2011	We showed that CBD induces endoplasmic reticulum stress and, subsequently, inhibits AKT and mTOR signaling as shown by decreased levels of phosphorylated mTOR and 4EBP1, and cyclin D1.	Cannabidiol	15-18	cyclin D1	Homo sapiens	174-183
21566064-7	2011	Analyzing further the cross-talk between the autophagic and apoptotic signaling pathways, we found that beclin1 plays a central role in the induction of CBD-mediated apoptosis in MDA-MB-231 breast cancer cells.	Cannabidiol	153-156	beclin 1	Homo sapiens	104-111
21477640-3	2011	Here, we report that CBD and THC inhibited the function of human 5-HT(3A) receptors (h5-HT(3A)Rs) expressed in HEK 293 cells.	Cannabidiol	21-24	5-hydroxytryptamine receptor 3A	Homo sapiens	65-72
22091481-4	2010	Cannabidiol has been reported as a GPR55 antagonist in the literature to GPR55 activation by O1062, but this could not be confirmed our laboratory (Dr. Abood & Dr. Barak).	Cannabidiol	0-11	G protein-coupled receptor 55	Homo sapiens	35-40
22091481-4	2010	Cannabidiol has been reported as a GPR55 antagonist in the literature to GPR55 activation by O1062, but this could not be confirmed our laboratory (Dr. Abood & Dr. Barak).	Cannabidiol	0-11	G protein-coupled receptor 55	Homo sapiens	73-78
21238476-0	2011	Cannabidiol inhibits the hyperphagia induced by cannabinoid-1 or serotonin-1A receptor agonists.	Cannabidiol	0-11	5-hydroxytryptamine receptor 1A	Rattus norvegicus	65-86
21492165-12	2011	Furthermore, a putative GPR55 antagonist, cannabidiol, also showed a similar inhibitory effect to that of CP55940.	Cannabidiol	42-53	G protein-coupled receptor 55	Rattus norvegicus	24-29
21356216-6	2011	For CYP3A7, Delta(9)-THC, CBD, and CBN inhibited the activity to a similar extent (IC(50)=23-31 muM).	Cannabidiol	26-29	latexin	Homo sapiens	96-99
21238476-4	2011	Since both the cannabinoid and serotoninergic systems have been implicated in food intake control, the aim of the present work was to investigate the effects caused by CBD on hyperphagia induced by agonists of CB1 or 5-HT1A receptors.	Cannabidiol	168-171	cannabinoid receptor 1	Rattus norvegicus	210-213
21238476-4	2011	Since both the cannabinoid and serotoninergic systems have been implicated in food intake control, the aim of the present work was to investigate the effects caused by CBD on hyperphagia induced by agonists of CB1 or 5-HT1A receptors.	Cannabidiol	168-171	5-hydroxytryptamine receptor 1A	Rattus norvegicus	217-223
21483776-0	2011	Role of myeloid-derived suppressor cells in amelioration of experimental autoimmune hepatitis following activation of TRPV1 receptors by cannabidiol.	Cannabidiol	137-148	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	118-123
21172406-0	2011	Cannabidiol decreases body weight gain in rats: involvement of CB2 receptors.	Cannabidiol	0-11	cannabinoid receptor 2	Rattus norvegicus	63-66
20945065-0	2011	The anxiolytic-like effects of cannabidiol injected into the bed nucleus of the stria terminalis are mediated by 5-HT1A receptors.	Cannabidiol	31-42	5-hydroxytryptamine receptor 1A	Homo sapiens	113-119
21356216-7	2011	CBD competitively inhibited the activity of CYP3A4, CYP3A5, and HLMs (K(i)=1.00, 0.195, and 6.14 muM, respectively).	Cannabidiol	0-3	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	44-50
21356216-7	2011	CBD competitively inhibited the activity of CYP3A4, CYP3A5, and HLMs (K(i)=1.00, 0.195, and 6.14 muM, respectively).	Cannabidiol	0-3	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	52-58
21356216-7	2011	CBD competitively inhibited the activity of CYP3A4, CYP3A5, and HLMs (K(i)=1.00, 0.195, and 6.14 muM, respectively).	Cannabidiol	0-3	latexin	Homo sapiens	97-100
21356216-8	2011	On the other hand, CBD inhibited the CYP3A7 activity in a mixed manner (K(i)=12.3 muM).	Cannabidiol	19-22	cytochrome P450 family 3 subfamily A member 7	Homo sapiens	37-43
21356216-8	2011	On the other hand, CBD inhibited the CYP3A7 activity in a mixed manner (K(i)=12.3 muM).	Cannabidiol	19-22	latexin	Homo sapiens	82-85
21356216-10	2011	The lesser inhibitory effects of monomethyl and dimethyl ethers of CBD indicated that the ability of CYP3A inhibition by the cannabinoid attenuated with the number of methylation on the phenolic hydroxyl groups in the resorcinol moiety.	Cannabidiol	67-70	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	101-106
21356216-11	2011	SIGNIFICANCE: This study indicated that CBD most potently inhibited catalytic activity of human CYP3A enzymes, especially CYP3A4 and CYP3A5.	Cannabidiol	40-43	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	96-101
21356216-11	2011	SIGNIFICANCE: This study indicated that CBD most potently inhibited catalytic activity of human CYP3A enzymes, especially CYP3A4 and CYP3A5.	Cannabidiol	40-43	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	122-128
21356216-11	2011	SIGNIFICANCE: This study indicated that CBD most potently inhibited catalytic activity of human CYP3A enzymes, especially CYP3A4 and CYP3A5.	Cannabidiol	40-43	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	133-139
21356216-12	2011	These results suggest that two phenolic hydroxyl groups in the resorcinol moiety of CBD may play an important role in the CYP3A inhibition.	Cannabidiol	84-87	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	122-127
20942863-1	2011	BACKGROUND AND PURPOSE: Two non-psychoactive cannabinoids, cannabidiol (CBD) and cannabichromene (CBC), are known to modulate in vitro the activity of proteins involved in nociceptive mechanisms, including transient receptor potential (TRP) channels of vanilloid type-1 (TRPV1) and of ankyrin type-1 (TRPA1), the equilibrative nucleoside transporter and proteins facilitating endocannabinoid inactivation.	Cannabidiol	59-70	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	271-276
20942863-1	2011	BACKGROUND AND PURPOSE: Two non-psychoactive cannabinoids, cannabidiol (CBD) and cannabichromene (CBC), are known to modulate in vitro the activity of proteins involved in nociceptive mechanisms, including transient receptor potential (TRP) channels of vanilloid type-1 (TRPV1) and of ankyrin type-1 (TRPA1), the equilibrative nucleoside transporter and proteins facilitating endocannabinoid inactivation.	Cannabidiol	59-70	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	301-306
20942863-1	2011	BACKGROUND AND PURPOSE: Two non-psychoactive cannabinoids, cannabidiol (CBD) and cannabichromene (CBC), are known to modulate in vitro the activity of proteins involved in nociceptive mechanisms, including transient receptor potential (TRP) channels of vanilloid type-1 (TRPV1) and of ankyrin type-1 (TRPA1), the equilibrative nucleoside transporter and proteins facilitating endocannabinoid inactivation.	Cannabidiol	72-75	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	271-276
20942863-1	2011	BACKGROUND AND PURPOSE: Two non-psychoactive cannabinoids, cannabidiol (CBD) and cannabichromene (CBC), are known to modulate in vitro the activity of proteins involved in nociceptive mechanisms, including transient receptor potential (TRP) channels of vanilloid type-1 (TRPV1) and of ankyrin type-1 (TRPA1), the equilibrative nucleoside transporter and proteins facilitating endocannabinoid inactivation.	Cannabidiol	72-75	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	301-306
19939866-9	2011	In the hippocampus CBD (15 mg/kg) reversed the d-AMPH-induced damage and increased (30 mg/kg) brain-derived neurotrophic factor (BDNF) expression.	Cannabidiol	19-22	brain-derived neurotrophic factor	Rattus norvegicus	94-127
19939866-9	2011	In the hippocampus CBD (15 mg/kg) reversed the d-AMPH-induced damage and increased (30 mg/kg) brain-derived neurotrophic factor (BDNF) expression.	Cannabidiol	19-22	brain-derived neurotrophic factor	Rattus norvegicus	129-133
19939866-13	2011	In conclusion, we could not observe effects on locomotion, but CBD protect against d-AMPH-induced oxidative protein damage and increased BDNF levels in the reversal model and these effects vary depending on the brain regions evaluated and doses of CBD administered.	Cannabidiol	63-66	brain-derived neurotrophic factor	Rattus norvegicus	137-141
20825410-6	2011	The effects of CBD in culture were significantly reduced in the presence of the cannabinoid receptor (CB(1) ) inverse agonist, LY320135 but were unaffected by the 5-HT(1A) receptor antagonist, WAY100135.	Cannabidiol	15-18	cannabinoid receptor 1	Rattus norvegicus	102-107
20825410-7	2011	In hippocampal slices, CBD inhibited basal synaptic transmission, an effect that was abolished by the proposed CB(1) receptor antagonist, AM251, in addition to LY320135 and WAY100135.	Cannabidiol	23-26	cannabinoid receptor 1	Rattus norvegicus	111-116
20825410-8	2011	CONCLUSIONS AND IMPLICATIONS: Cannabidiol reduces synaptic transmission in hippocampal in vitro preparations and we propose a role for both 5-HT(1A) and CB(1) receptors in these CBD-mediated effects.	Cannabidiol	30-41	5-hydroxytryptamine receptor 1A	Rattus norvegicus	140-147
20825410-8	2011	CONCLUSIONS AND IMPLICATIONS: Cannabidiol reduces synaptic transmission in hippocampal in vitro preparations and we propose a role for both 5-HT(1A) and CB(1) receptors in these CBD-mediated effects.	Cannabidiol	30-41	cannabinoid receptor 1	Rattus norvegicus	153-158
20945065-8	2011	Moreover, pretreatment with the 5-HT1A receptor antagonist WAY100635 (0.37 nmol) blocked the effects of CBD in both models.	Cannabidiol	104-107	5-hydroxytryptamine receptor 1A	Homo sapiens	32-47
21042286-8	2010	In addition, CBD at concentrations devoid of cytotoxic effects (1-4 micromol/L) attenuated OVA-induced IFN-gamma production by OVA-primed splenocytes, whereas IL-4 was unaffected.	Cannabidiol	13-16	interferon gamma	Mus musculus	103-112
22163051-0	2011	Cannabidiol reduces Abeta-induced neuroinflammation and promotes hippocampal neurogenesis through PPARgamma involvement.	Cannabidiol	0-11	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	98-107
20457188-0	2010	Intra-dorsal periaqueductal gray administration of cannabidiol blocks panic-like response by activating 5-HT1A receptors.	Cannabidiol	51-62	5-hydroxytryptamine receptor 1A	Rattus norvegicus	104-110
20457188-2	2010	Cannabidiol (CBD), a major non-psychotomimetic compound present in Cannabis sativa, causes anxiolytic-like effects after intra-dPAG microinjections by activating 5-HT1A receptors.	Cannabidiol	0-11	5-hydroxytryptamine receptor 1A	Rattus norvegicus	162-168
20457188-2	2010	Cannabidiol (CBD), a major non-psychotomimetic compound present in Cannabis sativa, causes anxiolytic-like effects after intra-dPAG microinjections by activating 5-HT1A receptors.	Cannabidiol	13-16	5-hydroxytryptamine receptor 1A	Rattus norvegicus	162-168
20668920-0	2010	Decrease of plasminogen activator inhibitor-1 may contribute to the anti-invasive action of cannabidiol on human lung cancer cells.	Cannabidiol	92-103	serpin family E member 1	Homo sapiens	12-45
20668920-1	2010	PURPOSE: Using human lung cancer cells, we evaluated the involvement of plasminogen activator inhibitor-1 (PAI-1) in the anti-invasive action of cannabidiol, a non-psychoactive cannabinoid.	Cannabidiol	145-156	serpin family E member 1	Homo sapiens	72-105
20668920-1	2010	PURPOSE: Using human lung cancer cells, we evaluated the involvement of plasminogen activator inhibitor-1 (PAI-1) in the anti-invasive action of cannabidiol, a non-psychoactive cannabinoid.	Cannabidiol	145-156	serpin family E member 1	Homo sapiens	107-112
20668920-4	2010	RESULTS: Cannabidiol caused a profound inhibition of A549 cell invasion, accompanied by a decreased expression and secretion of PAI-1.	Cannabidiol	9-20	serpin family E member 1	Homo sapiens	128-133
20668920-5	2010	Cannabidiol"s effects on PAI-1 secretion and invasion were suppressed by antagonists to CB(1) and CB(2) receptors as well as to transient receptor potential vanilloid 1.	Cannabidiol	0-11	serpin family E member 1	Homo sapiens	25-30
20668920-7	2010	Evidence for a causal link between cannabidiol"s effects on PAI-1 and invasion was provided by experiments showing a reversal of its anti-invasive action by addition of recombinant PAI-1 at non-proinvasive concentrations.	Cannabidiol	35-46	serpin family E member 1	Homo sapiens	60-65
20668920-7	2010	Evidence for a causal link between cannabidiol"s effects on PAI-1 and invasion was provided by experiments showing a reversal of its anti-invasive action by addition of recombinant PAI-1 at non-proinvasive concentrations.	Cannabidiol	35-46	serpin family E member 1	Homo sapiens	181-186
20668920-9	2010	In vivo, a significant downregulation of PAI-1 protein by cannabidiol was demonstrated in A549 xenografts.	Cannabidiol	58-69	serpin family E member 1	Homo sapiens	41-46
20806080-0	2010	Cannabidiol protects retinal neurons by preserving glutamine synthetase activity in diabetes.	Cannabidiol	0-11	glutamate-ammonia ligase	Rattus norvegicus	51-71
27713369-2	2010	Previously, we have demonstrated that the psychoactive D9-tetrahydrocannabinol (THC) and the non-psychotropic cannabidiol (CBD) modulate mitogen-induced Th1-type immune responses in peripheral blood mononuclear cells (PBMC).	Cannabidiol	110-121	negative elongation factor complex member C/D	Homo sapiens	153-156
27713369-2	2010	Previously, we have demonstrated that the psychoactive D9-tetrahydrocannabinol (THC) and the non-psychotropic cannabidiol (CBD) modulate mitogen-induced Th1-type immune responses in peripheral blood mononuclear cells (PBMC).	Cannabidiol	123-126	negative elongation factor complex member C/D	Homo sapiens	153-156
20546877-3	2010	The calcium permeability of TRPV2 channels in T24 cells was investigated using a calcium imaging assay that used cannabidiol (CBD), a relatively selective TRPV2 agonist, and ruthenium red (RuR), a nonselective TRPV channel antagonist.	Cannabidiol	113-124	transient receptor potential cation channel subfamily V member 2	Homo sapiens	28-33
20546877-3	2010	The calcium permeability of TRPV2 channels in T24 cells was investigated using a calcium imaging assay that used cannabidiol (CBD), a relatively selective TRPV2 agonist, and ruthenium red (RuR), a nonselective TRPV channel antagonist.	Cannabidiol	126-129	transient receptor potential cation channel subfamily V member 2	Homo sapiens	28-33
20117100-0	2010	Characterization of major phytocannabinoids, cannabidiol and cannabinol, as isoform-selective and potent inhibitors of human CYP1 enzymes.	Cannabidiol	45-56	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	125-129
20695034-0	2010	Cannabidiol inhibitory effect on marble-burying behaviour: involvement of CB1 receptors.	Cannabidiol	0-11	cannabinoid receptor 1	Homo sapiens	74-77
20117100-3	2010	CBD most potently inhibited the CYP1A1 activity; the apparent K(i) value (0.155microM) was at least one-seventeenth of the values for other CYP1 isoforms.	Cannabidiol	0-3	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	32-38
20117100-3	2010	CBD most potently inhibited the CYP1A1 activity; the apparent K(i) value (0.155microM) was at least one-seventeenth of the values for other CYP1 isoforms.	Cannabidiol	0-3	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	32-36
20117100-6	2010	The preincubation of CBD resulted in a time- and concentration-dependent decrease in catalytic activity of all the recombinant CYP1 enzymes and human liver microsomes.	Cannabidiol	21-24	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	127-131
20117100-9	2010	The inactivation of recombinant CYP1A1 and human liver microsomes by CBD required NADPH, was not influenced by dialysis and by glutathione, N-acetylcysteine, and superoxide dismutase as trapping agents.	Cannabidiol	69-72	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	32-38
20298715-5	2010	Whether GPR55 responds to the endocannabinoid ligands anandamide and 2-arachidonylglycerol and the phytocannabinoids, delta-9-tetrahydrocannabidiol and cannabidiol, is cell type and tissue-dependent.	Cannabidiol	136-147	G protein-coupled receptor 55	Mus musculus	8-13
20128798-0	2010	Cannabidiol ameliorates cognitive and motor impairments in bile-duct ligated mice via 5-HT1A receptor activation.	Cannabidiol	0-11	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	86-101
19914218-0	2010	Cannabidiol inhibits cancer cell invasion via upregulation of tissue inhibitor of matrix metalloproteinases-1.	Cannabidiol	0-11	TIMP metallopeptidase inhibitor 1	Homo sapiens	62-109
19914218-3	2010	Using Matrigel invasion assays we found a cannabidiol-driven impaired invasion of human cervical cancer (HeLa, C33A) and human lung cancer cells (A549) that was reversed by antagonists to both CB(1) and CB(2) receptors as well as to transient receptor potential vanilloid 1 (TRPV1).	Cannabidiol	42-53	transient receptor potential cation channel subfamily V member 1	Homo sapiens	233-273
19914218-3	2010	Using Matrigel invasion assays we found a cannabidiol-driven impaired invasion of human cervical cancer (HeLa, C33A) and human lung cancer cells (A549) that was reversed by antagonists to both CB(1) and CB(2) receptors as well as to transient receptor potential vanilloid 1 (TRPV1).	Cannabidiol	42-53	transient receptor potential cation channel subfamily V member 1	Homo sapiens	275-280
19914218-4	2010	The decrease of invasion by cannabidiol appeared concomitantly with upregulation of tissue inhibitor of matrix metalloproteinases-1 (TIMP-1).	Cannabidiol	28-39	TIMP metallopeptidase inhibitor 1	Homo sapiens	84-131
19914218-4	2010	The decrease of invasion by cannabidiol appeared concomitantly with upregulation of tissue inhibitor of matrix metalloproteinases-1 (TIMP-1).	Cannabidiol	28-39	TIMP metallopeptidase inhibitor 1	Homo sapiens	133-139
19914218-5	2010	Knockdown of cannabidiol-induced TIMP-1 expression by siRNA led to a reversal of the cannabidiol-elicited decrease in tumor cell invasiveness, implying a causal link between the TIMP-1-upregulating and anti-invasive action of cannabidiol.	Cannabidiol	13-24	TIMP metallopeptidase inhibitor 1	Homo sapiens	33-39
19914218-5	2010	Knockdown of cannabidiol-induced TIMP-1 expression by siRNA led to a reversal of the cannabidiol-elicited decrease in tumor cell invasiveness, implying a causal link between the TIMP-1-upregulating and anti-invasive action of cannabidiol.	Cannabidiol	13-24	TIMP metallopeptidase inhibitor 1	Homo sapiens	178-184
19914218-5	2010	Knockdown of cannabidiol-induced TIMP-1 expression by siRNA led to a reversal of the cannabidiol-elicited decrease in tumor cell invasiveness, implying a causal link between the TIMP-1-upregulating and anti-invasive action of cannabidiol.	Cannabidiol	85-96	TIMP metallopeptidase inhibitor 1	Homo sapiens	33-39
19914218-5	2010	Knockdown of cannabidiol-induced TIMP-1 expression by siRNA led to a reversal of the cannabidiol-elicited decrease in tumor cell invasiveness, implying a causal link between the TIMP-1-upregulating and anti-invasive action of cannabidiol.	Cannabidiol	85-96	TIMP metallopeptidase inhibitor 1	Homo sapiens	178-184
19914218-5	2010	Knockdown of cannabidiol-induced TIMP-1 expression by siRNA led to a reversal of the cannabidiol-elicited decrease in tumor cell invasiveness, implying a causal link between the TIMP-1-upregulating and anti-invasive action of cannabidiol.	Cannabidiol	85-96	TIMP metallopeptidase inhibitor 1	Homo sapiens	33-39
19914218-5	2010	Knockdown of cannabidiol-induced TIMP-1 expression by siRNA led to a reversal of the cannabidiol-elicited decrease in tumor cell invasiveness, implying a causal link between the TIMP-1-upregulating and anti-invasive action of cannabidiol.	Cannabidiol	85-96	TIMP metallopeptidase inhibitor 1	Homo sapiens	178-184
20346144-5	2010	Abn-CBD is a synthetic isomer of the phytocannabinoid cannabidiol (CBD) and is inactive at CB1 or CB2 receptors, but functions as a selective agonist at this Gi/o-coupled GPCR.	Cannabidiol	4-7	G protein-coupled bile acid receptor 1	Mus musculus	171-175
20236533-9	2010	Cannabidiol was also associated with restriction in elevation of microglial density in the dorsal spinal cord and elevation in phosphorylated p38 MAPK.	Cannabidiol	0-11	mitogen-activated protein kinase 14	Mus musculus	142-150
20128798-1	2010	BACKGROUND AND PURPOSE: We aimed to demonstrate the involvement of 5-HT(1A) receptors in the therapeutic effect of cannabidiol, a non-psychoactive constituent of Cannabis sativa, in a model of hepatic encephalopathy induced by bile-duct ligation (BDL) in mice.	Cannabidiol	115-126	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	67-74
20128798-8	2010	KEY RESULTS: Cannabidiol improved cognition and locomotion, which were impaired by BDL, and restored hippocampal expression of the tumour necrosis factor-alpha receptor 1 and the BDNF genes, which increased and decreased, respectively, following BDL.	Cannabidiol	13-24	brain derived neurotrophic factor	Mus musculus	179-183
20128798-10	2010	All the effects of cannabidiol, except for that on BDNF expression, were blocked by WAY-100635, indicating 5-HT(1A) receptor involvement in cannabidiol"s effects.	Cannabidiol	140-151	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	107-124
20128798-13	2010	Cannabidiol reverses these effects through a combination of anti-inflammatory activity and activation of this receptor, leading to improvement of the neurological deficits without affecting 5-HT(1A) receptor expression or liver function.	Cannabidiol	0-11	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	190-207
20128798-14	2010	BDNF up-regulation by cannabidiol does not seem to account for the cognitive improvement.	Cannabidiol	22-33	brain derived neurotrophic factor	Mus musculus	0-4
19910459-0	2010	Cannabinoids Delta(9)-tetrahydrocannabinol and cannabidiol differentially inhibit the lipopolysaccharide-activated NF-kappaB and interferon-beta/STAT proinflammatory pathways in BV-2 microglial cells.	Cannabidiol	47-58	interferon beta 1, fibroblast	Mus musculus	129-144
19910459-10	2010	However, both CBD and THC decreased the activation of the LPS-induced STAT1 transcription factor, a key player in IFNbeta-dependent proinflammatory processes.	Cannabidiol	14-17	signal transducer and activator of transcription 1	Mus musculus	70-75
19910459-10	2010	However, both CBD and THC decreased the activation of the LPS-induced STAT1 transcription factor, a key player in IFNbeta-dependent proinflammatory processes.	Cannabidiol	14-17	interferon beta 1, fibroblast	Mus musculus	114-121
19910459-11	2010	In summary, our observations show that CBD and THC vary in their effects on the anti-inflammatory pathways, including the NF-kappaB and IFNbeta-dependent pathways.	Cannabidiol	39-42	interferon beta 1, fibroblast	Mus musculus	136-143
20002102-0	2010	Antidepressant-like effects of cannabidiol in mice: possible involvement of 5-HT1A receptors.	Cannabidiol	31-42	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	76-82
19800921-5	2010	RESULTS: Confirming previous results systemic administration of CBD (10mg/kg) decreased contextual fear and associated c-Fos expression in the prefrontal cortex (prelimbic and infralimbic regions).	Cannabidiol	64-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
20002102-9	2010	BDNF protein levels were measured in the hippocampus of another group of mice treated with CBD (30 mg*kg(-1)) and submitted to the forced swimming test.	Cannabidiol	91-94	brain derived neurotrophic factor	Mus musculus	0-4
19805329-6	2009	These stimulatory effects on osteoclast function were attenuated in osteoclasts generated from GPR55(-/-) macrophages and by the GPR55 antagonist cannabidiol (CBD).	Cannabidiol	146-157	G protein-coupled receptor 55	Mus musculus	129-134
19735690-4	2009	The reasons for these curves are still unclear, but since these drugs can also activate TRPV1 receptors and increase glutamate release, we hypothesized that, at high doses, cannabidiol and WIN 55,212-2, a CB1 receptor agonist, could activate TRPV1 receptors, facilitating glutamate neurotransmission and anxiety responses.	Cannabidiol	173-184	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	88-93
19735690-4	2009	The reasons for these curves are still unclear, but since these drugs can also activate TRPV1 receptors and increase glutamate release, we hypothesized that, at high doses, cannabidiol and WIN 55,212-2, a CB1 receptor agonist, could activate TRPV1 receptors, facilitating glutamate neurotransmission and anxiety responses.	Cannabidiol	173-184	cannabinoid receptor 1	Rattus norvegicus	205-208
19735690-4	2009	The reasons for these curves are still unclear, but since these drugs can also activate TRPV1 receptors and increase glutamate release, we hypothesized that, at high doses, cannabidiol and WIN 55,212-2, a CB1 receptor agonist, could activate TRPV1 receptors, facilitating glutamate neurotransmission and anxiety responses.	Cannabidiol	173-184	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	242-247
19690824-8	2009	Cannabidiol reduced colon injury, inducible iNOS (but not cyclooxygenase-2) expression, and interleukin-1beta, interleukin-10, and endocannabinoid changes associated with 2,4,6-dinitrobenzene sulfonic acid administration.	Cannabidiol	0-11	nitric oxide synthase 2, inducible	Mus musculus	44-48
19690824-8	2009	Cannabidiol reduced colon injury, inducible iNOS (but not cyclooxygenase-2) expression, and interleukin-1beta, interleukin-10, and endocannabinoid changes associated with 2,4,6-dinitrobenzene sulfonic acid administration.	Cannabidiol	0-11	interleukin 1 beta	Mus musculus	92-109
19683810-4	2009	The increases in gene expression (Sox9, Aggrecan, fibronectin and collagen II), accumulation of chondrogenic matrices and decrease of collagen X gene expression during TGF-beta3 induction were only observed for those beads containing 10mg/g CBD-RGD initially, with 20.18+/-0.73% of that released in a week.	Cannabidiol	241-244	transforming growth factor beta 3	Homo sapiens	168-177
19805329-6	2009	These stimulatory effects on osteoclast function were attenuated in osteoclasts generated from GPR55(-/-) macrophages and by the GPR55 antagonist cannabidiol (CBD).	Cannabidiol	159-162	G protein-coupled receptor 55	Mus musculus	129-134
19721229-0	2009	Therapeutic time window of cannabidiol treatment on delayed ischemic damage via high-mobility group box1-inhibiting mechanism.	Cannabidiol	27-38	high mobility group box 1	Mus musculus	80-104
19721229-1	2009	Cannabidiol decreases cerebral infarction and high-mobility group box1 (HMGB1) in plasma in ischemic early phase.	Cannabidiol	0-11	high mobility group box 1	Mus musculus	46-70
19721229-1	2009	Cannabidiol decreases cerebral infarction and high-mobility group box1 (HMGB1) in plasma in ischemic early phase.	Cannabidiol	0-11	high mobility group box 1	Mus musculus	72-77
19721229-9	2009	Cannabidiol may provide therapeutic possibilities for the progressing brain injury via HMGB1-inhibiting mechanism.	Cannabidiol	0-11	high mobility group box 1	Mus musculus	87-92
19630026-5	2009	The method has also been validated for cannabinol (CBD) and cannabidiol (CDN), two cannabinoids that were shown not to interfere with the method.	Cannabidiol	60-71	5', 3'-nucleotidase, cytosolic	Homo sapiens	73-76
19285060-8	2009	The aim of the present study was to investigate whether another pharmacologically active phytocannabinoid, cannabidiol, similarly activates PPARgamma.	Cannabidiol	107-118	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	140-149
19285060-11	2009	Cannabidiol caused time-dependent (over 2 h) vasorelaxation of pre-constricted aortae, sensitive to PPARgamma antagonism (GW9662, 1 microM) and super oxide dismutase inhibition.	Cannabidiol	0-11	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	100-109
19285060-15	2009	In a reporter gene assay, cannabidiol increased the transcriptional activity of PPARgamma.	Cannabidiol	26-37	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	80-89
19285060-16	2009	Cannabidiol was also found to bind to PPARgamma and stimulate the differentiation of 3T3-L1 fibroblasts into adipocytes, a PPARgamma-mediated response.	Cannabidiol	0-11	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	38-47
19285060-16	2009	Cannabidiol was also found to bind to PPARgamma and stimulate the differentiation of 3T3-L1 fibroblasts into adipocytes, a PPARgamma-mediated response.	Cannabidiol	0-11	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	123-132
19285060-17	2009	These results show that cannabidiol binds to and activates PPARgamma, which partially underlies the time-dependent vascular effects of cannabidiol.	Cannabidiol	24-35	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	59-68
19285060-17	2009	These results show that cannabidiol binds to and activates PPARgamma, which partially underlies the time-dependent vascular effects of cannabidiol.	Cannabidiol	135-146	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	59-68
19167098-1	2009	Nanomolar concentrations of Delta9-tetrahydrocannabinol or cannabidiol are demonstrated to enhance mitogen-induced degradation of tryptophan in human peripheral blood mononuclear cells in dependence of CB1- or CB2-receptor activation.	Cannabidiol	59-70	cannabinoid receptor 1	Homo sapiens	202-205
19070683-0	2009	Cannabidiol decreases bone resorption by inhibiting RANK/RANKL expression and pro-inflammatory cytokines during experimental periodontitis in rats.	Cannabidiol	0-11	TNF superfamily member 11	Rattus norvegicus	57-62
19133999-0	2009	5-HT1A receptors are involved in the cannabidiol-induced attenuation of behavioural and cardiovascular responses to acute restraint stress in rats.	Cannabidiol	37-48	5-hydroxytryptamine receptor 1A	Rattus norvegicus	0-6
18641283-10	2008	CBD inhibited adenosine uptake via equilibrative nucleoside transporter 1 and synergistically enhanced adenosine"s TNF-alpha suppression after treatment with LPS.	Cannabidiol	0-3	tumor necrosis factor	Rattus norvegicus	115-124
18656454-5	2008	While all of these observations support the fact that CBD suppresses T cell function, we now demonstrate that CBD suppressed IL-2 and IFN-gamma production in purified splenic T cells.	Cannabidiol	110-113	interleukin 2	Mus musculus	125-129
18656454-5	2008	While all of these observations support the fact that CBD suppresses T cell function, we now demonstrate that CBD suppressed IL-2 and IFN-gamma production in purified splenic T cells.	Cannabidiol	110-113	interferon gamma	Mus musculus	134-143
18619955-3	2008	Indeed, the cannabinoids enhanced the intracellular accumulation of two ABCC1 substrates, Fluo3 and vincristine, in ovarian carcinoma cells over-expressing ABCC1 (2008/MRP1) with a rank order of potency: cannabidiol>cannabinol>Delta(9)-tetrahydrocannabinol.	Cannabidiol	204-215	ATP binding cassette subfamily C member 1	Homo sapiens	156-161
18373655-5	2008	Cannabidiol also regulates the activity of fatty acid amide hydrolase (FAAH) which is the main enzyme involved in endocannabinoid breakdown and which modulates gastrointestinal motility.	Cannabidiol	0-11	fatty acid amide hydrolase	Mus musculus	71-75
18373655-11	2008	The increase in FAAH expression was completely reversed by cannabidiol but not affected by AM251.	Cannabidiol	59-70	fatty acid amide hydrolase	Mus musculus	16-20
18354058-1	2008	The plant cannabinoids (phytocannabinoids), cannabidiol (CBD), and Delta(9)-tetrahydrocannabinol (THC) were previously shown to activate transient receptor potential channels of both vanilloid type 1 (TRPV1) and ankyrin type 1 (TRPA1), respectively.	Cannabidiol	44-55	transient receptor potential cation channel subfamily V member 1	Homo sapiens	201-206
18446323-0	2008	Involvement of 5HT1A receptors in the anxiolytic-like effects of cannabidiol injected into the dorsolateral periaqueductal gray of rats.	Cannabidiol	65-76	5-hydroxytryptamine receptor 1A	Rattus norvegicus	15-20
18469842-9	2008	CONCLUSIONS AND IMPLICATIONS: Cannabidiol selectively reduces croton oil-induced hypermotility in mice in vivo and this effect involves cannabinoid CB1 receptors and FAAH.	Cannabidiol	30-41	cannabinoid receptor 1 (brain)	Mus musculus	148-151
18469842-9	2008	CONCLUSIONS AND IMPLICATIONS: Cannabidiol selectively reduces croton oil-induced hypermotility in mice in vivo and this effect involves cannabinoid CB1 receptors and FAAH.	Cannabidiol	30-41	fatty acid amide hydrolase	Mus musculus	166-170
18550765-0	2008	TRPV2 is activated by cannabidiol and mediates CGRP release in cultured rat dorsal root ganglion neurons.	Cannabidiol	22-33	transient receptor potential cation channel, subfamily V, member 2	Rattus norvegicus	0-5
18550765-5	2008	We also demonstrated that cannabidiol evoked a concentration-dependent release of calcitonin gene-related peptide (CGRP) from cultured rat dorsal root ganglion neurons in a cannabinoid receptor- and TRPV1-independent manner.	Cannabidiol	26-37	calcitonin-related polypeptide alpha	Rattus norvegicus	82-113
18550765-5	2008	We also demonstrated that cannabidiol evoked a concentration-dependent release of calcitonin gene-related peptide (CGRP) from cultured rat dorsal root ganglion neurons in a cannabinoid receptor- and TRPV1-independent manner.	Cannabidiol	26-37	calcitonin-related polypeptide alpha	Rattus norvegicus	115-119
18550765-5	2008	We also demonstrated that cannabidiol evoked a concentration-dependent release of calcitonin gene-related peptide (CGRP) from cultured rat dorsal root ganglion neurons in a cannabinoid receptor- and TRPV1-independent manner.	Cannabidiol	26-37	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	199-204
18550765-6	2008	Moreover, the cannabidiol-evoked CGRP release depended on extracellular calcium and was blocked by the nonselective TRP channel blocker, ruthenium red.	Cannabidiol	14-25	calcitonin-related polypeptide alpha	Rattus norvegicus	33-37
18550765-7	2008	We further provide evidence through the use of small interfering RNA knockdown and repetitive stimulation studies, to show that cannabidiol-evoked CGRP release is mediated, at least in part, by TRPV2.	Cannabidiol	128-139	calcitonin-related polypeptide alpha	Rattus norvegicus	147-151
18550765-7	2008	We further provide evidence through the use of small interfering RNA knockdown and repetitive stimulation studies, to show that cannabidiol-evoked CGRP release is mediated, at least in part, by TRPV2.	Cannabidiol	128-139	transient receptor potential cation channel, subfamily V, member 2	Rattus norvegicus	194-199
18550765-8	2008	Together, these data suggest not only that TRPV2 may comprise a mechanism whereby cannabidiol exerts its clinically beneficial effects in vivo, but also that TRPV2 may constitute a viable, new drug target.	Cannabidiol	82-93	transient receptor potential cation channel, subfamily V, member 2	Rattus norvegicus	43-48
18390906-6	2008	At moderately hyperpolarized potentials, THC and CBD inhibited peak Ca(V)3.1 and Ca(V)3.2 currents with IC(50) values of approximately 1 mum but were less potent on Ca(V)3.3 channels.	Cannabidiol	49-52	calcium voltage-gated channel subunit alpha1 G	Homo sapiens	68-76
18390906-6	2008	At moderately hyperpolarized potentials, THC and CBD inhibited peak Ca(V)3.1 and Ca(V)3.2 currents with IC(50) values of approximately 1 mum but were less potent on Ca(V)3.3 channels.	Cannabidiol	49-52	caveolin 3	Homo sapiens	68-74
18390906-6	2008	At moderately hyperpolarized potentials, THC and CBD inhibited peak Ca(V)3.1 and Ca(V)3.2 currents with IC(50) values of approximately 1 mum but were less potent on Ca(V)3.3 channels.	Cannabidiol	49-52	immunoglobulin lambda variable 7-46	Homo sapiens	165-173
18390906-8	2008	However, in recordings made from a holding potential of -70 mV, 100 nm THC or CBD inhibited more than 50% of the peak Ca(V)3.1 current.	Cannabidiol	78-81	calcium voltage-gated channel subunit alpha1 G	Homo sapiens	118-126
18390906-9	2008	THC and CBD produced a significant hyperpolarizing shift in the steady state inactivation potentials for each of the Ca(V)3 channels, which accounts for inhibition of channel currents.	Cannabidiol	8-11	caveolin 3	Homo sapiens	117-123
18390906-12	2008	Thus, THC and CBD inhibit Ca(V)3 channels at pharmacologically relevant concentrations.	Cannabidiol	14-17	caveolin 3	Homo sapiens	26-32
18354058-1	2008	The plant cannabinoids (phytocannabinoids), cannabidiol (CBD), and Delta(9)-tetrahydrocannabinol (THC) were previously shown to activate transient receptor potential channels of both vanilloid type 1 (TRPV1) and ankyrin type 1 (TRPA1), respectively.	Cannabidiol	44-55	transient receptor potential cation channel subfamily A member 1	Homo sapiens	228-233
18354058-1	2008	The plant cannabinoids (phytocannabinoids), cannabidiol (CBD), and Delta(9)-tetrahydrocannabinol (THC) were previously shown to activate transient receptor potential channels of both vanilloid type 1 (TRPV1) and ankyrin type 1 (TRPA1), respectively.	Cannabidiol	57-60	transient receptor potential cation channel subfamily V member 1	Homo sapiens	201-206
18354058-1	2008	The plant cannabinoids (phytocannabinoids), cannabidiol (CBD), and Delta(9)-tetrahydrocannabinol (THC) were previously shown to activate transient receptor potential channels of both vanilloid type 1 (TRPV1) and ankyrin type 1 (TRPA1), respectively.	Cannabidiol	57-60	transient receptor potential cation channel subfamily A member 1	Homo sapiens	228-233
19052649-13	2008	Treatment with 1 microM CBD inhibited ROS formation and p38 MAPK activation, NO and TNF-alpha formation, and maintained cell morphology.	Cannabidiol	24-27	mitogen activated protein kinase 14	Rattus norvegicus	56-59
18028339-0	2008	5-Lipoxygenase and anandamide hydrolase (FAAH) mediate the antitumor activity of cannabidiol, a non-psychoactive cannabinoid.	Cannabidiol	81-92	arachidonate 5-lipoxygenase	Mus musculus	0-14
18028339-0	2008	5-Lipoxygenase and anandamide hydrolase (FAAH) mediate the antitumor activity of cannabidiol, a non-psychoactive cannabinoid.	Cannabidiol	81-92	fatty acid amide hydrolase	Mus musculus	41-45
18028339-6	2008	In addition, in vivo treatment with CBD markedly stimulated ( approximately 175%) the activity of fatty acid amide hydrolase (FAAH), the main anandamide-degrading enzyme, while decreasing anandamide content ( approximately 30%) and binding to CB1 cannabinoid receptors ( approximately 25%).	Cannabidiol	36-39	fatty acid amide hydrolase	Mus musculus	98-124
18028339-6	2008	In addition, in vivo treatment with CBD markedly stimulated ( approximately 175%) the activity of fatty acid amide hydrolase (FAAH), the main anandamide-degrading enzyme, while decreasing anandamide content ( approximately 30%) and binding to CB1 cannabinoid receptors ( approximately 25%).	Cannabidiol	36-39	fatty acid amide hydrolase	Mus musculus	126-130
18028339-7	2008	In vitro pre-treatment of U87 glioma cells with MK-886, a specific 5-LOX inhibitor, significantly enhanced the antimitotic effect of CBD, whereas the pre-treatment with indomethacin (pan-COX inhibitor) or celecoxib (COX-2 inhibitor), did not alter CBD effect.	Cannabidiol	133-136	arachidonate 5-lipoxygenase	Mus musculus	69-72
17950393-0	2008	Cannabidiol-induced apoptosis in primary lymphocytes is associated with oxidative stress-dependent activation of caspase-8.	Cannabidiol	0-11	caspase 8	Mus musculus	113-122
17950393-8	2008	Pretreatment of splenocytes with a cell-permeable inhibitor for caspase-8 significantly attenuated, in a concentration-dependent manner, CBD-mediated apoptosis, but not ROS production.	Cannabidiol	137-140	caspase 8	Mus musculus	64-73
17714746-4	2008	In addition, the level of the proinflammatory cytokine IL-12 produced by splenocytes was significantly reduced, whereas the level of the anti-inflammatory IL-10 was significantly elevated following CBD-treatment.	Cannabidiol	198-201	interleukin 10	Mus musculus	155-160
19052649-13	2008	Treatment with 1 microM CBD inhibited ROS formation and p38 MAPK activation, NO and TNF-alpha formation, and maintained cell morphology.	Cannabidiol	24-27	tumor necrosis factor	Rattus norvegicus	84-93
17927685-9	2007	In conclusion, both DRB1*13 and rs3117099TT homozygosity are associated with CBD in *Glu69-negative subjects, while DPB1*Glu69 is associated with CBD and BeS compared with Be-exp.	Cannabidiol	77-80	major histocompatibility complex, class II, DR beta 1	Homo sapiens	20-24
17927685-9	2007	In conclusion, both DRB1*13 and rs3117099TT homozygosity are associated with CBD in *Glu69-negative subjects, while DPB1*Glu69 is associated with CBD and BeS compared with Be-exp.	Cannabidiol	146-149	major histocompatibility complex, class II, DP beta 1	Homo sapiens	116-120
17704825-1	2007	CB1 and CB2 receptors mediate most responses to cannabinoids but not some of the cardiovascular actions of endocannabinoids such as anandamide and virodhamine, or those of some synthetic agents, like abnormal cannabidiol (abn-cbd).	Cannabidiol	209-220	cannabinoid receptor 1 (brain)	Mus musculus	0-3
17704825-1	2007	CB1 and CB2 receptors mediate most responses to cannabinoids but not some of the cardiovascular actions of endocannabinoids such as anandamide and virodhamine, or those of some synthetic agents, like abnormal cannabidiol (abn-cbd).	Cannabidiol	209-220	cannabinoid receptor 2 (macrophage)	Mus musculus	8-11
17704827-6	2007	KEY RESULTS: Atypical cannabinoids O-1602 and abnormal cannabidiol both stimulated GPR55-dependent GTPgammaS activity (EC50 approximately 2 nM), whereas the CB1 and CB2-selective agonist WIN 55,212-2 showed no effect in GPR55-expressing HEK293T cell membranes.	Cannabidiol	55-66	G protein-coupled receptor 55	Homo sapiens	83-88
17704827-6	2007	KEY RESULTS: Atypical cannabinoids O-1602 and abnormal cannabidiol both stimulated GPR55-dependent GTPgammaS activity (EC50 approximately 2 nM), whereas the CB1 and CB2-selective agonist WIN 55,212-2 showed no effect in GPR55-expressing HEK293T cell membranes.	Cannabidiol	55-66	G protein-coupled receptor 55	Homo sapiens	220-225
17906686-3	2007	Here we address the interaction of cannabinol (CBN), cannabidiol (CBD) and delta 9-tetrahydrocannabinol (THC) with the related multidrug transporter, ABCG2.	Cannabidiol	53-64	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	150-155
17906686-3	2007	Here we address the interaction of cannabinol (CBN), cannabidiol (CBD) and delta 9-tetrahydrocannabinol (THC) with the related multidrug transporter, ABCG2.	Cannabidiol	66-69	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	150-155
17906686-7	2007	KEY RESULTS: CBN, CBD and THC increased the intracellular accumulation of the Abcg2/ABCG2 substrate, mitoxantrone, in an over-expressing cell line.	Cannabidiol	18-21	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	78-83
17906686-7	2007	KEY RESULTS: CBN, CBD and THC increased the intracellular accumulation of the Abcg2/ABCG2 substrate, mitoxantrone, in an over-expressing cell line.	Cannabidiol	18-21	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	84-89
18025276-0	2007	Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells.	Cannabidiol	0-11	inhibitor of DNA binding 1, HLH protein	Homo sapiens	36-40
18025276-7	2007	Here, we report that cannabidiol (CBD), a cannabinoid with a low-toxicity profile, could down-regulate Id-1 expression in aggressive human breast cancer cells.	Cannabidiol	21-32	inhibitor of DNA binding 1, HLH protein	Homo sapiens	103-107
18025276-7	2007	Here, we report that cannabidiol (CBD), a cannabinoid with a low-toxicity profile, could down-regulate Id-1 expression in aggressive human breast cancer cells.	Cannabidiol	34-37	inhibitor of DNA binding 1, HLH protein	Homo sapiens	103-107
18025276-12	2007	In conclusion, CBD represents the first nontoxic exogenous agent that can significantly decrease Id-1 expression in metastatic breast cancer cells leading to the down-regulation of tumor aggressiveness.	Cannabidiol	15-18	inhibitor of DNA binding 1, HLH protein	Homo sapiens	97-101
17516913-3	2007	To identify CBD-binding sites on type I collagen and collagen peptides with the capacity to compete CBD binding of gelatin and thereby inhibit gelatinolysis by MMP-2, we screened a one-bead one-peptide combinatorial peptide library with recombinant CBD as bait.	Cannabidiol	12-15	matrix metallopeptidase 2	Homo sapiens	160-165
17876300-3	2007	GPR55 was activated by a range of plant, synthetic and endogenous cannabinoids and blocked by the non-psychoactive phytocannabinoid, cannabidiol.	Cannabidiol	133-144	G protein-coupled receptor 55	Mus musculus	0-5
17876302-7	2007	Ligands such as cannabidiol and abnormal cannabidiol which exhibit no CB1 or CB2 activity and are believed to function at a novel cannabinoid receptor, also showed activity at GPR55.	Cannabidiol	16-27	cannabinoid receptor 1	Homo sapiens	70-73
17876302-7	2007	Ligands such as cannabidiol and abnormal cannabidiol which exhibit no CB1 or CB2 activity and are believed to function at a novel cannabinoid receptor, also showed activity at GPR55.	Cannabidiol	16-27	G protein-coupled receptor 55	Homo sapiens	176-181
17876302-7	2007	Ligands such as cannabidiol and abnormal cannabidiol which exhibit no CB1 or CB2 activity and are believed to function at a novel cannabinoid receptor, also showed activity at GPR55.	Cannabidiol	41-52	G protein-coupled receptor 55	Homo sapiens	176-181
18035205-2	2007	Delta(9)-Tetrahydrocannabinol/cannabidiol (THC/CBD), an endocannabinoid system modulator, has demonstrated efficacy for up to 4 weeks in randomized controlled trials in the treatment of CNP in patients with MS.	Cannabidiol	30-41	2',3'-cyclic nucleotide 3' phosphodiesterase	Homo sapiens	186-189
18035205-2	2007	Delta(9)-Tetrahydrocannabinol/cannabidiol (THC/CBD), an endocannabinoid system modulator, has demonstrated efficacy for up to 4 weeks in randomized controlled trials in the treatment of CNP in patients with MS.	Cannabidiol	47-50	2',3'-cyclic nucleotide 3' phosphodiesterase	Homo sapiens	186-189
18035205-24	2007	CONCLUSIONS: THC/CBD was effective, with no evidence of tolerance, in these select patients with CNP and MS who completed approximately 2 years of treatment (n = 28).	Cannabidiol	17-20	2',3'-cyclic nucleotide 3' phosphodiesterase	Homo sapiens	97-100
17516913-11	2007	These experiments identified a CBD-binding site on type I collagen and demonstrated that a corresponding synthetic peptide can inhibit hydrolysis of type I and IV collagens by competing CBD-mediated gelatin binding to MMP-2.	Cannabidiol	31-34	matrix metallopeptidase 2	Homo sapiens	218-223
17516913-11	2007	These experiments identified a CBD-binding site on type I collagen and demonstrated that a corresponding synthetic peptide can inhibit hydrolysis of type I and IV collagens by competing CBD-mediated gelatin binding to MMP-2.	Cannabidiol	186-189	matrix metallopeptidase 2	Homo sapiens	218-223
17592514-0	2007	Cannabidiol in vivo blunts beta-amyloid induced neuroinflammation by suppressing IL-1beta and iNOS expression.	Cannabidiol	0-11	interleukin 1 beta	Mus musculus	81-89
17592514-0	2007	Cannabidiol in vivo blunts beta-amyloid induced neuroinflammation by suppressing IL-1beta and iNOS expression.	Cannabidiol	0-11	nitric oxide synthase 2, inducible	Mus musculus	94-98
17592514-9	2007	KEY RESULTS: In contrast to vehicle, CBD dose-dependently and significantly inhibited GFAP mRNA and protein expression in Abeta injected animals.	Cannabidiol	37-40	glial fibrillary acidic protein	Mus musculus	86-90
17672854-5	2007	The administration of CBD, but not ACEA or HU-308, completely reversed 3NP-induced reductions in GABA contents and mRNA levels for SP, NSE and SOD-2, and partially attenuated those found in SOD-1 and PENK.	Cannabidiol	22-25	enolase 2	Rattus norvegicus	135-138
17672854-5	2007	The administration of CBD, but not ACEA or HU-308, completely reversed 3NP-induced reductions in GABA contents and mRNA levels for SP, NSE and SOD-2, and partially attenuated those found in SOD-1 and PENK.	Cannabidiol	22-25	superoxide dismutase 2	Rattus norvegicus	143-148
17672854-5	2007	The administration of CBD, but not ACEA or HU-308, completely reversed 3NP-induced reductions in GABA contents and mRNA levels for SP, NSE and SOD-2, and partially attenuated those found in SOD-1 and PENK.	Cannabidiol	22-25	superoxide dismutase 1	Rattus norvegicus	190-195
17672854-5	2007	The administration of CBD, but not ACEA or HU-308, completely reversed 3NP-induced reductions in GABA contents and mRNA levels for SP, NSE and SOD-2, and partially attenuated those found in SOD-1 and PENK.	Cannabidiol	22-25	proenkephalin	Rattus norvegicus	200-204
16766924-4	2006	RESULTS: Results indicate that GCLC TNR genotype 7/7 is negatively associated with CBD (odds ratio [OR] = 0.28, 95% confidence interval [CI] = 0.08-0.95) and the GCLM-588 C/C SNP genotype is associated with CBD susceptibility (OR = 3.07, 95% CI = 1.00-9.37).	Cannabidiol	83-86	glutamate-cysteine ligase catalytic subunit	Homo sapiens	31-35
17239356-4	2007	The NAA/tCr in the putamen/globus pallidum region correlated significantly with cannabidiol (R(2) = .66, p = .004).	Cannabidiol	80-91	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	8-11
17466911-0	2007	Suppressive effects of cannabidiol on antigen-specific antibody production and functional activity of splenocytes in ovalbumin-sensitized BALB/c mice.	Cannabidiol	23-34	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	117-126
17466911-4	2007	The serum level of OVA-specific IgM was significantly attenuated by a high dose of CBD (20 mg/kg), and OVA-specific IgG(1) and IgG(2a) by all 3 doses of CBD.	Cannabidiol	153-156	immunoglobulin heavy variable V1-9	Mus musculus	127-133
17466911-5	2007	Concordantly, splenocytes of mice administered with CBD (5 or 20 mg/kg) produced less IL-2, IL-4 and IFN-gamma than those of vehicle-treated controls, upon ex vivo stimulation with phorbol ester plus calcium ionophore.	Cannabidiol	52-55	interleukin 2	Mus musculus	86-90
17466911-5	2007	Concordantly, splenocytes of mice administered with CBD (5 or 20 mg/kg) produced less IL-2, IL-4 and IFN-gamma than those of vehicle-treated controls, upon ex vivo stimulation with phorbol ester plus calcium ionophore.	Cannabidiol	52-55	interleukin 4	Mus musculus	92-96
17466911-5	2007	Concordantly, splenocytes of mice administered with CBD (5 or 20 mg/kg) produced less IL-2, IL-4 and IFN-gamma than those of vehicle-treated controls, upon ex vivo stimulation with phorbol ester plus calcium ionophore.	Cannabidiol	52-55	interferon gamma	Mus musculus	101-110
17245363-0	2007	Cannabidiol displays unexpectedly high potency as an antagonist of CB1 and CB2 receptor agonists in vitro.	Cannabidiol	0-11	cannabinoid receptor 1	Homo sapiens	67-70
17245363-0	2007	Cannabidiol displays unexpectedly high potency as an antagonist of CB1 and CB2 receptor agonists in vitro.	Cannabidiol	0-11	cannabinoid receptor 2	Homo sapiens	75-78
17245363-1	2007	BACKGROUND AND PURPOSE: A nonpsychoactive constituent of the cannabis plant, cannabidiol has been demonstrated to have low affinity for both cannabinoid CB1 and CB2 receptors.	Cannabidiol	77-88	cannabinoid receptor 1	Homo sapiens	153-156
17245363-1	2007	BACKGROUND AND PURPOSE: A nonpsychoactive constituent of the cannabis plant, cannabidiol has been demonstrated to have low affinity for both cannabinoid CB1 and CB2 receptors.	Cannabidiol	77-88	cannabinoid receptor 2	Homo sapiens	161-164
17245363-6	2007	KEY RESULTS: This paper reports firstly that cannabidiol displays inverse agonism at the human CB2 receptor.	Cannabidiol	45-56	cannabinoid receptor 2	Homo sapiens	95-98
17245363-7	2007	Secondly, we demonstrate that cannabidiol is a high potency antagonist of cannabinoid receptor agonists in mouse brain and in membranes from CHO cells transfected with human CB2 receptors.	Cannabidiol	30-41	cannabinoid receptor 2	Homo sapiens	174-177
17245363-8	2007	CONCLUSIONS AND IMPLICATIONS: This study has provided the first evidence that cannabidiol can display CB2 receptor inverse agonism, an action that appears to be responsible for its antagonism of CP55940 at the human CB2 receptor.	Cannabidiol	78-89	cannabinoid receptor 2	Homo sapiens	102-105
17245363-8	2007	CONCLUSIONS AND IMPLICATIONS: This study has provided the first evidence that cannabidiol can display CB2 receptor inverse agonism, an action that appears to be responsible for its antagonism of CP55940 at the human CB2 receptor.	Cannabidiol	78-89	cannabinoid receptor 2	Homo sapiens	216-219
17245363-9	2007	The ability of cannabidiol to behave as a CB2 receptor inverse agonist may contribute to its documented anti-inflammatory properties.	Cannabidiol	15-26	cannabinoid receptor 2	Homo sapiens	42-45
16971387-6	2006	Deleting CBD completely abolished the dimerization and phosphatase activity of Laforin.	Cannabidiol	9-12	EPM2A glucan phosphatase, laforin	Homo sapiens	79-86
16909207-3	2006	CBD produced a gradual, time-dependent activation of caspase-3, which preceded the appearance of apoptotic death.	Cannabidiol	0-3	caspase 3	Homo sapiens	53-62
16909207-5	2006	The exposure to CBD caused in glioma cells an early production of ROS, depletion of intracellular glutathione and increase activity of glutathione reductase and glutathione peroxidase enzymes.	Cannabidiol	16-19	glutathione-disulfide reductase	Homo sapiens	135-156
16754784-9	2006	Together, the results from this study reveal that cannabidiol, acting through CB2 and regulation of Nox4 and p22(phox) expression, may be a novel and highly selective treatment for leukemia.	Cannabidiol	50-61	cannabinoid receptor 2	Homo sapiens	78-81
16754784-0	2006	Cannabidiol-induced apoptosis in human leukemia cells: A novel role of cannabidiol in the regulation of p22phox and Nox4 expression.	Cannabidiol	0-11	cytochrome b-245 alpha chain	Homo sapiens	104-111
16754784-0	2006	Cannabidiol-induced apoptosis in human leukemia cells: A novel role of cannabidiol in the regulation of p22phox and Nox4 expression.	Cannabidiol	0-11	NADPH oxidase 4	Homo sapiens	116-120
16754784-0	2006	Cannabidiol-induced apoptosis in human leukemia cells: A novel role of cannabidiol in the regulation of p22phox and Nox4 expression.	Cannabidiol	71-82	cytochrome b-245 alpha chain	Homo sapiens	104-111
16754784-0	2006	Cannabidiol-induced apoptosis in human leukemia cells: A novel role of cannabidiol in the regulation of p22phox and Nox4 expression.	Cannabidiol	71-82	NADPH oxidase 4	Homo sapiens	116-120
16754784-2	2006	Exposure of leukemia cells to cannabidiol led to cannabinoid receptor 2 (CB2)-mediated reduction in cell viability and induction in apoptosis.	Cannabidiol	30-41	cannabinoid receptor 2	Homo sapiens	49-71
16754784-2	2006	Exposure of leukemia cells to cannabidiol led to cannabinoid receptor 2 (CB2)-mediated reduction in cell viability and induction in apoptosis.	Cannabidiol	30-41	cannabinoid receptor 2	Homo sapiens	73-76
16754784-4	2006	From a mechanistic standpoint, cannabidiol exposure resulted in activation of caspase-8, caspase-9, and caspase-3, cleavage of poly(ADP-ribose) polymerase, and a decrease in full-length Bid, suggesting possible cross-talk between the intrinsic and extrinsic apoptotic pathways.	Cannabidiol	31-42	caspase 8	Homo sapiens	78-87
16754784-4	2006	From a mechanistic standpoint, cannabidiol exposure resulted in activation of caspase-8, caspase-9, and caspase-3, cleavage of poly(ADP-ribose) polymerase, and a decrease in full-length Bid, suggesting possible cross-talk between the intrinsic and extrinsic apoptotic pathways.	Cannabidiol	31-42	caspase 9	Homo sapiens	89-98
16754784-4	2006	From a mechanistic standpoint, cannabidiol exposure resulted in activation of caspase-8, caspase-9, and caspase-3, cleavage of poly(ADP-ribose) polymerase, and a decrease in full-length Bid, suggesting possible cross-talk between the intrinsic and extrinsic apoptotic pathways.	Cannabidiol	31-42	caspase 3	Homo sapiens	104-113
16754784-4	2006	From a mechanistic standpoint, cannabidiol exposure resulted in activation of caspase-8, caspase-9, and caspase-3, cleavage of poly(ADP-ribose) polymerase, and a decrease in full-length Bid, suggesting possible cross-talk between the intrinsic and extrinsic apoptotic pathways.	Cannabidiol	31-42	poly(ADP-ribose) polymerase 1	Homo sapiens	127-154
16754784-4	2006	From a mechanistic standpoint, cannabidiol exposure resulted in activation of caspase-8, caspase-9, and caspase-3, cleavage of poly(ADP-ribose) polymerase, and a decrease in full-length Bid, suggesting possible cross-talk between the intrinsic and extrinsic apoptotic pathways.	Cannabidiol	31-42	BH3 interacting domain death agonist	Homo sapiens	186-189
16754784-5	2006	The role of the mitochondria was further suggested as exposure to cannabidiol led to loss of mitochondrial membrane potential and release of cytochrome c.	Cannabidiol	66-77	cytochrome c, somatic	Homo sapiens	141-153
16754784-6	2006	It is noteworthy that cannabidiol exposure led to an increase in reactive oxygen species (ROS) production as well as an increase in the expression of the NAD(P)H oxidases Nox4 and p22(phox).	Cannabidiol	22-33	NADPH oxidase 4	Homo sapiens	171-175
16754784-6	2006	It is noteworthy that cannabidiol exposure led to an increase in reactive oxygen species (ROS) production as well as an increase in the expression of the NAD(P)H oxidases Nox4 and p22(phox).	Cannabidiol	22-33	calcineurin like EF-hand protein 1	Homo sapiens	180-183
16754784-8	2006	Finally, cannabidiol exposure led to a decrease in the levels of p-p38 mitogen-activated protein kinase, which could be blocked by treatment with a CB2-selective antagonist or ROS scavenger.	Cannabidiol	9-20	cannabinoid receptor 2	Homo sapiens	148-151
16754784-9	2006	Together, the results from this study reveal that cannabidiol, acting through CB2 and regulation of Nox4 and p22(phox) expression, may be a novel and highly selective treatment for leukemia.	Cannabidiol	50-61	NADPH oxidase 4	Homo sapiens	100-104
16754784-9	2006	Together, the results from this study reveal that cannabidiol, acting through CB2 and regulation of Nox4 and p22(phox) expression, may be a novel and highly selective treatment for leukemia.	Cannabidiol	50-61	calcineurin like EF-hand protein 1	Homo sapiens	109-112
16844117-6	2006	Icv injections of CBD (10 microg/5microl) induced an enhancement of c-Fos expression in waking-related brain areas such as hypothalamus and dorsal raphe nucleus (DRD).	Cannabidiol	18-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
16969427-3	2006	GW Pharmaceuticals have developed Sativex (GW- 1,000-02), a combined cannabinoid medicine that delivers and maintains therapeutic levels of two principal cannabinoids, delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD), via an oromucosal pump spray, that aims to minimize psychotropic side effects.	Cannabidiol	207-218	trinucleotide repeat containing adaptor 6A	Homo sapiens	43-55
16969427-3	2006	GW Pharmaceuticals have developed Sativex (GW- 1,000-02), a combined cannabinoid medicine that delivers and maintains therapeutic levels of two principal cannabinoids, delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD), via an oromucosal pump spray, that aims to minimize psychotropic side effects.	Cannabidiol	220-223	trinucleotide repeat containing adaptor 6A	Homo sapiens	43-55
16540122-8	2006	Moreover, degenerative change was more evident in CA2 than in CA1, as noted in some cases of tauopathy with accumulation of 4-repeat tau such as CBD.	Cannabidiol	145-148	carbonic anhydrase 2	Homo sapiens	50-53
16540122-8	2006	Moreover, degenerative change was more evident in CA2 than in CA1, as noted in some cases of tauopathy with accumulation of 4-repeat tau such as CBD.	Cannabidiol	145-148	carbonic anhydrase 1	Homo sapiens	62-65
16540122-8	2006	Moreover, degenerative change was more evident in CA2 than in CA1, as noted in some cases of tauopathy with accumulation of 4-repeat tau such as CBD.	Cannabidiol	145-148	microtubule associated protein tau	Homo sapiens	93-96
16805813-4	2006	We demonstrated that treatment of cultured rat pineals with 9-carboxy-11-nor-delta-9-tetrahydrocannabinol (THC), cannabidiol or cannabinol significantly reduced norepinephrine-induced arylalkylamine N-acetyltransferase (AANAT) activity and melatonin biosynthesis.	Cannabidiol	113-124	aralkylamine N-acetyltransferase	Rattus norvegicus	184-218
16805813-4	2006	We demonstrated that treatment of cultured rat pineals with 9-carboxy-11-nor-delta-9-tetrahydrocannabinol (THC), cannabidiol or cannabinol significantly reduced norepinephrine-induced arylalkylamine N-acetyltransferase (AANAT) activity and melatonin biosynthesis.	Cannabidiol	113-124	aralkylamine N-acetyltransferase	Rattus norvegicus	220-225
16766924-4	2006	RESULTS: Results indicate that GCLC TNR genotype 7/7 is negatively associated with CBD (odds ratio [OR] = 0.28, 95% confidence interval [CI] = 0.08-0.95) and the GCLM-588 C/C SNP genotype is associated with CBD susceptibility (OR = 3.07, 95% CI = 1.00-9.37).	Cannabidiol	207-210	glutamate-cysteine ligase catalytic subunit	Homo sapiens	31-35
16766924-4	2006	RESULTS: Results indicate that GCLC TNR genotype 7/7 is negatively associated with CBD (odds ratio [OR] = 0.28, 95% confidence interval [CI] = 0.08-0.95) and the GCLM-588 C/C SNP genotype is associated with CBD susceptibility (OR = 3.07, 95% CI = 1.00-9.37).	Cannabidiol	207-210	glutamate-cysteine ligase modifier subunit	Homo sapiens	162-166
16672367-1	2006	The plant-derived cannabinoids delta9-tetrahydrocannabinol (THC) and cannabidiol (CBD) both have immunosuppressive effects; although some effects of THC are mediated by the CB2 receptor, CB2 binds CBD weakly.	Cannabidiol	69-80	cannabinoid receptor 2 (macrophage)	Mus musculus	173-176
16672367-1	2006	The plant-derived cannabinoids delta9-tetrahydrocannabinol (THC) and cannabidiol (CBD) both have immunosuppressive effects; although some effects of THC are mediated by the CB2 receptor, CB2 binds CBD weakly.	Cannabidiol	69-80	cannabinoid receptor 2 (macrophage)	Mus musculus	187-190
16672367-1	2006	The plant-derived cannabinoids delta9-tetrahydrocannabinol (THC) and cannabidiol (CBD) both have immunosuppressive effects; although some effects of THC are mediated by the CB2 receptor, CB2 binds CBD weakly.	Cannabidiol	82-85	cannabinoid receptor 2 (macrophage)	Mus musculus	173-176
16490313-0	2006	Cannabidiol inhibits inducible nitric oxide synthase protein expression and nitric oxide production in beta-amyloid stimulated PC12 neurons through p38 MAP kinase and NF-kappaB involvement.	Cannabidiol	0-11	mitogen activated protein kinase 14	Rattus norvegicus	148-162
16490313-3	2006	In parallel, cannabidiol has been described to have anti-inflammatory properties in acute models of inflammation but the possible inhibitory effect of cannabidiol on iNOS protein expression and nitrite production in the nitrosative stress induced by Abeta in neuronal cell-line is un-investigated.	Cannabidiol	151-162	nitric oxide synthase 2	Rattus norvegicus	166-170
16490313-5	2006	CBD (10(-6) to 10(-4) M) inhibited both nitrite production and iNOS protein expression induced by Abeta (1-42).	Cannabidiol	0-3	nitric oxide synthase 2	Rattus norvegicus	63-67
16490313-6	2006	Cannabidiol effect was mediated through the inhibition of phosphorylated form of p38 MAP kinase and transcription factor nuclear factor-kappaB activation in a concentration-dependent manner.	Cannabidiol	0-11	mitogen activated protein kinase 14	Rattus norvegicus	81-84
16698671-4	2006	CBD treatment also resulted in the significant reduction of plasma levels of the pro-inflammatory cytokines, IFN-gamma and TNF-alpha.	Cannabidiol	0-3	interferon gamma	Mus musculus	109-118
16439618-2	2006	The purpose of this study was to investigate the possible interaction of P-gp with each of four major marijuana constituents: Delta(9)-tetrahydrocannabinol (THC), 11-nor-Delta(9)-tetrahydrocannabinol-carboxylic acid (THC-COOH), cannabinol (CBN), and cannabidiol (CBD).	Cannabidiol	250-261	phosphoglycolate phosphatase	Homo sapiens	73-77
16439618-2	2006	The purpose of this study was to investigate the possible interaction of P-gp with each of four major marijuana constituents: Delta(9)-tetrahydrocannabinol (THC), 11-nor-Delta(9)-tetrahydrocannabinol-carboxylic acid (THC-COOH), cannabinol (CBN), and cannabidiol (CBD).	Cannabidiol	263-266	phosphoglycolate phosphatase	Homo sapiens	73-77
16458258-7	2006	However, in CEM/VLB(100) cells, prolonged 72 h exposure to the cannabinoids, THC and CBD, decreased P-gp expression to a similar extent as the flavonoid, curcumin (turmeric).	Cannabidiol	85-88	ATP binding cassette subfamily B member 1	Homo sapiens	100-104
16052245-1	2006	Cannabidiol, a nonpsychoactive constituent of the Cannabis sativa plant, has been reported to act as an agonist of the vanilloid 1 channel in the transient receptor potential family (TRPV1) and also to inhibit the hydrolysis and cellular uptake of the endogenous cannabinoid anandamide.	Cannabidiol	0-11	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	183-188
16052245-12	2006	prevented the reversal of MK-801-induced disruption of PPI by cannabidiol, providing preliminary evidence that TRPV1 receptors are involved in the reversal of MK-801-induced sensorimotor gating deficits by cannabidiol.	Cannabidiol	62-73	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	111-116
16052245-12	2006	prevented the reversal of MK-801-induced disruption of PPI by cannabidiol, providing preliminary evidence that TRPV1 receptors are involved in the reversal of MK-801-induced sensorimotor gating deficits by cannabidiol.	Cannabidiol	206-217	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	111-116
16698671-4	2006	CBD treatment also resulted in the significant reduction of plasma levels of the pro-inflammatory cytokines, IFN-gamma and TNF-alpha.	Cannabidiol	0-3	tumor necrosis factor	Mus musculus	123-132
15750822-3	2005	Although a glutamic acid in position 69 of the human leukocyte antigen-DP beta chain (HLA-DPB1-Glu69) is associated with the development of CBD, it cannot fully explain susceptibility.	Cannabidiol	140-143	major histocompatibility complex, class II, DP beta 1	Homo sapiens	86-94
16389547-0	2006	The marijuana component cannabidiol inhibits beta-amyloid-induced tau protein hyperphosphorylation through Wnt/beta-catenin pathway rescue in PC12 cells.	Cannabidiol	24-35	Wnt family member 2	Rattus norvegicus	107-110
16389547-0	2006	The marijuana component cannabidiol inhibits beta-amyloid-induced tau protein hyperphosphorylation through Wnt/beta-catenin pathway rescue in PC12 cells.	Cannabidiol	24-35	catenin beta 1	Rattus norvegicus	111-123
16389547-9	2006	The effect of cannabidiol is mediated through the Wnt/beta-catenin pathway rescue in Abeta-stimulated PC12 cells.	Cannabidiol	14-25	Wnt family member 2	Rattus norvegicus	50-53
16389547-9	2006	The effect of cannabidiol is mediated through the Wnt/beta-catenin pathway rescue in Abeta-stimulated PC12 cells.	Cannabidiol	14-25	catenin beta 1	Rattus norvegicus	54-66
15964831-10	2005	Pulse stimulation of cells on CBD or HepII with lysophosphatidic acid elevates Rho GTP loading to the same level, but the lysophosphatidic acid-stimulated MLC phosphorylation is significantly lower in cells on HepII than on CBD.	Cannabidiol	224-227	modulator of VRAC current 1	Homo sapiens	155-158
15960180-6	2005	In previous reports, there was a difference between the dopamine D2 receptor binding capacity of CBD and that of HPHA.	Cannabidiol	97-100	dopamine receptor D2	Homo sapiens	56-76
15845890-8	2005	Moreover, the neuroprotective effect of cannabidiol was inhibited by WAY100135, a serotonin 5-hydroxytriptamine1A (5-HT1A) receptor antagonist but not capsazepine a vanilloid receptor antagonist.	Cannabidiol	40-51	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	115-131
15845890-12	2005	These results suggested that the neuroprotective effect of cannabidiol may be related to the increase in CBF through the serotonergic 5-HT1A receptor.	Cannabidiol	59-70	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	134-149
15588739-1	2004	Delta9-Tetrahydrocannabinol (Delta9-THC) and (-)-cannabidiol are major constituents of the Cannabis sativa plant with different pharmacological profiles: (-)-Delta9-tetrahydrocannabinol, but not (-)-cannabidiol, activates cannabinoid CB1 and CB2 receptors and induces psychoactive and peripheral effects.	Cannabidiol	45-60	cannabinoid receptor 1 (brain)	Mus musculus	234-237
15910887-1	2005	Delta-9 tetrahydrocannabinol (Delta(9)-THC) and (-)-cannabidiol ((-)-CBD) are major constituents of the Cannabis sativa plant with different pharmacological profiles: (Delta(9)-THC activates cannabinoid CB(1) and CB(2) receptors and induces psychoactive and peripheral effects.	Cannabidiol	48-63	cannabinoid receptor 1 (brain)	Mus musculus	203-208
15910887-1	2005	Delta-9 tetrahydrocannabinol (Delta(9)-THC) and (-)-cannabidiol ((-)-CBD) are major constituents of the Cannabis sativa plant with different pharmacological profiles: (Delta(9)-THC activates cannabinoid CB(1) and CB(2) receptors and induces psychoactive and peripheral effects.	Cannabidiol	65-72	cannabinoid receptor 1 (brain)	Mus musculus	203-208
15910887-5	2005	Of the five (+)-CBD derivatives, all with CB(1) receptor affinity, only (+)-7-OH-CBD-DMH (DMH=1,1-dimethylheptyl), acted centrally, while all five arrested defecation.	Cannabidiol	12-19	cannabinoid receptor 1 (brain)	Mus musculus	42-47
15652407-2	2005	We examined the ability of in vivo and in vitro cannabidiol to interfere with the production of interleukin (IL)-12 and IL-10 by murine macrophages and to modulate macrophage chemotaxis.	Cannabidiol	48-59	interleukin 10	Mus musculus	120-125
15652407-3	2005	Cannabidiol added in vitro to peritoneal macrophages significantly increased IL-12 and decreased IL-10 production.	Cannabidiol	0-11	interleukin 10	Mus musculus	97-102
15588739-1	2004	Delta9-Tetrahydrocannabinol (Delta9-THC) and (-)-cannabidiol are major constituents of the Cannabis sativa plant with different pharmacological profiles: (-)-Delta9-tetrahydrocannabinol, but not (-)-cannabidiol, activates cannabinoid CB1 and CB2 receptors and induces psychoactive and peripheral effects.	Cannabidiol	45-60	cannabinoid receptor 2 (macrophage)	Mus musculus	242-245
15588739-3	2004	Although all (+)-cannabidiols bind to cannabinoid CB1 and CB2 receptors, only (+)-7-OH-cannabidiol-DMH was centrally active, while all (+)-cannabidiol analogues completely arrested defecation.	Cannabidiol	13-29	cannabinoid receptor 1 (brain)	Mus musculus	50-53
15588739-3	2004	Although all (+)-cannabidiols bind to cannabinoid CB1 and CB2 receptors, only (+)-7-OH-cannabidiol-DMH was centrally active, while all (+)-cannabidiol analogues completely arrested defecation.	Cannabidiol	13-29	cannabinoid receptor 2 (macrophage)	Mus musculus	58-61
15588739-3	2004	Although all (+)-cannabidiols bind to cannabinoid CB1 and CB2 receptors, only (+)-7-OH-cannabidiol-DMH was centrally active, while all (+)-cannabidiol analogues completely arrested defecation.	Cannabidiol	13-28	cannabinoid receptor 1 (brain)	Mus musculus	50-53
15588739-3	2004	Although all (+)-cannabidiols bind to cannabinoid CB1 and CB2 receptors, only (+)-7-OH-cannabidiol-DMH was centrally active, while all (+)-cannabidiol analogues completely arrested defecation.	Cannabidiol	13-28	cannabinoid receptor 2 (macrophage)	Mus musculus	58-61
15158372-0	2004	Cannabidiol increases Fos expression in the nucleus accumbens but not in the dorsal striatum.	Cannabidiol	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-25
15640760-0	2004	Cannabidiol prevents infarction via the non-CB1 cannabinoid receptor mechanism.	Cannabidiol	0-11	cannabinoid receptor 1 (brain)	Mus musculus	44-47
15314281-5	2004	CBD could induce cytochrome c release from isolated mitochondria, but much less potent than tBid.	Cannabidiol	0-3	cytochrome c, somatic	Homo sapiens	17-29
15314281-6	2004	Free cardiolipin inhibited the CBD-induced cytochrome c release, suggesting that it may be mediated by interfering with mitochondrial cardiolipin, especially with the interaction between cytochrome c and cardiolipin.	Cannabidiol	31-34	cytochrome c, somatic	Homo sapiens	43-55
15314281-6	2004	Free cardiolipin inhibited the CBD-induced cytochrome c release, suggesting that it may be mediated by interfering with mitochondrial cardiolipin, especially with the interaction between cytochrome c and cardiolipin.	Cannabidiol	31-34	cytochrome c, somatic	Homo sapiens	187-199
15313881-0	2004	Vanilloid TRPV1 receptor mediates the antihyperalgesic effect of the nonpsychoactive cannabinoid, cannabidiol, in a rat model of acute inflammation.	Cannabidiol	98-109	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	10-15
15273960-2	2004	However, the relationship between HLA-DPB1 and beryllium sensitization, and whether the presence of one or two HLA-DPB1(Glu69) alleles is differentially associated with CBD and beryllium sensitization have not been completely resolved.	Cannabidiol	169-172	major histocompatibility complex, class II, DP beta 1	Homo sapiens	111-119
15273960-4	2004	RESULTS: HLA-DPB1(Glu69) was associated with both CBD (OR = 9.4; 95% CI = 5.4, 16.6) and sensitization (OR = 3.3, 95% CI = 1.9, 5.9).	Cannabidiol	50-53	major histocompatibility complex, class II, DP beta 1	Homo sapiens	9-17
15158372-2	2004	In the present paper we employed the detection of Fos protein to investigate neuronal activation in the dorsal striatum and nucleus accumbens of male Wistar rats after systemic administration of CBD (120 mg/kg), haloperidol (1 mg/kg) or clozapine (20 mg/kg).	Cannabidiol	195-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
15140635-0	2004	Cannabidiol lacks the vanilloid VR1-mediated vasorespiratory effects of capsaicin and anandamide in anaesthetised rats.	Cannabidiol	0-11	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	32-35
15140635-7	2004	It has previously been shown using human embryonic kidney (HEK) cells over-expressing vanilloid human VR1 (hVR1) receptors that cannabidiol is a full agonist at vanilloid VR1 receptors in vitro.	Cannabidiol	128-139	transient receptor potential cation channel subfamily V member 1	Homo sapiens	102-105
15140635-7	2004	It has previously been shown using human embryonic kidney (HEK) cells over-expressing vanilloid human VR1 (hVR1) receptors that cannabidiol is a full agonist at vanilloid VR1 receptors in vitro.	Cannabidiol	128-139	transient receptor potential cation channel subfamily V member 1	Homo sapiens	107-111
15140635-7	2004	It has previously been shown using human embryonic kidney (HEK) cells over-expressing vanilloid human VR1 (hVR1) receptors that cannabidiol is a full agonist at vanilloid VR1 receptors in vitro.	Cannabidiol	128-139	transient receptor potential cation channel subfamily V member 1	Homo sapiens	108-111
15140635-9	2004	We conclude that there are substantial functional differences between human and rat vanilloid VR1 receptors with respect to the actions of cannabidiol as an agonist at vanilloid VR1 receptors.	Cannabidiol	139-150	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	94-97
15140635-9	2004	We conclude that there are substantial functional differences between human and rat vanilloid VR1 receptors with respect to the actions of cannabidiol as an agonist at vanilloid VR1 receptors.	Cannabidiol	139-150	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	178-181
12379658-5	2002	As in the case of KCBP with CBD, the interaction of chimeric motors with MTs, as well as their MT-stimulated ATPase activity, was inhibited by Ca(2+)-CaM.	Cannabidiol	28-31	Calmodulin	Drosophila melanogaster	143-153
14975942-6	2004	The Be-stimulated upregulation of TNF-alpha mature-mRNA levels with TNF-alpha protein production was a unique property of CBD BAL cells, and did not occur in BAL cells from Be-sensitized patients without CBD, or sarcoidosis BAL cells.	Cannabidiol	122-125	tumor necrosis factor	Homo sapiens	34-43
14975942-6	2004	The Be-stimulated upregulation of TNF-alpha mature-mRNA levels with TNF-alpha protein production was a unique property of CBD BAL cells, and did not occur in BAL cells from Be-sensitized patients without CBD, or sarcoidosis BAL cells.	Cannabidiol	122-125	tumor necrosis factor	Homo sapiens	68-77
15030397-5	2004	Treatment of the cells with cannabidiol (10(-7)-10(-4)m) prior to beta-amyloid peptide exposure significantly elevated cell survival while it decreased ROS production, lipid peroxidation, caspase 3 levels, DNA fragmentation and intracellular calcium.	Cannabidiol	28-39	caspase 3	Rattus norvegicus	188-197
15030397-6	2004	Our results indicate that cannabidiol exerts a combination of neuroprotective, anti-oxidative and anti-apoptotic effects against beta-amyloid peptide toxicity, and that inhibition of caspase 3 appearance from its inactive precursor, pro-caspase 3, by cannabidiol is involved in the signalling pathway for this neuroprotection.	Cannabidiol	26-37	caspase 3	Rattus norvegicus	237-246
14617682-5	2004	By contrast, the CB1 cannabinoid receptor antagonist N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboximide hydrochloride (SR141716; SR1), capsazepine (vanilloid receptor antagonist), the inhibitors of ceramide generation, or pertussis toxin did not counteract CBD effects.	Cannabidiol	302-305	cannabinoid receptor 1	Homo sapiens	17-20
14673106-9	2003	Further Ca2+ binding to the N-terminal EF-hands promotes secondary CaM interactions with CBD, which enhance facilitation and cause a conformational change that initiates CDI.	Cannabidiol	89-92	calmodulin 1	Homo sapiens	67-70
12915448-5	2003	Both in vitro and in vivo assay have shown that the interaction is specific and that laforin probably uses its N-terminal CBD-4 domain to interact with the C-terminal NifU-like domain of the HIRIP5 protein.	Cannabidiol	122-125	EPM2A glucan phosphatase, laforin	Homo sapiens	85-92
12915448-5	2003	Both in vitro and in vivo assay have shown that the interaction is specific and that laforin probably uses its N-terminal CBD-4 domain to interact with the C-terminal NifU-like domain of the HIRIP5 protein.	Cannabidiol	122-125	NFU1 iron-sulfur cluster scaffold	Homo sapiens	191-197
12571139-6	2003	CBD also induced a significant decrease in CO activity of the PBC in most animals and a distinct delay, as well as prolongation of the maturational process, especially when induced close to P3 and P11-P13.	Cannabidiol	0-3	S100 calcium binding protein A10	Rattus norvegicus	197-200
12443781-1	2002	1",1"-Cyclopropyl side chain substituents enhance the affinities of Delta(8)-tetrahydrocannabinol and respective cannabidiol analogues for the CB1 and CB2 cannabinoid receptors.	Cannabidiol	113-124	cannabinoid receptor 1	Homo sapiens	143-146
12443781-1	2002	1",1"-Cyclopropyl side chain substituents enhance the affinities of Delta(8)-tetrahydrocannabinol and respective cannabidiol analogues for the CB1 and CB2 cannabinoid receptors.	Cannabidiol	113-124	cannabinoid receptor 2	Homo sapiens	151-154
12443781-2	2002	The results support the hypothesis for a subsite within CB1 and CB2 binding domain at the level of the benzylic side chain carbon in the tetrahydrocannabinol and cannabidiol series.	Cannabidiol	162-173	cannabinoid receptor 1	Homo sapiens	56-59
12443781-2	2002	The results support the hypothesis for a subsite within CB1 and CB2 binding domain at the level of the benzylic side chain carbon in the tetrahydrocannabinol and cannabidiol series.	Cannabidiol	162-173	cannabinoid receptor 2	Homo sapiens	64-67
12450575-2	2002	We have found that cannabidiol can also interact with cannabinoid CB(1) receptor agonists in the mouse vas deferens, a tissue in which prejunctional cannabinoid CB(1) receptors mediate inhibition of electrically evoked contractions by suppressing noradrenaline and/or ATP release.	Cannabidiol	19-30	cannabinoid receptor 1 (brain)	Mus musculus	66-71
12450575-2	2002	We have found that cannabidiol can also interact with cannabinoid CB(1) receptor agonists in the mouse vas deferens, a tissue in which prejunctional cannabinoid CB(1) receptors mediate inhibition of electrically evoked contractions by suppressing noradrenaline and/or ATP release.	Cannabidiol	19-30	cannabinoid receptor 1 (brain)	Mus musculus	161-166
11935262-3	2002	Tau-positive doughnut-shaped structures were also found occasionally in the cerebellar molecular layer in 6 of the 13 patients with PSP (46%) and 2 of the 7 patients with CBD (29%).	Cannabidiol	171-174	microtubule associated protein tau	Homo sapiens	0-3
12784694-7	2002	In conclusion, measurement of tau protein levels in CSF may be useful for the differential diagnosis of CBD from PSP.	Cannabidiol	104-107	microtubule associated protein tau	Homo sapiens	30-33
11606325-0	2001	Molecular targets for cannabidiol and its synthetic analogues: effect on vanilloid VR1 receptors and on the cellular uptake and enzymatic hydrolysis of anandamide.	Cannabidiol	22-33	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	83-86
11809870-7	2002	Enhancement of IL-2 was also demonstrated with CP55940, Delta(9)-tetrahydrocannabinol, and cannabidiol, thus suggesting that the phenomenon is not unique to CBN.	Cannabidiol	91-102	interleukin 2	Mus musculus	15-19
11606325-8	2001	Both CBD and (+)-CBD, but not the other analogues, stimulated VR1 with EC(50)=3.2 - 3.5 microM, and with a maximal effect similar in efficacy to that of capsaicin, i.e. 67 - 70% of the effect obtained with ionomycin (4 microM).	Cannabidiol	5-8	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	62-65
11606325-8	2001	Both CBD and (+)-CBD, but not the other analogues, stimulated VR1 with EC(50)=3.2 - 3.5 microM, and with a maximal effect similar in efficacy to that of capsaicin, i.e. 67 - 70% of the effect obtained with ionomycin (4 microM).	Cannabidiol	13-20	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	62-65
11606325-9	2001	CBD (10 microM) desensitized VR1 to the action of capsaicin.	Cannabidiol	0-3	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	29-32
11606325-19	2001	These findings suggest that VR1 receptors, or increased levels of endogenous AEA, might mediate some of the pharmacological effects of CBD and its analogues.	Cannabidiol	135-138	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	28-31
11207315-3	2001	Immunogenetic studies have demonstrated a strong association between CBD and possession of alleles of HLA-DP containing glutamic acid (Glu) at position 69 in the HLA-DP beta-chain.	Cannabidiol	69-72	major histocompatibility complex, class II, DP beta 1	Homo sapiens	102-108
11373682-4	2001	First, although facilitation and inactivation are two competing processes, both require Ca2+-CaM binding to a single "IQ-like" domain on the carboxy tail of alpha1A; a previously identified "CBD" CaM-binding site has no detectable role.	Cannabidiol	191-194	calcium voltage-gated channel subunit alpha1 A	Homo sapiens	157-164
11373682-4	2001	First, although facilitation and inactivation are two competing processes, both require Ca2+-CaM binding to a single "IQ-like" domain on the carboxy tail of alpha1A; a previously identified "CBD" CaM-binding site has no detectable role.	Cannabidiol	191-194	calmodulin 1	Homo sapiens	196-199
11370939-7	2001	Genetic studies also demonstrated an association of CBD with HLA-DPB1 alleles that contain glutamine at position 69 in up to 97 percent of subjects with CBD but also 30-40 percent of controls.	Cannabidiol	52-55	major histocompatibility complex, class II, DP beta 1	Homo sapiens	61-69
11370939-7	2001	Genetic studies also demonstrated an association of CBD with HLA-DPB1 alleles that contain glutamine at position 69 in up to 97 percent of subjects with CBD but also 30-40 percent of controls.	Cannabidiol	153-156	major histocompatibility complex, class II, DP beta 1	Homo sapiens	61-69
11207315-3	2001	Immunogenetic studies have demonstrated a strong association between CBD and possession of alleles of HLA-DP containing glutamic acid (Glu) at position 69 in the HLA-DP beta-chain.	Cannabidiol	69-72	major histocompatibility complex, class II, DP beta 1	Homo sapiens	162-168
10570211-4	1999	Here we show that "abnormal cannabidiol" (Abn-cbd) is a neurobehaviorally inactive cannabinoid that does not bind to CB1 receptors, yet causes SR141716A-sensitive hypotension and mesenteric vasodilation in wild-type mice and in mice lacking CB1 receptors or both CB1 and CB2 receptors.	Cannabidiol	28-39	cannabinoid receptor 1 (brain)	Mus musculus	241-244
10570211-4	1999	Here we show that "abnormal cannabidiol" (Abn-cbd) is a neurobehaviorally inactive cannabinoid that does not bind to CB1 receptors, yet causes SR141716A-sensitive hypotension and mesenteric vasodilation in wild-type mice and in mice lacking CB1 receptors or both CB1 and CB2 receptors.	Cannabidiol	28-39	cannabinoid receptor 1 (brain)	Mus musculus	241-244
10570211-4	1999	Here we show that "abnormal cannabidiol" (Abn-cbd) is a neurobehaviorally inactive cannabinoid that does not bind to CB1 receptors, yet causes SR141716A-sensitive hypotension and mesenteric vasodilation in wild-type mice and in mice lacking CB1 receptors or both CB1 and CB2 receptors.	Cannabidiol	28-39	cannabinoid receptor 2 (macrophage)	Mus musculus	271-274
10415070-5	1999	Individuals with DPB1 Glu69 in both alleles were almost exclusively found in the CBD group (6/20) vs the control group (1/75).	Cannabidiol	81-84	major histocompatibility complex, class II, DP beta 1	Homo sapiens	17-21
10415070-6	1999	Whereas most Glu69 carriers from the control group had a DPB1 allele *0201 (68%), most Glu69 carriers from the CBD group had a non-*0201 DPB1 Glu69-carrying allele (84%).	Cannabidiol	111-114	major histocompatibility complex, class II, DP beta 1	Homo sapiens	137-141
9858061-3	1998	We investigated the effect of delta9 tetrahydrocannabinol (THC) and cannabidiol (CBD) on cytokine production in vitro by human leukemic T, B, eosinophilic and CD8+ NK cell lines as models.	Cannabidiol	81-84	CD8a molecule	Homo sapiens	159-162
18636596-5	1997	Optimization of inducer (isophenyl-thio-beta-D-galactopyranoside) concentration and the time of induction led to soluble, fully active CBD(Cex) production levels in excess of 8 g/L.	Cannabidiol	135-138	cloacin lysis protein	Escherichia coli	139-142
8977230-7	1997	The data demonstrate that levels of the alpha subunit of the soluble IL-2 receptor, but not IFN-gamma, are elevated in the serum (median = 1428 U/ml; interquartile range = 823-2137 U/ml) and bronchoalveolar lavage fluid (median = 1.56 U/ml, interquartile range = 1.04-4.22 U/ml) of patients with CBD and correlate with the degree of pulmonary lymphocytosis and clinical measures of disease severity.	Cannabidiol	296-299	interleukin 2	Homo sapiens	69-73
8721631-2	1996	Animals were given intraperitoneally different doses (8,40 or 200 mg.kg.-1 daily) of CBD for 21 days, and the following dose-dependent events were observed: liver damage, significant increase in liver lipid peroxides, and decreases in activities of erythrocytic glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD).	Cannabidiol	85-88	glutathione peroxidase 1	Rattus norvegicus	286-292
2393963-5	1990	Western blotting analysis showed a marked decrease in the male-specific cytochrome P450 UT-2 in the hepatic microsomes, especially 24 to 48 h after pretreatment with CBD.	Cannabidiol	166-169	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	72-92
7584607-3	1995	Cannabidiol inactivated cytochrome P450 UT-2 (CYP2C11) not equal to in male rats and a member of 3A subfamily in mouse liver.	Cannabidiol	0-11	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	24-44
7584607-3	1995	Cannabidiol inactivated cytochrome P450 UT-2 (CYP2C11) not equal to in male rats and a member of 3A subfamily in mouse liver.	Cannabidiol	0-11	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	46-53
7753807-6	1995	The gene encoding lactoferrin is an estrogen-responsive gene in the mouse uterus that was rapidly and transiently up-regulated by THC, but not by CBD, in ovariectomized mice in the absence of ovarian steroids.	Cannabidiol	146-149	lactotransferrin	Mus musculus	18-29
7572077-3	1995	Epitopes spanning the entire length of the tau protein were present in CBD inclusions.	Cannabidiol	71-74	microtubule associated protein tau	Homo sapiens	43-46
18613043-2	1993	Transcription from the lac promoter coupled with translation from a consensus prokaryotic ribosome binding site led to the production of large quantities of CBD(Cex) (up to 25% total soluble cell protein).	Cannabidiol	157-160	cloacin lysis protein	Escherichia coli	161-164
18613043-6	1993	Absence of free thiols indicated that the two Cys residues of CBD(Cex) form a disulfide bridge.	Cannabidiol	62-65	cloacin lysis protein	Escherichia coli	66-69
18613043-7	1993	It had the same N-terminal amino acid sequence as CBD(Cex) prepared from Cex by proteolysis, plus two additional N-terminal amino acid residues (Ala and Ser) encoded by the Nhel site introduced during plasmid construction.	Cannabidiol	50-53	cloacin lysis protein	Escherichia coli	54-57
18613043-7	1993	It had the same N-terminal amino acid sequence as CBD(Cex) prepared from Cex by proteolysis, plus two additional N-terminal amino acid residues (Ala and Ser) encoded by the Nhel site introduced during plasmid construction.	Cannabidiol	50-53	cloacin lysis protein	Escherichia coli	73-76
18613043-8	1993	CBD(Cex) bound to a variety of beta-1, 4-glycans with different affinities and saturation levels.	Cannabidiol	0-3	cloacin lysis protein	Escherichia coli	4-7
8466552-5	1993	Immunoprecipitation of microsomal protein with antibodies raised against either P450 2C or 3A revealed that approximately equal amounts of [14C]-CBD were bound to each of these P450s after CBD-mediated inactivation.	Cannabidiol	145-148	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	80-87
8466552-7	1993	Although > 80% of the enzyme activities attributed to P450s 2C and 3A were inactivated by CBD at the anticonvulsant dose of 120 mg/kg, P450 2C was approximately 3-fold more sensitive than P450 3A at the lower CBD doses tested.	Cannabidiol	93-96	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	138-145
1802990-7	1991	The results indicate that CBDHQ, which is an oxidation product of CBD, inhibits the hepatic microsomal drug-metabolizing enzymes through the decrease of cytochrome P-450 content.	Cannabidiol	26-29	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	153-169
1667651-3	1991	Concentrations of THC and CBD, comparable to plasma levels found after smoking marijuana (10-100 ng/ml), increased the concentration of measurable IFN (139 and 68%), while high concentrations of both cannabinoids (5-20 micrograms/ml) completely blocked synthesis and/or release of this cytokine.	Cannabidiol	26-29	interferon gamma	Homo sapiens	147-150
1667651-4	1991	CBD was also shown to decrease the measurable quantity of both IL-1 and TNF.	Cannabidiol	0-3	interleukin 1 alpha	Homo sapiens	63-67
1667651-4	1991	CBD was also shown to decrease the measurable quantity of both IL-1 and TNF.	Cannabidiol	0-3	tumor necrosis factor	Homo sapiens	72-75
1678894-4	1991	In addition, both CBD and haloperidol reduced the occurrence of stereotyped biting induced by apomorphine (6.4 mg/kg), increased plasma prolactin levels and produced palpebral ptosis, as compared to control solutions.	Cannabidiol	18-21	prolactin	Rattus norvegicus	136-145
2393963-7	1990	In the later stages from 24 to 48 h after CBD treatment, the reduction in content of the male-specific cytochrome P450 UT-2 may play a major role in the inhibitory effect of CBD on the hepatic drug-metabolizing enzyme system in the adult male rat in vivo.	Cannabidiol	42-45	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	103-123
34054347-1	2021	Objective: To study airway pathophysiology and the role of dendritic cells (DCs) and IL-17 receptor (IL-17R) signals in a mouse model for CBD.	Cannabidiol	138-141	interleukin 17 receptor A	Mus musculus	101-107
33817834-5	2021	In human SH-SY5Y neuronal cells, CBD prevented neurite lesion induced by Abeta1-42 and increased the expression of fatty acid amide hydrolase (FAAH) and cannabinoid receptor 1 (CB1R).	Cannabidiol	33-36	fatty acid amide hydrolase	Homo sapiens	115-141
33817834-5	2021	In human SH-SY5Y neuronal cells, CBD prevented neurite lesion induced by Abeta1-42 and increased the expression of fatty acid amide hydrolase (FAAH) and cannabinoid receptor 1 (CB1R).	Cannabidiol	33-36	fatty acid amide hydrolase	Homo sapiens	143-147
33817834-5	2021	In human SH-SY5Y neuronal cells, CBD prevented neurite lesion induced by Abeta1-42 and increased the expression of fatty acid amide hydrolase (FAAH) and cannabinoid receptor 1 (CB1R).	Cannabidiol	33-36	cannabinoid receptor 1	Homo sapiens	153-175
33817834-5	2021	In human SH-SY5Y neuronal cells, CBD prevented neurite lesion induced by Abeta1-42 and increased the expression of fatty acid amide hydrolase (FAAH) and cannabinoid receptor 1 (CB1R).	Cannabidiol	33-36	cannabinoid receptor 1	Homo sapiens	177-181
33817834-8	2021	The neuroprotective effect of CBD was further explored by observing the dopaminergic neurons using transgenic dat-1: GFP strains using the confocal microscope.	Cannabidiol	30-33	Sodium-dependent dopamine transporter	Caenorhabditis elegans	110-115
33763863-13	2021	CONCLUSION: Regardless of the morphology of astrocytic tau lesions, semi-quantitative tau pathology scores in select brain regions are sufficient to distinguish PSP and CBD.	Cannabidiol	169-172	microtubule associated protein tau	Homo sapiens	86-89
33802282-2	2021	9-Tetrahydrocannabinol (THC) and cannabidiol (CBD) are the best-characterized components of Cannabis sativa plants with modulating effects on cannabinoid receptors 1 and 2 (CB1 and CB2) and on orphan receptors such as GPR18 or GPR55.	Cannabidiol	33-44	cannabinoid receptor 1	Homo sapiens	173-176
33807975-5	2021	Since CB2 is expressed mainly in the immune cells, we hypothesized that CBD treatment could alter the activity of polymorphonuclear neutrophils (PMNs) in a similar way that it does with microglia/macrophages and others circulating leukocytes.	Cannabidiol	72-75	cannabinoid receptor 2	Homo sapiens	6-9
33802282-2	2021	9-Tetrahydrocannabinol (THC) and cannabidiol (CBD) are the best-characterized components of Cannabis sativa plants with modulating effects on cannabinoid receptors 1 and 2 (CB1 and CB2) and on orphan receptors such as GPR18 or GPR55.	Cannabidiol	33-44	cannabinoid receptor 2	Homo sapiens	181-184
33802282-2	2021	9-Tetrahydrocannabinol (THC) and cannabidiol (CBD) are the best-characterized components of Cannabis sativa plants with modulating effects on cannabinoid receptors 1 and 2 (CB1 and CB2) and on orphan receptors such as GPR18 or GPR55.	Cannabidiol	33-44	G protein-coupled receptor 18	Homo sapiens	218-223
33802282-2	2021	9-Tetrahydrocannabinol (THC) and cannabidiol (CBD) are the best-characterized components of Cannabis sativa plants with modulating effects on cannabinoid receptors 1 and 2 (CB1 and CB2) and on orphan receptors such as GPR18 or GPR55.	Cannabidiol	33-44	G protein-coupled receptor 55	Homo sapiens	227-232
33802282-2	2021	9-Tetrahydrocannabinol (THC) and cannabidiol (CBD) are the best-characterized components of Cannabis sativa plants with modulating effects on cannabinoid receptors 1 and 2 (CB1 and CB2) and on orphan receptors such as GPR18 or GPR55.	Cannabidiol	46-49	cannabinoid receptor 1	Homo sapiens	173-176
33802282-2	2021	9-Tetrahydrocannabinol (THC) and cannabidiol (CBD) are the best-characterized components of Cannabis sativa plants with modulating effects on cannabinoid receptors 1 and 2 (CB1 and CB2) and on orphan receptors such as GPR18 or GPR55.	Cannabidiol	46-49	cannabinoid receptor 2	Homo sapiens	181-184
33802282-2	2021	9-Tetrahydrocannabinol (THC) and cannabidiol (CBD) are the best-characterized components of Cannabis sativa plants with modulating effects on cannabinoid receptors 1 and 2 (CB1 and CB2) and on orphan receptors such as GPR18 or GPR55.	Cannabidiol	46-49	G protein-coupled receptor 18	Homo sapiens	218-223
33802282-2	2021	9-Tetrahydrocannabinol (THC) and cannabidiol (CBD) are the best-characterized components of Cannabis sativa plants with modulating effects on cannabinoid receptors 1 and 2 (CB1 and CB2) and on orphan receptors such as GPR18 or GPR55.	Cannabidiol	46-49	G protein-coupled receptor 55	Homo sapiens	227-232
33802282-3	2021	Previous studies have demonstrated anti-tumorigenic effects of THC and CBD in several tumor entities including GBM, mostly mediated via CB1 or CB2.	Cannabidiol	71-74	cannabinoid receptor 1	Homo sapiens	136-139
33802282-3	2021	Previous studies have demonstrated anti-tumorigenic effects of THC and CBD in several tumor entities including GBM, mostly mediated via CB1 or CB2.	Cannabidiol	71-74	cannabinoid receptor 2	Homo sapiens	143-146
34864001-5	2022	However, it is unknown which brain regions CBD stimulates CB1 receptors and how it interferes with local activity-related plasticity to produce these effects.	Cannabidiol	43-46	cannabinoid receptor 1	Rattus norvegicus	58-61
32244040-0	2020	MyD88-dependent and -independent signalling via TLR3 and TLR4 are differentially modulated by Delta9-tetrahydrocannabinol and cannabidiol in human macrophages.	Cannabidiol	126-137	MYD88 innate immune signal transduction adaptor	Homo sapiens	0-5
32244040-0	2020	MyD88-dependent and -independent signalling via TLR3 and TLR4 are differentially modulated by Delta9-tetrahydrocannabinol and cannabidiol in human macrophages.	Cannabidiol	126-137	toll like receptor 3	Homo sapiens	48-52
32244040-0	2020	MyD88-dependent and -independent signalling via TLR3 and TLR4 are differentially modulated by Delta9-tetrahydrocannabinol and cannabidiol in human macrophages.	Cannabidiol	126-137	toll like receptor 4	Homo sapiens	57-61
32244040-7	2020	THC and CBD (both at 10 muM) attenuated TLR3/4-induced IRF3 activation and induction of CXCL10/IFN-beta, while both phytocannabinoids failed to impact TLR4-induced IkappaB-alpha degradation and TNF-alpha/CXCL8 expression.	Cannabidiol	8-11	toll like receptor 3	Homo sapiens	40-44
32244040-7	2020	THC and CBD (both at 10 muM) attenuated TLR3/4-induced IRF3 activation and induction of CXCL10/IFN-beta, while both phytocannabinoids failed to impact TLR4-induced IkappaB-alpha degradation and TNF-alpha/CXCL8 expression.	Cannabidiol	8-11	interferon regulatory factor 3	Homo sapiens	55-59
32244040-7	2020	THC and CBD (both at 10 muM) attenuated TLR3/4-induced IRF3 activation and induction of CXCL10/IFN-beta, while both phytocannabinoids failed to impact TLR4-induced IkappaB-alpha degradation and TNF-alpha/CXCL8 expression.	Cannabidiol	8-11	C-X-C motif chemokine ligand 10	Homo sapiens	88-94
32244040-7	2020	THC and CBD (both at 10 muM) attenuated TLR3/4-induced IRF3 activation and induction of CXCL10/IFN-beta, while both phytocannabinoids failed to impact TLR4-induced IkappaB-alpha degradation and TNF-alpha/CXCL8 expression.	Cannabidiol	8-11	IFN1@	Homo sapiens	95-103
32244040-7	2020	THC and CBD (both at 10 muM) attenuated TLR3/4-induced IRF3 activation and induction of CXCL10/IFN-beta, while both phytocannabinoids failed to impact TLR4-induced IkappaB-alpha degradation and TNF-alpha/CXCL8 expression.	Cannabidiol	8-11	NFKB inhibitor alpha	Homo sapiens	164-177
32244040-7	2020	THC and CBD (both at 10 muM) attenuated TLR3/4-induced IRF3 activation and induction of CXCL10/IFN-beta, while both phytocannabinoids failed to impact TLR4-induced IkappaB-alpha degradation and TNF-alpha/CXCL8 expression.	Cannabidiol	8-11	tumor necrosis factor	Homo sapiens	194-203
32244040-7	2020	THC and CBD (both at 10 muM) attenuated TLR3/4-induced IRF3 activation and induction of CXCL10/IFN-beta, while both phytocannabinoids failed to impact TLR4-induced IkappaB-alpha degradation and TNF-alpha/CXCL8 expression.	Cannabidiol	8-11	C-X-C motif chemokine ligand 8	Homo sapiens	204-209
34864001-8	2022	Animals that received post-retrieval systemic CBD treatment presented relatively fewer cells expressing Zif268/Egr1 protein, a proxy for synaptic plasticity related to reconsolidation, in the AC and PL.	Cannabidiol	46-49	early growth response 1	Rattus norvegicus	104-110
34864001-8	2022	Animals that received post-retrieval systemic CBD treatment presented relatively fewer cells expressing Zif268/Egr1 protein, a proxy for synaptic plasticity related to reconsolidation, in the AC and PL.	Cannabidiol	46-49	early growth response 1	Rattus norvegicus	111-115
34450240-0	2022	Cannabidiol reverses memory impairments and activates components of the Akt/GSK3beta pathway in an experimental model of estrogen depletion.	Cannabidiol	0-11	AKT serine/threonine kinase 1	Rattus norvegicus	72-75
34662693-3	2022	To elucidate the role of accumbal D1 and D2 dopamine receptor families in Cannabidiol"s inhibitory impact on the acquisition and expression phases of methamphetamine (MET), the conditioned place preference (CPP) procedure as a common method to assay reward characteristics of drugs was carried out.	Cannabidiol	74-85	dopamine receptor D2	Rattus norvegicus	41-61
34662693-3	2022	To elucidate the role of accumbal D1 and D2 dopamine receptor families in Cannabidiol"s inhibitory impact on the acquisition and expression phases of methamphetamine (MET), the conditioned place preference (CPP) procedure as a common method to assay reward characteristics of drugs was carried out.	Cannabidiol	74-85	MET proto-oncogene, receptor tyrosine kinase	Rattus norvegicus	167-170
34662693-5	2022	In the second step of the study, animals received SCH23390 or Sulpiride in the NAc before Cannabidiol (50 mug/5 muL) infusion into the LV in the expression phase of MET to illuminate the influence of SCH23390 or Sulpiride on the inhibitory impact of Cannabidiol on the expression of MET-induced CPP.	Cannabidiol	250-261	MET proto-oncogene, receptor tyrosine kinase	Rattus norvegicus	283-286
34662693-6	2022	Intra-NAc administration of either SCH23390 or Sulpiride impaired Cannabidiol"s suppressive impact on the expression phase, while just Sulpiride could suppress the Cannabidiol"s impact on the acquisition phase of the MET-induced CPP.	Cannabidiol	164-175	MET proto-oncogene, receptor tyrosine kinase	Rattus norvegicus	217-220
34662693-8	2022	It seems that Cannabidiol prevents the expression and acquisition phases of MET-induced CPP partly through the dopaminergic system in the NAc.	Cannabidiol	14-25	MET proto-oncogene, receptor tyrosine kinase	Rattus norvegicus	76-79
34688811-8	2022	After cannabidiol 20 mg/kg treatment, increased levels of CB1 receptor protein were found in the prelimbic and orbitofrontal regions of the prefrontal cortex, and in the ventral striatum; an effect paralleled by a reduction of striatal  FosB accumulation and an increment of GluR2 AMPA receptor subunits.	Cannabidiol	6-17	FBJ osteosarcoma oncogene B	Mus musculus	237-241
34688811-13	2022	Our results reveal a series of complex CB1-related changes induced by cannabidiol with a varying impact on the reinstatement of cocaine-seeking behaviour that could limit its therapeutic applications.	Cannabidiol	70-81	cannabinoid receptor 1 (brain)	Mus musculus	39-42
34269108-0	2022	CBD Promotes Oral Ulcer Healing via Inhibiting CMPK2-Mediated Inflammasome.	Cannabidiol	0-3	cytidine monophosphate (UMP-CMP) kinase 2, mitochondrial	Mus musculus	47-52
34269108-4	2022	Notably, the enrichment of genes associated with the NOD, LRR, and NLRP3 pyrin domain-containing protein 3 (NLRP3) inflammasome pathway is downregulated after CBD treatment.	Cannabidiol	159-162	NLR family, pyrin domain containing 3	Mus musculus	108-113
34269108-6	2022	In addition, CBD decreases the expression of cytidine/uridine monophosphate kinase 2 (CMPK2), which subsequently inhibits the generation of oxidized mitochondria DNA and suppresses inflammasome activation.	Cannabidiol	13-16	cytidine monophosphate (UMP-CMP) kinase 2, mitochondrial	Mus musculus	45-84
34269108-6	2022	In addition, CBD decreases the expression of cytidine/uridine monophosphate kinase 2 (CMPK2), which subsequently inhibits the generation of oxidized mitochondria DNA and suppresses inflammasome activation.	Cannabidiol	13-16	cytidine monophosphate (UMP-CMP) kinase 2, mitochondrial	Mus musculus	86-91
34269108-7	2022	These immunomodulating effects of CBD are mostly blocked by peroxisome proliferator activated receptor gamma (PPARgamma) antagonist and partially antagonized by CB1 receptor antagonist.	Cannabidiol	34-37	peroxisome proliferator activated receptor gamma	Mus musculus	60-108
34269108-7	2022	These immunomodulating effects of CBD are mostly blocked by peroxisome proliferator activated receptor gamma (PPARgamma) antagonist and partially antagonized by CB1 receptor antagonist.	Cannabidiol	34-37	peroxisome proliferator activated receptor gamma	Mus musculus	110-119
34269108-8	2022	Our results demonstrate that CBD accelerates oral ulcer healing by inhibiting CMPK2-mediated NLRP3 inflammasome activation and pyroptosis, which are mediated mostly by PPARgamma in the nucleus and partially by CB1 in the plasma membrane.	Cannabidiol	29-32	cytidine monophosphate (UMP-CMP) kinase 2, mitochondrial	Mus musculus	78-83
34269108-8	2022	Our results demonstrate that CBD accelerates oral ulcer healing by inhibiting CMPK2-mediated NLRP3 inflammasome activation and pyroptosis, which are mediated mostly by PPARgamma in the nucleus and partially by CB1 in the plasma membrane.	Cannabidiol	29-32	NLR family, pyrin domain containing 3	Mus musculus	93-98
34269108-8	2022	Our results demonstrate that CBD accelerates oral ulcer healing by inhibiting CMPK2-mediated NLRP3 inflammasome activation and pyroptosis, which are mediated mostly by PPARgamma in the nucleus and partially by CB1 in the plasma membrane.	Cannabidiol	29-32	peroxisome proliferator activated receptor gamma	Mus musculus	168-177
34269108-8	2022	Our results demonstrate that CBD accelerates oral ulcer healing by inhibiting CMPK2-mediated NLRP3 inflammasome activation and pyroptosis, which are mediated mostly by PPARgamma in the nucleus and partially by CB1 in the plasma membrane.	Cannabidiol	29-32	cannabinoid receptor 1 (brain)	Mus musculus	210-213
34736642-2	2022	We have demonstrated for the first time that cannabidiol (CBD) and 11-nor-Delta9-tetrahydrocannabinol-9-carboxylic acid (carboxy-THC) act as extracellular ligands for the growth hormone secretagogue receptor (GHS-R1a), strongly promoting the binding of ghrelin (GHR), the endogenous ligand of GHS-R1a.	Cannabidiol	45-56	growth hormone secretagogue receptor	Homo sapiens	171-207
34736642-2	2022	We have demonstrated for the first time that cannabidiol (CBD) and 11-nor-Delta9-tetrahydrocannabinol-9-carboxylic acid (carboxy-THC) act as extracellular ligands for the growth hormone secretagogue receptor (GHS-R1a), strongly promoting the binding of ghrelin (GHR), the endogenous ligand of GHS-R1a.	Cannabidiol	58-61	growth hormone secretagogue receptor	Homo sapiens	171-207
34736642-3	2022	The affinity profiles of CBD and carboxy-THC are significantly different from the profiles of synthetic GHR mimetics such as CJC-1295 or (D-Arg1-D-Phe5-D-Trp7,9-Leu11)-Substance P peptides, which are the most common interferents; the cannabinoids promoted the GHR/GHS-R1a interaction, while the ghrelin mimetics acted rather as competitive inhibitors.	Cannabidiol	25-28	arginase 1	Homo sapiens	140-144
34450240-0	2022	Cannabidiol reverses memory impairments and activates components of the Akt/GSK3beta pathway in an experimental model of estrogen depletion.	Cannabidiol	0-11	glycogen synthase kinase 3 alpha	Rattus norvegicus	76-84
34904193-12	2022	Thus, PECS-101, a new fluorinated CBD analog, could represent a novel therapeutic alternative to prevent mechanical and cold allodynia induced by PTX potentially through the activation of PPARgamma in macrophages.	Cannabidiol	34-37	peroxisome proliferator activated receptor gamma	Mus musculus	188-197
34915361-0	2022	Cannabidiol activates PINK1-Parkin-dependent mitophagy and mitochondrial-derived vesicles.	Cannabidiol	0-11	PTEN induced kinase 1	Homo sapiens	22-27
34915361-4	2022	Here we present evidence that cannabidiol (CBD) activates the PINK1-Parkin pathway in a unique manner.	Cannabidiol	30-41	PTEN induced kinase 1	Homo sapiens	62-67
34915361-4	2022	Here we present evidence that cannabidiol (CBD) activates the PINK1-Parkin pathway in a unique manner.	Cannabidiol	43-46	PTEN induced kinase 1	Homo sapiens	62-67
34915361-6	2022	The mitochondrial permeability transition pore inhibitor cyclosporine A exclusively diminished the CBD-induced PINK1/Parkin activation and its associated mitochondrial effects.	Cannabidiol	99-102	PTEN induced kinase 1	Homo sapiens	111-116
34971020-0	2022	The effects of cannabidiol via TRPV2 channel in chronic myeloid leukemia cells and its combination with imatinib.	Cannabidiol	15-26	transient receptor potential cation channel subfamily V member 2	Homo sapiens	31-36
34973413-10	2022	Altogether, our study supports the hypothesis that MSEW induces profound long-lasting molecular changes in mTOR signalling and brain energy metabolism related to depressive-like and anxiety-like behaviours in female mice, which were partially ameliorated by CBD administration.	Cannabidiol	258-261	mechanistic target of rapamycin kinase	Mus musculus	107-111
34918945-6	2021	Objective: Considering the major CES1-mediated metabolism of RDV on systemic administration, we intend to explore the remarkable CES1 plus CYP3A4 inhibitory activity of cannabidiol (CBD) against in vitro microsomal metabolism of RDV to indicate its therapeutic potential as an adjuvant to RDV in the treatment and management of COVID-19.	Cannabidiol	169-180	carboxylesterase 1	Homo sapiens	129-133
34918945-6	2021	Objective: Considering the major CES1-mediated metabolism of RDV on systemic administration, we intend to explore the remarkable CES1 plus CYP3A4 inhibitory activity of cannabidiol (CBD) against in vitro microsomal metabolism of RDV to indicate its therapeutic potential as an adjuvant to RDV in the treatment and management of COVID-19.	Cannabidiol	169-180	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	139-145
34918945-6	2021	Objective: Considering the major CES1-mediated metabolism of RDV on systemic administration, we intend to explore the remarkable CES1 plus CYP3A4 inhibitory activity of cannabidiol (CBD) against in vitro microsomal metabolism of RDV to indicate its therapeutic potential as an adjuvant to RDV in the treatment and management of COVID-19.	Cannabidiol	182-185	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	139-145
34918964-8	2021	Results: Our findings showed that inhalation of CBD was able to not only limit the tumor growth but also to alter the dynamics of TME by repressing P-selectin, apelin, and interleukin (IL)-8, as well as blocking a key immune checkpoint-indoleamine 2,3-dioxygenase (IDO).	Cannabidiol	48-51	selectin P	Homo sapiens	148-158
34918964-8	2021	Results: Our findings showed that inhalation of CBD was able to not only limit the tumor growth but also to alter the dynamics of TME by repressing P-selectin, apelin, and interleukin (IL)-8, as well as blocking a key immune checkpoint-indoleamine 2,3-dioxygenase (IDO).	Cannabidiol	48-51	apelin	Homo sapiens	160-166
34918964-8	2021	Results: Our findings showed that inhalation of CBD was able to not only limit the tumor growth but also to alter the dynamics of TME by repressing P-selectin, apelin, and interleukin (IL)-8, as well as blocking a key immune checkpoint-indoleamine 2,3-dioxygenase (IDO).	Cannabidiol	48-51	C-X-C motif chemokine ligand 8	Homo sapiens	172-190
34918964-8	2021	Results: Our findings showed that inhalation of CBD was able to not only limit the tumor growth but also to alter the dynamics of TME by repressing P-selectin, apelin, and interleukin (IL)-8, as well as blocking a key immune checkpoint-indoleamine 2,3-dioxygenase (IDO).	Cannabidiol	48-51	indoleamine 2,3-dioxygenase 1	Homo sapiens	225-263
34918964-8	2021	Results: Our findings showed that inhalation of CBD was able to not only limit the tumor growth but also to alter the dynamics of TME by repressing P-selectin, apelin, and interleukin (IL)-8, as well as blocking a key immune checkpoint-indoleamine 2,3-dioxygenase (IDO).	Cannabidiol	48-51	indoleamine 2,3-dioxygenase 1	Homo sapiens	265-268
34918964-9	2021	In addition, CBD enhanced the cluster of differentiation (CD) 103 expression, indicating improved antigen presentation, promoted CD8 immune responses, and reduced innate Lymphoid Cells within the tumor.	Cannabidiol	13-16	CD8a molecule	Homo sapiens	129-132
34537380-14	2021	Cannabidiol similarly inhibited IL-1beta-induced mBMDM M1 polarization via a reduction in Il1b and an increase in Cd206 and Il4 gene expression.	Cannabidiol	0-11	interleukin 1 beta	Mus musculus	90-94
34944028-0	2021	Cannabidiol Inhibits Tau Aggregation In Vitro.	Cannabidiol	0-11	microtubule associated protein tau	Homo sapiens	21-24
34944028-5	2021	Therefore, we hypothesize that CBD may serve as a potent substance to hamper tau aggregation in AD.	Cannabidiol	31-34	microtubule associated protein tau	Homo sapiens	77-80
34944028-6	2021	In this study, we aim to investigate the CBD effect on the aggregation of recombinant human tau protein 1N/4R isoform using biochemical methods in vitro and in silico.	Cannabidiol	41-44	microtubule associated protein tau	Homo sapiens	92-95
34944028-8	2021	Moreover, by quenching assay, docking, and job"s plot, we further demonstrated that one molecule of CBD interacts with one molecule of tau protein through a spontaneous binding.	Cannabidiol	100-103	microtubule associated protein tau	Homo sapiens	135-138
34944028-10	2021	Taken together, this study provides new insights about a natural substance, CBD, for tau therapy which may offer new hope for the treatment of AD.	Cannabidiol	76-79	microtubule associated protein tau	Homo sapiens	85-88
34493602-7	2021	THC and CBD showed mixed-type inhibition for CYP2C19 and CYP1A2, respectively.	Cannabidiol	8-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	45-52
34493602-7	2021	THC and CBD showed mixed-type inhibition for CYP2C19 and CYP1A2, respectively.	Cannabidiol	8-11	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	57-63
34792764-12	2021	Cannabidiol increased CB1 in DRG, reduced mechanical hyperalgesia and c-Fos expression in DRG and SC.	Cannabidiol	0-11	cannabinoid receptor 1 (brain)	Mus musculus	22-25
34792764-12	2021	Cannabidiol increased CB1 in DRG, reduced mechanical hyperalgesia and c-Fos expression in DRG and SC.	Cannabidiol	0-11	FBJ osteosarcoma oncogene	Mus musculus	70-75
34792764-15	2021	Oxaliplatin also increased Iba-1 in DRG, suggesting immune response modulation which was reduced by cannabidiol and enhanced by AM630.	Cannabidiol	100-111	induction of brown adipocytes 1	Mus musculus	27-32
34537380-14	2021	Cannabidiol similarly inhibited IL-1beta-induced mBMDM M1 polarization via a reduction in Il1b and an increase in Cd206 and Il4 gene expression.	Cannabidiol	0-11	mannose receptor, C type 1	Mus musculus	114-119
34537380-14	2021	Cannabidiol similarly inhibited IL-1beta-induced mBMDM M1 polarization via a reduction in Il1b and an increase in Cd206 and Il4 gene expression.	Cannabidiol	0-11	interleukin 4	Mus musculus	124-127
34643000-0	2021	Cannabidiol inhibits SARS-Cov-2 spike (S) protein-induced cytotoxicity and inflammation through a PPARgamma-dependent TLR4/NLRP3/Caspase-1 signaling suppression in Caco-2 cell line.	Cannabidiol	0-11	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	39-40
34218397-0	2021	Cannabidiol prevents lipopolysaccharide-induced sickness behavior and alters cytokine and neurotrophic factor levels in the brain.	Cannabidiol	0-11	neurotrophin 3	Homo sapiens	90-109
34218397-13	2021	In addition, CBD prevented endotoxin-induced increase in BDNF and NGF levels in the hippocampus of SB animals.	Cannabidiol	13-16	brain derived neurotrophic factor	Homo sapiens	57-61
34218397-13	2021	In addition, CBD prevented endotoxin-induced increase in BDNF and NGF levels in the hippocampus of SB animals.	Cannabidiol	13-16	nerve growth factor	Homo sapiens	66-69
34643000-0	2021	Cannabidiol inhibits SARS-Cov-2 spike (S) protein-induced cytotoxicity and inflammation through a PPARgamma-dependent TLR4/NLRP3/Caspase-1 signaling suppression in Caco-2 cell line.	Cannabidiol	0-11	peroxisome proliferator activated receptor gamma	Homo sapiens	98-107
34861907-0	2021	Implications of Cannabidiol in Pharmacogenomic-Based Drug Interactions with CYP2C19 Substrates.	Cannabidiol	16-27	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	76-83
34740670-0	2021	Cannabidiol selectively modulates interleukin (IL)-1beta and IL-6 production in toll-like receptor activated human peripheral blood monocytes.	Cannabidiol	0-11	interleukin 1 alpha	Homo sapiens	34-56
34740670-0	2021	Cannabidiol selectively modulates interleukin (IL)-1beta and IL-6 production in toll-like receptor activated human peripheral blood monocytes.	Cannabidiol	0-11	interleukin 6	Homo sapiens	61-65
34740670-4	2021	The objective of this study was to evaluate whether CBD modulates the innate immune response by human primary monocytes activated through toll-like receptors (TLR) 1-9.	Cannabidiol	52-55	toll like receptor 1	Homo sapiens	138-167
34740670-7	2021	CBD treatment significantly suppressed secretion of proinflammatory cytokine IL-1beta by monocytes activated through most TLRs, apart from TLRs 3 and 8.	Cannabidiol	0-3	interleukin 1 alpha	Homo sapiens	77-85
34740670-8	2021	Additionally, CBD treatment induced significant modulation of IL-6 production by monocytes activated through most TLRs, except for TLRs 1 and 3.	Cannabidiol	14-17	interleukin 6	Homo sapiens	62-66
34740670-11	2021	This study is of particular importance as it provides a direct and comprehensive assessment of the effects of CBD on TLR-activated primary human monocytes at a time when CBD containing products are being widely used by the public.	Cannabidiol	110-113	toll like receptor 1	Homo sapiens	117-120
34711111-10	2022	The level of cytochrome C release, apoptosis, oxidative stress, and cardiac biomarkers was considerably increased by AlP, which was compensated following CBD administration.	Cannabidiol	154-157	cytochrome c, somatic	Homo sapiens	13-25
34643000-0	2021	Cannabidiol inhibits SARS-Cov-2 spike (S) protein-induced cytotoxicity and inflammation through a PPARgamma-dependent TLR4/NLRP3/Caspase-1 signaling suppression in Caco-2 cell line.	Cannabidiol	0-11	toll like receptor 4	Homo sapiens	118-122
34643000-0	2021	Cannabidiol inhibits SARS-Cov-2 spike (S) protein-induced cytotoxicity and inflammation through a PPARgamma-dependent TLR4/NLRP3/Caspase-1 signaling suppression in Caco-2 cell line.	Cannabidiol	0-11	NLR family pyrin domain containing 3	Homo sapiens	123-128
34643000-0	2021	Cannabidiol inhibits SARS-Cov-2 spike (S) protein-induced cytotoxicity and inflammation through a PPARgamma-dependent TLR4/NLRP3/Caspase-1 signaling suppression in Caco-2 cell line.	Cannabidiol	0-11	caspase 1	Homo sapiens	129-138
34643000-5	2021	CBD caused a parallel inhibition of interleukin 1 beta (IL-1beta), IL-6, tumor necrosis factor alpha (TNF-alpha), and IL-18 by enzyme-linked immunosorbent assay (ELISA) assay.	Cannabidiol	0-3	interleukin 1 beta	Homo sapiens	36-54
34643000-5	2021	CBD caused a parallel inhibition of interleukin 1 beta (IL-1beta), IL-6, tumor necrosis factor alpha (TNF-alpha), and IL-18 by enzyme-linked immunosorbent assay (ELISA) assay.	Cannabidiol	0-3	interleukin 1 alpha	Homo sapiens	56-64
34643000-5	2021	CBD caused a parallel inhibition of interleukin 1 beta (IL-1beta), IL-6, tumor necrosis factor alpha (TNF-alpha), and IL-18 by enzyme-linked immunosorbent assay (ELISA) assay.	Cannabidiol	0-3	interleukin 6	Homo sapiens	67-71
34643000-5	2021	CBD caused a parallel inhibition of interleukin 1 beta (IL-1beta), IL-6, tumor necrosis factor alpha (TNF-alpha), and IL-18 by enzyme-linked immunosorbent assay (ELISA) assay.	Cannabidiol	0-3	tumor necrosis factor	Homo sapiens	73-100
34643000-5	2021	CBD caused a parallel inhibition of interleukin 1 beta (IL-1beta), IL-6, tumor necrosis factor alpha (TNF-alpha), and IL-18 by enzyme-linked immunosorbent assay (ELISA) assay.	Cannabidiol	0-3	tumor necrosis factor	Homo sapiens	102-111
34643000-5	2021	CBD caused a parallel inhibition of interleukin 1 beta (IL-1beta), IL-6, tumor necrosis factor alpha (TNF-alpha), and IL-18 by enzyme-linked immunosorbent assay (ELISA) assay.	Cannabidiol	0-3	interleukin 18	Homo sapiens	118-123
34832951-8	2021	Furthermore, we found that CBD activated the effector caspases 3/7, increased the expression of pro-apoptotic proteins, increased the levels of reactive oxygen species, as well as a leading to a loss of mitochondrial membrane potential in both populations.	Cannabidiol	27-30	caspase 3	Homo sapiens	54-66
34757526-4	2021	In-depth scRNA Seq analysis of CNS tissue demonstrated that CBD treatment resulted in a significant reduction in CXCL9, CXCL10 and IL-1beta expression within the CNS, leading to inhibited infiltration of inflammatory macrophages.	Cannabidiol	60-63	chemokine (C-X-C motif) ligand 9	Mus musculus	113-118
34757526-4	2021	In-depth scRNA Seq analysis of CNS tissue demonstrated that CBD treatment resulted in a significant reduction in CXCL9, CXCL10 and IL-1beta expression within the CNS, leading to inhibited infiltration of inflammatory macrophages.	Cannabidiol	60-63	chemokine (C-X-C motif) ligand 10	Mus musculus	120-126
34757526-4	2021	In-depth scRNA Seq analysis of CNS tissue demonstrated that CBD treatment resulted in a significant reduction in CXCL9, CXCL10 and IL-1beta expression within the CNS, leading to inhibited infiltration of inflammatory macrophages.	Cannabidiol	60-63	interleukin 1 alpha	Mus musculus	131-139
34727050-7	2021	At daily CBD doses of 10 to 20 mg/kg/d, hypoxia was observed in 5 dogs and increased serum alkaline phosphatase (ALP) activities (range, 301 to 978 U/L) was observed in 4 dogs.	Cannabidiol	9-12	alkaline phosphatase, biomineralization associated	Canis lupus familiaris	91-111
34727550-13	2021	CONCLUSION: It seems that CBD coated by nano-chitosan has good potential for reducing Abeta plaques, increasing brain CB1 and levels CB2, and improving learning and memory in Alz rats.	Cannabidiol	26-29	cannabinoid receptor 1	Rattus norvegicus	118-121
34727550-13	2021	CONCLUSION: It seems that CBD coated by nano-chitosan has good potential for reducing Abeta plaques, increasing brain CB1 and levels CB2, and improving learning and memory in Alz rats.	Cannabidiol	26-29	cannabinoid receptor 2	Rattus norvegicus	133-136
34727050-7	2021	At daily CBD doses of 10 to 20 mg/kg/d, hypoxia was observed in 5 dogs and increased serum alkaline phosphatase (ALP) activities (range, 301 to 978 U/L) was observed in 4 dogs.	Cannabidiol	9-12	alkaline phosphatase, biomineralization associated	Canis lupus familiaris	113-116
34331010-9	2021	Participants treated with CBD had lower levels of interleukin-6 (p = 0.017), vascular endothelial growth factor (p = 0.032), intermediate monocytes CD14+CD16+ (p = 0.024), and natural killer CD56negCD16hi (p = 0.000) compared with participants receiving placebo.	Cannabidiol	26-29	interleukin 6	Homo sapiens	50-63
34331010-9	2021	Participants treated with CBD had lower levels of interleukin-6 (p = 0.017), vascular endothelial growth factor (p = 0.032), intermediate monocytes CD14+CD16+ (p = 0.024), and natural killer CD56negCD16hi (p = 0.000) compared with participants receiving placebo.	Cannabidiol	26-29	vascular endothelial growth factor A	Homo sapiens	77-111
34331010-9	2021	Participants treated with CBD had lower levels of interleukin-6 (p = 0.017), vascular endothelial growth factor (p = 0.032), intermediate monocytes CD14+CD16+ (p = 0.024), and natural killer CD56negCD16hi (p = 0.000) compared with participants receiving placebo.	Cannabidiol	26-29	CD14 molecule	Homo sapiens	148-152
34331010-9	2021	Participants treated with CBD had lower levels of interleukin-6 (p = 0.017), vascular endothelial growth factor (p = 0.032), intermediate monocytes CD14+CD16+ (p = 0.024), and natural killer CD56negCD16hi (p = 0.000) compared with participants receiving placebo.	Cannabidiol	26-29	Fc gamma receptor IIIa	Homo sapiens	153-157
34331010-9	2021	Participants treated with CBD had lower levels of interleukin-6 (p = 0.017), vascular endothelial growth factor (p = 0.032), intermediate monocytes CD14+CD16+ (p = 0.024), and natural killer CD56negCD16hi (p = 0.000) compared with participants receiving placebo.	Cannabidiol	26-29	neural cell adhesion molecule 1	Homo sapiens	191-202
34102871-0	2021	Rates of self-directed perioperative cannabidiol use in patients undergoing total hip or knee arthroplasty.	Cannabidiol	37-48	hedgehog interacting protein	Homo sapiens	82-85
34102871-1	2021	Aim: To evaluate the prevalence of self-directed cannabidiol (CBD) use in patients with end-stage degenerative hip and knee arthritis who underwent total hip arthroplasty and total knee arthroplasty.	Cannabidiol	49-60	hedgehog interacting protein	Homo sapiens	154-157
34102871-1	2021	Aim: To evaluate the prevalence of self-directed cannabidiol (CBD) use in patients with end-stage degenerative hip and knee arthritis who underwent total hip arthroplasty and total knee arthroplasty.	Cannabidiol	62-65	hedgehog interacting protein	Homo sapiens	154-157
34776964-7	2021	Additionally, repeated KET administration increased ERK1/2 phosphorylation state in all regions examined, apart from the ventral hippocampus that was modulated by subsequent CBD treatment.	Cannabidiol	174-177	mitogen activated protein kinase 3	Rattus norvegicus	52-58
34628227-4	2021	OBJECTIVES: Study the biophysical gating effects of the curcumin-based diazepine on AMPAR variants and identify CBD binding sites on AMPARs with the hopes of discovering more potent drug candidates with less undesirable side effects.	Cannabidiol	112-115	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	133-139
34628227-7	2021	CBD-4 and CBD-5 show the most significant impact on AMPARs, reducing the current by 7-fold.	Cannabidiol	0-3	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	52-58
34628227-7	2021	CBD-4 and CBD-5 show the most significant impact on AMPARs, reducing the current by 7-fold.	Cannabidiol	10-13	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	52-58
34776964-8	2021	The present results show, for the first time, a stimulated motor output coupled with a specific glutamatergic-related status and ERK1/2 activation following chronic KET administration that were attenuated by CBD treatment, in a region-dependent manner.	Cannabidiol	208-211	mitogen activated protein kinase 3	Rattus norvegicus	129-135
34636529-3	2021	As a result, the growth mechanism of the CBD-Zn(O,S) layer varied as a function of KF PDT process time.	Cannabidiol	41-44	arylformamidase	Homo sapiens	83-85
34667212-6	2021	Moreover, topical treatment with CBD resulted in the penetration of CBD into the blood and, as a consequence, in direct modifications to the plasma protein structure by creating CBD adducts with molecules, such as proline-rich protein 30, transcription factor 19, or N-acetylglucosamine-6-sulfatase, what significantly changed the activity of these proteins.	Cannabidiol	33-36	proline rich 30	Rattus norvegicus	214-237
34667212-6	2021	Moreover, topical treatment with CBD resulted in the penetration of CBD into the blood and, as a consequence, in direct modifications to the plasma protein structure by creating CBD adducts with molecules, such as proline-rich protein 30, transcription factor 19, or N-acetylglucosamine-6-sulfatase, what significantly changed the activity of these proteins.	Cannabidiol	33-36	glucosamine (N-acetyl)-6-sulfatase	Rattus norvegicus	267-298
34667212-6	2021	Moreover, topical treatment with CBD resulted in the penetration of CBD into the blood and, as a consequence, in direct modifications to the plasma protein structure by creating CBD adducts with molecules, such as proline-rich protein 30, transcription factor 19, or N-acetylglucosamine-6-sulfatase, what significantly changed the activity of these proteins.	Cannabidiol	68-71	proline rich 30	Rattus norvegicus	214-237
34667212-6	2021	Moreover, topical treatment with CBD resulted in the penetration of CBD into the blood and, as a consequence, in direct modifications to the plasma protein structure by creating CBD adducts with molecules, such as proline-rich protein 30, transcription factor 19, or N-acetylglucosamine-6-sulfatase, what significantly changed the activity of these proteins.	Cannabidiol	68-71	glucosamine (N-acetyl)-6-sulfatase	Rattus norvegicus	267-298
34692831-9	2021	Pathological examination revealed more distribution of proliferative blood vessels in the animals treated with ADM modified with CBD-VEGF.	Cannabidiol	129-132	vascular endothelial growth factor A	Bos taurus	133-137
34416240-12	2021	Cannabidiol"s low micromolar CB1 antagonist pKB values suggest that at clinical blood levels (1-3 muM) it may act as a CB1 antagonist at prejunctional neuronal sites with more potency when ATP is the effector than for noradrenaline.	Cannabidiol	0-11	cannabinoid receptor 1	Rattus norvegicus	29-32
34416240-12	2021	Cannabidiol"s low micromolar CB1 antagonist pKB values suggest that at clinical blood levels (1-3 muM) it may act as a CB1 antagonist at prejunctional neuronal sites with more potency when ATP is the effector than for noradrenaline.	Cannabidiol	0-11	cannabinoid receptor 1	Rattus norvegicus	119-122
34289379-5	2021	Cannabidiol also significantly reduced the protein levels of proinflammatory cytokines (TNF-alpha and IL-1beta) and significantly increased the expression of tight junction proteins (claudin-5 and occludin).	Cannabidiol	0-11	tumor necrosis factor	Rattus norvegicus	88-97
34289379-5	2021	Cannabidiol also significantly reduced the protein levels of proinflammatory cytokines (TNF-alpha and IL-1beta) and significantly increased the expression of tight junction proteins (claudin-5 and occludin).	Cannabidiol	0-11	interleukin 1 alpha	Rattus norvegicus	102-110
34289379-5	2021	Cannabidiol also significantly reduced the protein levels of proinflammatory cytokines (TNF-alpha and IL-1beta) and significantly increased the expression of tight junction proteins (claudin-5 and occludin).	Cannabidiol	0-11	claudin 5	Rattus norvegicus	183-192
34289379-5	2021	Cannabidiol also significantly reduced the protein levels of proinflammatory cytokines (TNF-alpha and IL-1beta) and significantly increased the expression of tight junction proteins (claudin-5 and occludin).	Cannabidiol	0-11	occludin	Rattus norvegicus	197-205
34330718-0	2021	Cytochrome P450-Catalyzed Metabolism of Cannabidiol to the Active Metabolite 7-Hydroxy-Cannabidiol.	Cannabidiol	40-51	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-15
34330718-4	2021	Given the polymorphic nature of CYP2C19, we hypothesized that variable CYP2C19 expression may lead to interindividual differences in CBD metabolism to 7-OH-CBD.	Cannabidiol	133-136	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-39
34330718-4	2021	Given the polymorphic nature of CYP2C19, we hypothesized that variable CYP2C19 expression may lead to interindividual differences in CBD metabolism to 7-OH-CBD.	Cannabidiol	133-136	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-78
34330718-6	2021	The results from reaction phenotyping experiments with recombinant CYP enzymes and CYP-selective chemical inhibitors indicated that both CYP2C19 and CYP2C9 are capable of CBD metabolism to 7-OH-CBD.	Cannabidiol	171-174	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	137-144
34330718-6	2021	The results from reaction phenotyping experiments with recombinant CYP enzymes and CYP-selective chemical inhibitors indicated that both CYP2C19 and CYP2C9 are capable of CBD metabolism to 7-OH-CBD.	Cannabidiol	171-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
34330718-7	2021	CYP3A played a major role in CBD metabolic clearance via oxidation at sites other than the 7-position.	Cannabidiol	29-32	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-5
34330718-9	2021	In a subset of single-donor human liver microsomes with moderate to low CYP2C19 activity, CYP2C9 inhibition significantly reduced 7-OH-CBD formation, suggesting that CYP2C9 may play a greater role in CBD 7-hydroxylation than previously thought.	Cannabidiol	200-203	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
34330718-9	2021	In a subset of single-donor human liver microsomes with moderate to low CYP2C19 activity, CYP2C9 inhibition significantly reduced 7-OH-CBD formation, suggesting that CYP2C9 may play a greater role in CBD 7-hydroxylation than previously thought.	Cannabidiol	200-203	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	166-172
34330718-10	2021	Collectively, these data indicate that both CYP2C19 and CYP2C9 are important contributors in CBD metabolism to the active metabolite 7-OH-CBD.	Cannabidiol	93-96	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	44-51
34330718-10	2021	Collectively, these data indicate that both CYP2C19 and CYP2C9 are important contributors in CBD metabolism to the active metabolite 7-OH-CBD.	Cannabidiol	93-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
34330718-11	2021	Significance Statement This study demonstrates that both CYP2C19 and CYP2C9 are involved in CBD metabolism to the active metabolite 7-OH-CBD, and CYP3A4 is a major contributor to CBD metabolism through pathways other than 7-hydroxylation.	Cannabidiol	92-95	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	57-64
34330718-11	2021	Significance Statement This study demonstrates that both CYP2C19 and CYP2C9 are involved in CBD metabolism to the active metabolite 7-OH-CBD, and CYP3A4 is a major contributor to CBD metabolism through pathways other than 7-hydroxylation.	Cannabidiol	92-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
34330718-11	2021	Significance Statement This study demonstrates that both CYP2C19 and CYP2C9 are involved in CBD metabolism to the active metabolite 7-OH-CBD, and CYP3A4 is a major contributor to CBD metabolism through pathways other than 7-hydroxylation.	Cannabidiol	179-182	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	146-152
34834189-4	2021	Here, we report the preparation of original super-macroporous cryogels from 2-hydroxyethyl cellulose (HEC) and beta-cyclodextrin (beta-CD) designed for the topical delivery of CBD.	Cannabidiol	176-179	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	130-137
34587731-4	2021	The blank control group was treated without any repair materials;the ADM group was treated with collagen patch for repair and the ADM loaded with CBD-VEGF group was treated with collagen patch loaded with VEGF for repair.	Cannabidiol	146-149	vascular endothelial growth factor A	Homo sapiens	150-154
34274349-0	2021	Cannabidiol effectively reverses mechanical and thermal allodynia, hyperalgesia, and anxious behaviors in a neuropathic pain model: Possible role of CB1 and TRPV1 receptors.	Cannabidiol	0-11	cannabinoid receptor 1	Rattus norvegicus	149-152
34274349-0	2021	Cannabidiol effectively reverses mechanical and thermal allodynia, hyperalgesia, and anxious behaviors in a neuropathic pain model: Possible role of CB1 and TRPV1 receptors.	Cannabidiol	0-11	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	157-162
34303725-7	2021	However, in the long term, only the CB1 blockade reverted CBD positive results.	Cannabidiol	58-61	cannabinoid receptor 1	Rattus norvegicus	36-39
34303725-9	2021	Five days after the lesion, CBD treatment preserved ~35 % of synapses in the ventral horn, and such effect was partially reversed by CB1 inactivation.	Cannabidiol	28-31	cannabinoid receptor 1	Rattus norvegicus	133-136
34681188-6	2021	A key role of PPARgamma in mediating the therapeutic potential of CBD was revealed, whereas upregulation of multiple transient receptor potential channels demasked CBD-induced heat hyperalgesia.	Cannabidiol	66-69	peroxisome proliferator activated receptor gamma	Homo sapiens	14-23
34491040-7	2021	Since CYP2D6 is an important brain and liver P450 and is known to be inhibited by CBD, we investigated the interactions of four important highly prevalent CYP2D6 polymorphisms with selected phytocannabinoids (CBD, THC, CBDV, THCV, CBN, CBG, CBC, beta-carophyllene) that are rapidly gaining popularity.	Cannabidiol	82-85	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	6-12
34576119-5	2021	While CBD alone did not have any major effects on keratinocytes, the UVB treatment activated the extrinsic apoptotic pathway, with enhanced caspase 8 expression in both healthy and psoriatic keratinocytes.	Cannabidiol	6-9	caspase 8	Homo sapiens	140-149
34630100-7	2021	CBD treatment inhibited macrophage recruitment and suppressed activation of NFkappaB-NLRP3-pyroptosis pathway in mice livers.	Cannabidiol	0-3	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	76-84
34630100-7	2021	CBD treatment inhibited macrophage recruitment and suppressed activation of NFkappaB-NLRP3-pyroptosis pathway in mice livers.	Cannabidiol	0-3	NLR family, pyrin domain containing 3	Mus musculus	85-90
34576262-10	2021	We reported the inhibition of topoisomerase II beta and alpha, cullin 1, V-type proton ATPase, and CDK-6 in CBD-treated MCF7 cells for the first time as additional cytotoxic mechanisms of CBD, alongside sabotaged energy production and reduced mitochondrial translation.	Cannabidiol	108-111	DNA topoisomerase II beta	Homo sapiens	30-61
34576262-10	2021	We reported the inhibition of topoisomerase II beta and alpha, cullin 1, V-type proton ATPase, and CDK-6 in CBD-treated MCF7 cells for the first time as additional cytotoxic mechanisms of CBD, alongside sabotaged energy production and reduced mitochondrial translation.	Cannabidiol	108-111	cullin 1	Homo sapiens	63-71
34576262-10	2021	We reported the inhibition of topoisomerase II beta and alpha, cullin 1, V-type proton ATPase, and CDK-6 in CBD-treated MCF7 cells for the first time as additional cytotoxic mechanisms of CBD, alongside sabotaged energy production and reduced mitochondrial translation.	Cannabidiol	108-111	cyclin dependent kinase 6	Homo sapiens	99-104
34576262-10	2021	We reported the inhibition of topoisomerase II beta and alpha, cullin 1, V-type proton ATPase, and CDK-6 in CBD-treated MCF7 cells for the first time as additional cytotoxic mechanisms of CBD, alongside sabotaged energy production and reduced mitochondrial translation.	Cannabidiol	188-191	DNA topoisomerase II beta	Homo sapiens	30-61
34576262-10	2021	We reported the inhibition of topoisomerase II beta and alpha, cullin 1, V-type proton ATPase, and CDK-6 in CBD-treated MCF7 cells for the first time as additional cytotoxic mechanisms of CBD, alongside sabotaged energy production and reduced mitochondrial translation.	Cannabidiol	188-191	cullin 1	Homo sapiens	63-71
34576262-10	2021	We reported the inhibition of topoisomerase II beta and alpha, cullin 1, V-type proton ATPase, and CDK-6 in CBD-treated MCF7 cells for the first time as additional cytotoxic mechanisms of CBD, alongside sabotaged energy production and reduced mitochondrial translation.	Cannabidiol	188-191	cyclin dependent kinase 6	Homo sapiens	99-104
34576212-6	2021	Moreover, experimental studies on the effects of cannabidiol (plant-derived, non-psychoactive cannabinoid) in animal PH models have shown that cannabidiol reduces right ventricular systolic pressure and excessive remodelling and decreases pulmonary vascular hypertrophy and pulmonary vascular resistance.	Cannabidiol	49-60	phenylalanine hydroxylase	Homo sapiens	117-119
34576212-6	2021	Moreover, experimental studies on the effects of cannabidiol (plant-derived, non-psychoactive cannabinoid) in animal PH models have shown that cannabidiol reduces right ventricular systolic pressure and excessive remodelling and decreases pulmonary vascular hypertrophy and pulmonary vascular resistance.	Cannabidiol	143-154	phenylalanine hydroxylase	Homo sapiens	117-119
34576119-8	2021	Application of CBD partially attenuated these effects of UVB irradiation both in healthy and psoriatic keratinocytes, reducing the levels of 15-d-PGJ2, p-p38 and caspase 8 while increasing Bcl2 expression.	Cannabidiol	15-18	mitogen-activated protein kinase 14	Homo sapiens	154-157
34576119-8	2021	Application of CBD partially attenuated these effects of UVB irradiation both in healthy and psoriatic keratinocytes, reducing the levels of 15-d-PGJ2, p-p38 and caspase 8 while increasing Bcl2 expression.	Cannabidiol	15-18	caspase 8	Homo sapiens	162-171
34576119-8	2021	Application of CBD partially attenuated these effects of UVB irradiation both in healthy and psoriatic keratinocytes, reducing the levels of 15-d-PGJ2, p-p38 and caspase 8 while increasing Bcl2 expression.	Cannabidiol	15-18	BCL2 apoptosis regulator	Homo sapiens	189-193
34573232-8	2021	Particularly, the noncannabinoid receptor, peroxisome proliferator-activated receptor gamma, has been suggested to be involved in multiple functions of CBD.	Cannabidiol	152-155	peroxisome proliferator activated receptor gamma	Mus musculus	43-91
34500787-2	2021	In addition to their other pharmacological targets, both THC and CBD are competitive inhibitors of the equilibrative nucleoside transporter-1 (ENT-1), a primary inactivation mechanism for adenosine, and thereby increase adenosine signaling.	Cannabidiol	65-68	solute carrier family 29 (nucleoside transporters), member 1	Mus musculus	103-141
34564578-5	2021	We observed a reduction in IL-6 and TNF-alpha production from the group treated with CBD, but non-altered IL-10 levels.	Cannabidiol	85-88	interleukin 6	Canis lupus familiaris	27-31
34564578-5	2021	We observed a reduction in IL-6 and TNF-alpha production from the group treated with CBD, but non-altered IL-10 levels.	Cannabidiol	85-88	tumor necrosis factor	Canis lupus familiaris	36-45
34500787-2	2021	In addition to their other pharmacological targets, both THC and CBD are competitive inhibitors of the equilibrative nucleoside transporter-1 (ENT-1), a primary inactivation mechanism for adenosine, and thereby increase adenosine signaling.	Cannabidiol	65-68	solute carrier family 29 (nucleoside transporters), member 1	Mus musculus	143-148
34500787-3	2021	The goal of this study was to examine the role of adenosine A2A receptor activation in the effects of intraperitoneally administered THC alone and in combination with CBD or PECS-101, a 4"-fluorinated derivative of CBD, in the cannabinoid tetrad, elevated plus maze (EPM) and marble bury assays.	Cannabidiol	215-218	adenosine A2a receptor	Mus musculus	50-72
34126352-10	2021	Moreover, CBD restores the PLAE-induced increased levels of TNFalpha and IL-6 in the hippocampus.	Cannabidiol	10-13	tumor necrosis factor	Mus musculus	60-68
34572327-2	2021	We investigated the binding kinetics of CBD to Nav1.4 channels on the muscle membrane.	Cannabidiol	40-43	sodium voltage-gated channel alpha subunit 4	Homo sapiens	47-53
34572327-4	2021	The CDOCKER program was employed to model CBD docking onto the Nav1.4 channel to determine its binding sites.	Cannabidiol	42-45	sodium voltage-gated channel alpha subunit 4	Homo sapiens	63-69
34572327-8	2021	Five proposed CBD binding sites in a bundle crossing region of the Nav1.4 channels pore was identified as Val793, Leu794, Phe797, and Cys759 in domain I/S6, and Ile1279 in domain II/S6.	Cannabidiol	14-17	sodium voltage-gated channel alpha subunit 4	Homo sapiens	67-73
34572327-9	2021	Our findings imply that CBD favorably binds to the Nav1.4 channel in its slow-inactivated state.	Cannabidiol	24-27	sodium voltage-gated channel alpha subunit 4	Homo sapiens	51-57
34126352-10	2021	Moreover, CBD restores the PLAE-induced increased levels of TNFalpha and IL-6 in the hippocampus.	Cannabidiol	10-13	interleukin 6	Mus musculus	73-77
34192579-0	2021	Cannabidiol in the prelimbic cortex modulates the comorbid condition between the chronic neuropathic pain and depression-like behaviour in rats: The role of medial prefrontal cortex 5-HT1A and CB1 receptors.	Cannabidiol	0-11	5-hydroxytryptamine receptor 1A	Rattus norvegicus	182-188
34192579-0	2021	Cannabidiol in the prelimbic cortex modulates the comorbid condition between the chronic neuropathic pain and depression-like behaviour in rats: The role of medial prefrontal cortex 5-HT1A and CB1 receptors.	Cannabidiol	0-11	cannabinoid receptor 1	Rattus norvegicus	193-196
34265088-1	2021	OBJECTIVE: We conducted a post hoc analysis of two randomized controlled trials, GWPCARE1 (NCT02091375) and GWPCARE2 (NCT02224703), to estimate the time to onset of cannabidiol (CBD) treatment effects (seizure reduction and adverse events (AEs)) in patients with Dravet syndrome (DS).	Cannabidiol	165-176	opsin 1, medium wave sensitive	Homo sapiens	178-181
34121064-8	2021	However, CBD significantly inhibited CYP3A4 and CYP2C19-mediated metabolism of citalopram and its stereoisomer escitalopram at physiologically relevant concentrations, suggesting a possible in vivo DDI.	Cannabidiol	9-12	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	37-43
34121064-8	2021	However, CBD significantly inhibited CYP3A4 and CYP2C19-mediated metabolism of citalopram and its stereoisomer escitalopram at physiologically relevant concentrations, suggesting a possible in vivo DDI.	Cannabidiol	9-12	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	48-55
34577578-0	2021	Cannabidiol Application Increases Cutaneous Aquaporin-3 and Exerts a Skin Moisturizing Effect.	Cannabidiol	0-11	aquaporin 3	Mus musculus	44-55
34577578-7	2021	However, only aquaporin-3 (AQP3), a member of the aquaporin family, showed significantly higher levels in the CBD-treated group than in the control group at both the mRNA and protein levels.	Cannabidiol	110-113	aquaporin 3	Mus musculus	14-25
34577578-7	2021	However, only aquaporin-3 (AQP3), a member of the aquaporin family, showed significantly higher levels in the CBD-treated group than in the control group at both the mRNA and protein levels.	Cannabidiol	110-113	aquaporin 3	Mus musculus	27-31
34281647-13	2021	CBD at 4 microg/mL significantly reduced production of IFN-gamma and TNF-alpha (P < .05).	Cannabidiol	0-3	interferon gamma	Equus caballus	55-64
34445394-0	2021	Tamoxifen Sensitizes Acute Lymphoblastic Leukemia Cells to Cannabidiol by Targeting Cyclophilin-D and Altering Mitochondrial Ca2+ Homeostasis.	Cannabidiol	59-70	peptidylprolyl isomerase D	Homo sapiens	84-97
34281647-13	2021	CBD at 4 microg/mL significantly reduced production of IFN-gamma and TNF-alpha (P < .05).	Cannabidiol	0-3	tumor necrosis factor	Equus caballus	69-78
34176244-0	2021	Cannabidiol-mediated RISK PI3K/AKT and MAPK/ERK pathways decreasing reperfusion myocardial damage.	Cannabidiol	0-11	AKT serine/threonine kinase 1	Rattus norvegicus	31-34
34143376-6	2021	According to our findings, repeated ICV administration of CBD improved cell proliferation and neurogenesis and increased the number of Ki-67 and DCX-positive cells in the abstinence period.	Cannabidiol	58-61	doublecortin	Rattus norvegicus	145-148
34176244-0	2021	Cannabidiol-mediated RISK PI3K/AKT and MAPK/ERK pathways decreasing reperfusion myocardial damage.	Cannabidiol	0-11	Eph receptor B1	Rattus norvegicus	44-47
34131037-0	2021	Cannabidiol inhibition of murine primary nociceptors: Tight binding to slow inactivated states of Nav1.8 channels.	Cannabidiol	0-11	sodium channel, voltage-gated, type X, alpha	Mus musculus	98-104
34131037-9	2021	We conclude that CBD might produce some of its analgesic effects by direct effects on neuronal excitability, with tight binding to the slow inactivated state of Nav1.8 channels contributing to effective inhibition of repetitive firing by modest depolarizations.Significance Statement:Cannabidiol has been shown to inhibit pain in various rodent models but the mechanism of this effect is unknown.	Cannabidiol	17-20	sodium channel, voltage-gated, type X, alpha	Mus musculus	161-167
34131037-9	2021	We conclude that CBD might produce some of its analgesic effects by direct effects on neuronal excitability, with tight binding to the slow inactivated state of Nav1.8 channels contributing to effective inhibition of repetitive firing by modest depolarizations.Significance Statement:Cannabidiol has been shown to inhibit pain in various rodent models but the mechanism of this effect is unknown.	Cannabidiol	284-295	sodium channel, voltage-gated, type X, alpha	Mus musculus	161-167
34131037-12	2021	The results suggest that CBD can exert analgesic effects in part by directly inhibiting repetitive firing of primary nociceptors and suggest a strategy of identifying compounds that bind selectively to slow inactivated states of Nav1.8 channels for developing effective analgesics.	Cannabidiol	25-28	sodium channel, voltage-gated, type X, alpha	Mus musculus	229-235
34439405-7	2021	As a consequence of reductions in phospholipase A2 and cyclooxygenases activity following UV irradiation, CBD upregulates the level of 2-arachidonoylglycerol and downregulates prostaglandin E2 and leukotriene B4.	Cannabidiol	106-109	phospholipase A2 group IB	Rattus norvegicus	34-50
34349839-8	2021	Highly purified cannabidiol, recently approved in the US as Epidiolex  for TSC-associated seizures in patients >=1 years of age, and the KD, may also participate in the regulation of the mTOR pathway.	Cannabidiol	16-27	TSC complex subunit 1	Homo sapiens	75-78
34349839-8	2021	Highly purified cannabidiol, recently approved in the US as Epidiolex  for TSC-associated seizures in patients >=1 years of age, and the KD, may also participate in the regulation of the mTOR pathway.	Cannabidiol	16-27	mechanistic target of rapamycin kinase	Homo sapiens	187-191
34249397-9	2021	However, CBD treatment has no changes in gene expression including beta-catenin, but the decreased beta-catenin expression by testosterone or PMA was restored by CBD pretreatment, suggesting that potential regulatory effect on alopecia induction of testosterone and PMA.	Cannabidiol	9-12	catenin beta 1	Homo sapiens	99-111
34249397-9	2021	However, CBD treatment has no changes in gene expression including beta-catenin, but the decreased beta-catenin expression by testosterone or PMA was restored by CBD pretreatment, suggesting that potential regulatory effect on alopecia induction of testosterone and PMA.	Cannabidiol	162-165	catenin beta 1	Homo sapiens	99-111
34182795-0	2021	Perinatal CBD or THC Exposure Results in Lasting Resistance to Fluoxetine in the Forced Swim Test: Reversal by Fatty Acid Amide Hydrolase Inhibition.	Cannabidiol	10-13	fatty acid amide hydrolase	Mus musculus	122-137
34262461-10	2021	Gene expression analyses revealed a long-term increase of corticotropin releasing factor (Crf) that was significantly normalized with the combination CBD plus STR.	Cannabidiol	150-153	corticotropin releasing hormone	Mus musculus	58-88
34262461-12	2021	Interestingly, CBD and STR alone or combined induced a significant and marked increase of Slc6a4 gene expression.	Cannabidiol	15-18	solute carrier family 6 (neurotransmitter transporter, serotonin), member 4	Mus musculus	90-96
34079465-2	2021	Although the mechanism of anticonvulsant action of cannabidiol is unknown, emerging data suggests involvement of the transient receptor potential cation channel subfamily V member 1 (Trpv1).	Cannabidiol	51-62	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	183-188
34249397-0	2021	Regulatory Effect of Cannabidiol (CBD) on Decreased beta-Catenin Expression in Alopecia Models by Testosterone and PMA Treatment in Dermal Papilla Cells.	Cannabidiol	21-32	catenin beta 1	Homo sapiens	52-64
34249397-0	2021	Regulatory Effect of Cannabidiol (CBD) on Decreased beta-Catenin Expression in Alopecia Models by Testosterone and PMA Treatment in Dermal Papilla Cells.	Cannabidiol	34-37	catenin beta 1	Homo sapiens	52-64
34189291-0	2021	Characterisation of inverse agonism of the orphan-G protein-coupled receptor GPR52 by cannabinoid ligands Cannabidiol and O-1918.	Cannabidiol	106-117	G protein-coupled receptor 52	Homo sapiens	77-82
34189291-1	2021	The identification of cannabinoid ligands Cannabidiol and O-1918 as inverse agonists of the orphan receptor GPR52 is reported.	Cannabidiol	42-53	G protein-coupled receptor 52	Homo sapiens	108-113
34063802-3	2021	It was shown that CBD penetrated the blood and in UVB-irradiated rats was preferentially located in the membranes of polymorphonuclear leukocytes, which promoted reduction of ROS generation and up-regulation of antioxidant ability by increasing the activity of glutathione reductase and thioredoxin reductase, while the level of reduced glutathione decreased by UV radiation.	Cannabidiol	18-21	glutathione-disulfide reductase	Rattus norvegicus	261-282
34063802-3	2021	It was shown that CBD penetrated the blood and in UVB-irradiated rats was preferentially located in the membranes of polymorphonuclear leukocytes, which promoted reduction of ROS generation and up-regulation of antioxidant ability by increasing the activity of glutathione reductase and thioredoxin reductase, while the level of reduced glutathione decreased by UV radiation.	Cannabidiol	18-21	peroxiredoxin 5	Rattus norvegicus	287-308
34658452-1	2021	(-)-Cannabidiol ((-)-CBD) has recently gained prominence as a treatment for neuro-inflammation and other neurodegenerative disorders; interest is also developing in its synthetic enantiomer, (+)-CBD, which has a higher affinity to CB1 / CB2 receptors than the natural stereoisomer.	Cannabidiol	0-15	cannabinoid receptor 1	Homo sapiens	231-234
34658452-1	2021	(-)-Cannabidiol ((-)-CBD) has recently gained prominence as a treatment for neuro-inflammation and other neurodegenerative disorders; interest is also developing in its synthetic enantiomer, (+)-CBD, which has a higher affinity to CB1 / CB2 receptors than the natural stereoisomer.	Cannabidiol	0-15	cannabinoid receptor 2	Homo sapiens	237-240
34658452-1	2021	(-)-Cannabidiol ((-)-CBD) has recently gained prominence as a treatment for neuro-inflammation and other neurodegenerative disorders; interest is also developing in its synthetic enantiomer, (+)-CBD, which has a higher affinity to CB1 / CB2 receptors than the natural stereoisomer.	Cannabidiol	17-24	cannabinoid receptor 1	Homo sapiens	231-234
34658452-1	2021	(-)-Cannabidiol ((-)-CBD) has recently gained prominence as a treatment for neuro-inflammation and other neurodegenerative disorders; interest is also developing in its synthetic enantiomer, (+)-CBD, which has a higher affinity to CB1 / CB2 receptors than the natural stereoisomer.	Cannabidiol	17-24	cannabinoid receptor 2	Homo sapiens	237-240
35568225-0	2022	Effect of cannabidiol on apoptosis and cellular interferon and interferon-stimulated gene responses to the SARS-CoV-2 genes ORF8, ORF10 and M protein.	Cannabidiol	10-21	ORF8 protein	Severe acute respiratory syndrome coronavirus 2	124-128
35568225-0	2022	Effect of cannabidiol on apoptosis and cellular interferon and interferon-stimulated gene responses to the SARS-CoV-2 genes ORF8, ORF10 and M protein.	Cannabidiol	10-21	ORF10 protein	Severe acute respiratory syndrome coronavirus 2	130-135
35568225-0	2022	Effect of cannabidiol on apoptosis and cellular interferon and interferon-stimulated gene responses to the SARS-CoV-2 genes ORF8, ORF10 and M protein.	Cannabidiol	10-21	membrane glycoprotein	Severe acute respiratory syndrome coronavirus 2	140-141
35568225-1	2022	AIMS: To study effects on cellular innate immune responses to ORF8, ORF10, and Membrane protein (M protein) from the Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes COVID-19, in combination with cannabidiol (CBD).	Cannabidiol	220-231	ORF8 protein	Severe acute respiratory syndrome coronavirus 2	62-66
35568225-1	2022	AIMS: To study effects on cellular innate immune responses to ORF8, ORF10, and Membrane protein (M protein) from the Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes COVID-19, in combination with cannabidiol (CBD).	Cannabidiol	220-231	membrane glycoprotein	Severe acute respiratory syndrome coronavirus 2	97-98
35568225-1	2022	AIMS: To study effects on cellular innate immune responses to ORF8, ORF10, and Membrane protein (M protein) from the Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes COVID-19, in combination with cannabidiol (CBD).	Cannabidiol	233-236	ORF8 protein	Severe acute respiratory syndrome coronavirus 2	62-66
35568225-1	2022	AIMS: To study effects on cellular innate immune responses to ORF8, ORF10, and Membrane protein (M protein) from the Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes COVID-19, in combination with cannabidiol (CBD).	Cannabidiol	233-236	membrane glycoprotein	Severe acute respiratory syndrome coronavirus 2	97-98
35462234-5	2022	Cannabidiol and cannabinol exhibited potent inhibitory activities (IC50 = 4.8 and 6.27 muM, respectively) towards the TET1 protein, whereas cannabigerol had no effect on the enzyme activity.	Cannabidiol	0-11	tet methylcytosine dioxygenase 1	Homo sapiens	118-122
35605018-11	2022	Achievable free CBD plasma concentrations ~100 nM can interact predominantly with high-affinity CBD targets, for example, TRPA1 and TRPM8 membrane channels that are abundantly expressed in pathological conditions.	Cannabidiol	16-19	transient receptor potential cation channel subfamily A member 1	Homo sapiens	122-127
34069407-3	2021	In recent decades, evidence has indicated a role for CBD in the modulation of mitochondrial processes, including respiration and bioenergetics, mitochondrial DNA epigenetics, intrinsic apoptosis, the regulation of mitochondrial and intracellular calcium concentrations, mitochondrial fission, fusion and biogenesis, and mitochondrial ferritin concentration and mitochondrial monoamine oxidase activity regulation.	Cannabidiol	53-56	ferritin mitochondrial	Homo sapiens	320-342
35398615-0	2022	Characterization of molecular interactions between cannabidiol and human plasma proteins (serum albumin and gamma-globulin) by surface plasmon resonance, microcalorimetry, and molecular docking.	Cannabidiol	51-62	albumin	Homo sapiens	90-103
35605018-11	2022	Achievable free CBD plasma concentrations ~100 nM can interact predominantly with high-affinity CBD targets, for example, TRPA1 and TRPM8 membrane channels that are abundantly expressed in pathological conditions.	Cannabidiol	16-19	transient receptor potential cation channel subfamily M member 8	Homo sapiens	132-137
35605018-11	2022	Achievable free CBD plasma concentrations ~100 nM can interact predominantly with high-affinity CBD targets, for example, TRPA1 and TRPM8 membrane channels that are abundantly expressed in pathological conditions.	Cannabidiol	96-99	transient receptor potential cation channel subfamily A member 1	Homo sapiens	122-127
35605018-11	2022	Achievable free CBD plasma concentrations ~100 nM can interact predominantly with high-affinity CBD targets, for example, TRPA1 and TRPM8 membrane channels that are abundantly expressed in pathological conditions.	Cannabidiol	96-99	transient receptor potential cation channel subfamily M member 8	Homo sapiens	132-137
35605606-5	2022	In vitro and in vivo genetic and pharmacologic (cannabidiol (CBD)) inhibition of ID1 on DMG tumor growth was assessed.	Cannabidiol	48-59	inhibitor of DNA binding 1, HLH protein	Homo sapiens	81-84
35605606-5	2022	In vitro and in vivo genetic and pharmacologic (cannabidiol (CBD)) inhibition of ID1 on DMG tumor growth was assessed.	Cannabidiol	61-64	inhibitor of DNA binding 1, HLH protein	Homo sapiens	81-84
35605606-13	2022	CONCLUSIONS: H3K27M-mediated re-activation of ID1 in DMG results in a SPARCL1+ migratory transcriptional program that is therapeutically targetable with CBD.	Cannabidiol	153-156	inhibitor of DNA binding 1, HLH protein	Homo sapiens	46-49
35605606-13	2022	CONCLUSIONS: H3K27M-mediated re-activation of ID1 in DMG results in a SPARCL1+ migratory transcriptional program that is therapeutically targetable with CBD.	Cannabidiol	153-156	SPARC like 1	Homo sapiens	70-77
35630804-6	2022	Administration of CBD increased TAC and GSH concentrations, glutathione reductase (GSR) activity, and decreased CB1-Rs expression and levels of inflammatory mediators such as TNF-alpha, IL -1beta, NF-kappaB, MCP-1 and CD68.	Cannabidiol	18-21	glutathione-disulfide reductase	Rattus norvegicus	60-81
35630804-6	2022	Administration of CBD increased TAC and GSH concentrations, glutathione reductase (GSR) activity, and decreased CB1-Rs expression and levels of inflammatory mediators such as TNF-alpha, IL -1beta, NF-kappaB, MCP-1 and CD68.	Cannabidiol	18-21	cannabinoid receptor 1	Rattus norvegicus	112-115
35630804-6	2022	Administration of CBD increased TAC and GSH concentrations, glutathione reductase (GSR) activity, and decreased CB1-Rs expression and levels of inflammatory mediators such as TNF-alpha, IL -1beta, NF-kappaB, MCP-1 and CD68.	Cannabidiol	18-21	tumor necrosis factor	Rattus norvegicus	175-184
35630804-6	2022	Administration of CBD increased TAC and GSH concentrations, glutathione reductase (GSR) activity, and decreased CB1-Rs expression and levels of inflammatory mediators such as TNF-alpha, IL -1beta, NF-kappaB, MCP-1 and CD68.	Cannabidiol	18-21	interleukin 1 alpha	Rattus norvegicus	186-195
35630804-6	2022	Administration of CBD increased TAC and GSH concentrations, glutathione reductase (GSR) activity, and decreased CB1-Rs expression and levels of inflammatory mediators such as TNF-alpha, IL -1beta, NF-kappaB, MCP-1 and CD68.	Cannabidiol	18-21	C-C motif chemokine ligand 2	Rattus norvegicus	208-213
35631293-9	2022	CBD did not influence food induced thermogenesis but did favorably modify early insulin and triglyceride responses.	Cannabidiol	0-3	insulin	Homo sapiens	80-87
35598400-0	2022	Cannabidiol exerts anti-proliferative activity via a cannabinoid receptor 2-dependent mechanism in human colorectal cancer cells.	Cannabidiol	0-11	cannabinoid receptor 2	Homo sapiens	53-75
35598400-5	2022	CBD treatment led to G1-phase cell cycle arrest and an increased sub-G1 population (apoptotic cells); it also downregulated protein expression of cyclin D1, cyclin D3, cyclin-dependent kinase 2 (CDK2), CDK4, and CDK6.	Cannabidiol	0-3	cyclin D1	Homo sapiens	146-155
35598400-5	2022	CBD treatment led to G1-phase cell cycle arrest and an increased sub-G1 population (apoptotic cells); it also downregulated protein expression of cyclin D1, cyclin D3, cyclin-dependent kinase 2 (CDK2), CDK4, and CDK6.	Cannabidiol	0-3	cyclin D3	Homo sapiens	157-166
35598400-5	2022	CBD treatment led to G1-phase cell cycle arrest and an increased sub-G1 population (apoptotic cells); it also downregulated protein expression of cyclin D1, cyclin D3, cyclin-dependent kinase 2 (CDK2), CDK4, and CDK6.	Cannabidiol	0-3	cyclin dependent kinase 2	Homo sapiens	168-193
35598400-5	2022	CBD treatment led to G1-phase cell cycle arrest and an increased sub-G1 population (apoptotic cells); it also downregulated protein expression of cyclin D1, cyclin D3, cyclin-dependent kinase 2 (CDK2), CDK4, and CDK6.	Cannabidiol	0-3	cyclin dependent kinase 2	Homo sapiens	195-199
35598400-5	2022	CBD treatment led to G1-phase cell cycle arrest and an increased sub-G1 population (apoptotic cells); it also downregulated protein expression of cyclin D1, cyclin D3, cyclin-dependent kinase 2 (CDK2), CDK4, and CDK6.	Cannabidiol	0-3	cyclin dependent kinase 4	Homo sapiens	202-206
35598400-5	2022	CBD treatment led to G1-phase cell cycle arrest and an increased sub-G1 population (apoptotic cells); it also downregulated protein expression of cyclin D1, cyclin D3, cyclin-dependent kinase 2 (CDK2), CDK4, and CDK6.	Cannabidiol	0-3	cyclin dependent kinase 6	Homo sapiens	212-216
35628181-3	2022	A high-affinity agonist of TRPV2 named cannabidiol is one of the candidate drugs for AD.	Cannabidiol	39-50	transient receptor potential cation channel, subfamily V, member 2	Mus musculus	27-32
35628181-5	2022	The present study investigated whether cannabidiol enhances the phagocytosis and clearance of microglial Abeta via the TRPV2 channel.	Cannabidiol	39-50	amyloid beta (A4) precursor protein	Mus musculus	105-110
35628181-8	2022	Cannabidiol enhanced microglial amyloid-beta phagocytosis through TRPV2 activation, which increased the mRNA expression of the phagocytosis-related receptors, but knockdown of TRPV2 or Trem2 rescued the expression.	Cannabidiol	0-11	transient receptor potential cation channel subfamily V member 2	Homo sapiens	66-71
35628181-8	2022	Cannabidiol enhanced microglial amyloid-beta phagocytosis through TRPV2 activation, which increased the mRNA expression of the phagocytosis-related receptors, but knockdown of TRPV2 or Trem2 rescued the expression.	Cannabidiol	0-11	transient receptor potential cation channel subfamily V member 2	Homo sapiens	176-181
35628181-8	2022	Cannabidiol enhanced microglial amyloid-beta phagocytosis through TRPV2 activation, which increased the mRNA expression of the phagocytosis-related receptors, but knockdown of TRPV2 or Trem2 rescued the expression.	Cannabidiol	0-11	triggering receptor expressed on myeloid cells 2	Mus musculus	185-190
35628181-10	2022	Furthermore, cannabidiol treatment successfully attenuated neuroinflammation while simultaneously improving mitochondrial function and ATP production via TRPV2 activation.	Cannabidiol	13-24	transient receptor potential cation channel subfamily V member 2	Homo sapiens	154-159
35537858-1	2022	BACKGROUND: Cannabidiol (CBD), a CBR2 agonist with limited psychic effects, antagonizes CB1/CB2 receptors.	Cannabidiol	12-23	cannabinoid receptor 1	Homo sapiens	88-91
35537858-1	2022	BACKGROUND: Cannabidiol (CBD), a CBR2 agonist with limited psychic effects, antagonizes CB1/CB2 receptors.	Cannabidiol	12-23	cannabinoid receptor 2	Homo sapiens	92-95
35537858-1	2022	BACKGROUND: Cannabidiol (CBD), a CBR2 agonist with limited psychic effects, antagonizes CB1/CB2 receptors.	Cannabidiol	25-28	cannabinoid receptor 1	Homo sapiens	88-91
35537858-1	2022	BACKGROUND: Cannabidiol (CBD), a CBR2 agonist with limited psychic effects, antagonizes CB1/CB2 receptors.	Cannabidiol	25-28	cannabinoid receptor 2	Homo sapiens	92-95
35537858-12	2022	CBD treatment-by-gene interactions suggest potential benefit for postprandial distress with CNR1 rs806378 T allele.	Cannabidiol	0-3	cannabinoid receptor 1	Homo sapiens	92-96
35524041-0	2022	Inhibition of human androgen receptor by delta 9-tetrahydro-cannabinol and cannabidiol related to reproductive dysfunction: A computational study.	Cannabidiol	75-86	androgen receptor	Homo sapiens	20-37
35524041-2	2022	Hence this study was aimed to ascertain the impact of tetrahydrocannabinol (THC) and cannabidiol (CBD) binding affinity on human androgen receptor (AR) via computational molecular dynamic simulation.	Cannabidiol	85-96	androgen receptor	Homo sapiens	129-146
35524041-2	2022	Hence this study was aimed to ascertain the impact of tetrahydrocannabinol (THC) and cannabidiol (CBD) binding affinity on human androgen receptor (AR) via computational molecular dynamic simulation.	Cannabidiol	85-96	androgen receptor	Homo sapiens	148-150
35524041-2	2022	Hence this study was aimed to ascertain the impact of tetrahydrocannabinol (THC) and cannabidiol (CBD) binding affinity on human androgen receptor (AR) via computational molecular dynamic simulation.	Cannabidiol	98-101	androgen receptor	Homo sapiens	129-146
35524041-2	2022	Hence this study was aimed to ascertain the impact of tetrahydrocannabinol (THC) and cannabidiol (CBD) binding affinity on human androgen receptor (AR) via computational molecular dynamic simulation.	Cannabidiol	98-101	androgen receptor	Homo sapiens	148-150
35524041-8	2022	Despite the diversity within the chemical space, both CBD and THC poses bond flexibility required to bind avidly to AR with the docking scores comparable to R18.	Cannabidiol	54-57	androgen receptor	Homo sapiens	116-118
35524041-12	2022	This study hypothesized that CBD and THC binds complimentarily to the pocket AR, indicating a likely inhibition of reproductive function and prostate cancer progression.	Cannabidiol	29-32	androgen receptor	Homo sapiens	77-79
35512806-4	2022	Oral MPH undergoes extensive pre-systemic metabolism by carboxylesterase 1 (CES1), a hepatic enzyme which can be inhibited by two prominent cannabinoids,  9-tetrahydrocannabinol (THC) and cannabidiol (CBD).	Cannabidiol	188-199	carboxylesterase 1	Homo sapiens	56-74
35512806-4	2022	Oral MPH undergoes extensive pre-systemic metabolism by carboxylesterase 1 (CES1), a hepatic enzyme which can be inhibited by two prominent cannabinoids,  9-tetrahydrocannabinol (THC) and cannabidiol (CBD).	Cannabidiol	188-199	carboxylesterase 1	Homo sapiens	76-80
35512806-4	2022	Oral MPH undergoes extensive pre-systemic metabolism by carboxylesterase 1 (CES1), a hepatic enzyme which can be inhibited by two prominent cannabinoids,  9-tetrahydrocannabinol (THC) and cannabidiol (CBD).	Cannabidiol	201-204	carboxylesterase 1	Homo sapiens	56-74
35512806-4	2022	Oral MPH undergoes extensive pre-systemic metabolism by carboxylesterase 1 (CES1), a hepatic enzyme which can be inhibited by two prominent cannabinoids,  9-tetrahydrocannabinol (THC) and cannabidiol (CBD).	Cannabidiol	201-204	carboxylesterase 1	Homo sapiens	76-80
35535052-10	2022	To that extent, CBD and other cannabis constituents such as cannabis seeds were found to reduce inflammation and expression of inflammatory cytokines including TNF-alpha and IL-1beta when evaluated in acne-like conditions.	Cannabidiol	16-19	tumor necrosis factor	Homo sapiens	160-169
35535052-10	2022	To that extent, CBD and other cannabis constituents such as cannabis seeds were found to reduce inflammation and expression of inflammatory cytokines including TNF-alpha and IL-1beta when evaluated in acne-like conditions.	Cannabidiol	16-19	interleukin 1 alpha	Homo sapiens	174-182
35358799-6	2022	In silico studies revealed a strong molecular interaction of cannabidiol with adipose triglyceride lipase, hormone-sensitive lipase, and monoglyceride lipase.	Cannabidiol	61-72	lipase G, endothelial type	Rattus norvegicus	99-105
35358799-6	2022	In silico studies revealed a strong molecular interaction of cannabidiol with adipose triglyceride lipase, hormone-sensitive lipase, and monoglyceride lipase.	Cannabidiol	61-72	lipase E, hormone sensitive type	Rattus norvegicus	107-131
35358799-6	2022	In silico studies revealed a strong molecular interaction of cannabidiol with adipose triglyceride lipase, hormone-sensitive lipase, and monoglyceride lipase.	Cannabidiol	61-72	monoglyceride lipase	Rattus norvegicus	137-157
34997862-12	2022	However, DRD1 agonist SKF81297 (10 muM) induced DA release and protein change in vitro, which was also blocked by CBD (1 muM) pretreatment.	Cannabidiol	114-117	dopamine receptor D1	Rattus norvegicus	9-13
34997862-13	2022	METH (2 mg/kg) significantly increased the DA level in the nucleus accumbens (NAc) of rats with activation of the DRD1-MeCP2-BDNF-TrkB signaling pathway, but these changes were blocked by CBD (40 or 80 mg/kg) pretreatment.	Cannabidiol	188-191	dopamine receptor D1	Rattus norvegicus	114-118
34997862-13	2022	METH (2 mg/kg) significantly increased the DA level in the nucleus accumbens (NAc) of rats with activation of the DRD1-MeCP2-BDNF-TrkB signaling pathway, but these changes were blocked by CBD (40 or 80 mg/kg) pretreatment.	Cannabidiol	188-191	methyl CpG binding protein 2	Rattus norvegicus	119-124
34997862-13	2022	METH (2 mg/kg) significantly increased the DA level in the nucleus accumbens (NAc) of rats with activation of the DRD1-MeCP2-BDNF-TrkB signaling pathway, but these changes were blocked by CBD (40 or 80 mg/kg) pretreatment.	Cannabidiol	188-191	brain-derived neurotrophic factor	Rattus norvegicus	125-129
34997862-13	2022	METH (2 mg/kg) significantly increased the DA level in the nucleus accumbens (NAc) of rats with activation of the DRD1-MeCP2-BDNF-TrkB signaling pathway, but these changes were blocked by CBD (40 or 80 mg/kg) pretreatment.	Cannabidiol	188-191	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	130-134
35484159-4	2022	Additionally, electrophysiological experiments show that the combination of 2-APB and cannabidiol has a synergetic effect on TRPV2 activation, and cryo-EM structures demonstrate that both drugs were able to bind simultaneously.	Cannabidiol	86-97	transient receptor potential cation channel, subfamily V, member 2	Rattus norvegicus	125-130
35445360-10	2022	Further investigation demonstrated that CBD-induced lifespan extension and increased neuronal health require sir-2.1/SIRT1.	Cannabidiol	40-43	Deacetylase sirtuin-type domain-containing protein;NAD-dependent protein deacetylase sir-2.1	Caenorhabditis elegans	109-116
34997862-0	2022	Cannabidiol inhibits methamphetamine-induced dopamine release via modulation of the DRD1-MeCP2-BDNF-TrkB signaling pathway.	Cannabidiol	0-11	dopamine receptor D1	Rattus norvegicus	84-88
34997862-0	2022	Cannabidiol inhibits methamphetamine-induced dopamine release via modulation of the DRD1-MeCP2-BDNF-TrkB signaling pathway.	Cannabidiol	0-11	methyl CpG binding protein 2	Rattus norvegicus	89-94
34997862-0	2022	Cannabidiol inhibits methamphetamine-induced dopamine release via modulation of the DRD1-MeCP2-BDNF-TrkB signaling pathway.	Cannabidiol	0-11	brain-derived neurotrophic factor	Rattus norvegicus	95-99
34997862-0	2022	Cannabidiol inhibits methamphetamine-induced dopamine release via modulation of the DRD1-MeCP2-BDNF-TrkB signaling pathway.	Cannabidiol	0-11	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	100-104
34997862-8	2022	Investigating the intervention effects of CBD on the DRD1-MeCP2-BDNF-TrkB signaling pathway could help clarify the underlying mechanisms and therapeutic potential of CBD in METH-related disorders.	Cannabidiol	42-45	dopamine receptor D1	Rattus norvegicus	53-57
34997862-8	2022	Investigating the intervention effects of CBD on the DRD1-MeCP2-BDNF-TrkB signaling pathway could help clarify the underlying mechanisms and therapeutic potential of CBD in METH-related disorders.	Cannabidiol	42-45	methyl CpG binding protein 2	Rattus norvegicus	58-63
34997862-8	2022	Investigating the intervention effects of CBD on the DRD1-MeCP2-BDNF-TrkB signaling pathway could help clarify the underlying mechanisms and therapeutic potential of CBD in METH-related disorders.	Cannabidiol	42-45	brain-derived neurotrophic factor	Rattus norvegicus	64-68
34997862-8	2022	Investigating the intervention effects of CBD on the DRD1-MeCP2-BDNF-TrkB signaling pathway could help clarify the underlying mechanisms and therapeutic potential of CBD in METH-related disorders.	Cannabidiol	42-45	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	69-73
34997862-8	2022	Investigating the intervention effects of CBD on the DRD1-MeCP2-BDNF-TrkB signaling pathway could help clarify the underlying mechanisms and therapeutic potential of CBD in METH-related disorders.	Cannabidiol	166-169	dopamine receptor D1	Rattus norvegicus	53-57
34997862-8	2022	Investigating the intervention effects of CBD on the DRD1-MeCP2-BDNF-TrkB signaling pathway could help clarify the underlying mechanisms and therapeutic potential of CBD in METH-related disorders.	Cannabidiol	166-169	methyl CpG binding protein 2	Rattus norvegicus	58-63
34997862-8	2022	Investigating the intervention effects of CBD on the DRD1-MeCP2-BDNF-TrkB signaling pathway could help clarify the underlying mechanisms and therapeutic potential of CBD in METH-related disorders.	Cannabidiol	166-169	brain-derived neurotrophic factor	Rattus norvegicus	64-68
34997862-8	2022	Investigating the intervention effects of CBD on the DRD1-MeCP2-BDNF-TrkB signaling pathway could help clarify the underlying mechanisms and therapeutic potential of CBD in METH-related disorders.	Cannabidiol	166-169	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	69-73
34997862-10	2022	METH (400 muM) significantly increased the expression levels of DRD1, BDNF, and TrkB, but decreased the expression of MeCP2 in the neurons, whereas CBD (1 muM) pretreatment notably inhibited the protein changes induced by METH.	Cannabidiol	148-151	dopamine receptor D1	Rattus norvegicus	64-68
34997862-10	2022	METH (400 muM) significantly increased the expression levels of DRD1, BDNF, and TrkB, but decreased the expression of MeCP2 in the neurons, whereas CBD (1 muM) pretreatment notably inhibited the protein changes induced by METH.	Cannabidiol	148-151	brain-derived neurotrophic factor	Rattus norvegicus	70-74
34997862-10	2022	METH (400 muM) significantly increased the expression levels of DRD1, BDNF, and TrkB, but decreased the expression of MeCP2 in the neurons, whereas CBD (1 muM) pretreatment notably inhibited the protein changes induced by METH.	Cannabidiol	148-151	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	80-84
35563697-8	2022	Our results revealed that CBD and, for the first time, THC significantly inhibited NLRP3 inflammasome activation following LPS + ATP stimulation, leading to a reduction in the levels of IL-1beta in THP-1 macrophages and HBECs.	Cannabidiol	26-29	NLR family pyrin domain containing 3	Homo sapiens	83-88
35563697-8	2022	Our results revealed that CBD and, for the first time, THC significantly inhibited NLRP3 inflammasome activation following LPS + ATP stimulation, leading to a reduction in the levels of IL-1beta in THP-1 macrophages and HBECs.	Cannabidiol	26-29	interleukin 1 alpha	Homo sapiens	186-194
35563697-8	2022	Our results revealed that CBD and, for the first time, THC significantly inhibited NLRP3 inflammasome activation following LPS + ATP stimulation, leading to a reduction in the levels of IL-1beta in THP-1 macrophages and HBECs.	Cannabidiol	26-29	GLI family zinc finger 2	Homo sapiens	198-203
35563697-10	2022	Our multiplex ELISA data revealed that CBD and THC significantly diminished the levels of IL-6, IL-8, and tumor necrosis factor-alpha (TNF-alpha) after LPS treatment in THP-1 macrophages and HBECs.	Cannabidiol	39-42	interleukin 6	Homo sapiens	90-94
35563697-10	2022	Our multiplex ELISA data revealed that CBD and THC significantly diminished the levels of IL-6, IL-8, and tumor necrosis factor-alpha (TNF-alpha) after LPS treatment in THP-1 macrophages and HBECs.	Cannabidiol	39-42	C-X-C motif chemokine ligand 8	Homo sapiens	96-100
35563697-10	2022	Our multiplex ELISA data revealed that CBD and THC significantly diminished the levels of IL-6, IL-8, and tumor necrosis factor-alpha (TNF-alpha) after LPS treatment in THP-1 macrophages and HBECs.	Cannabidiol	39-42	tumor necrosis factor	Homo sapiens	106-133
35563697-10	2022	Our multiplex ELISA data revealed that CBD and THC significantly diminished the levels of IL-6, IL-8, and tumor necrosis factor-alpha (TNF-alpha) after LPS treatment in THP-1 macrophages and HBECs.	Cannabidiol	39-42	tumor necrosis factor	Homo sapiens	135-144
35563697-10	2022	Our multiplex ELISA data revealed that CBD and THC significantly diminished the levels of IL-6, IL-8, and tumor necrosis factor-alpha (TNF-alpha) after LPS treatment in THP-1 macrophages and HBECs.	Cannabidiol	39-42	GLI family zinc finger 2	Homo sapiens	169-174
35563697-11	2022	In addition, the phosphorylation of STAT3 was significantly downregulated by CBD and THC in THP-1 macrophages and HBECs, which was in turn attributed to the reduced phosphorylation of tyrosine kinase-2 (TYK2) by CBD and THC after LPS stimulation in these cells.	Cannabidiol	77-80	signal transducer and activator of transcription 3	Homo sapiens	36-41
35563697-11	2022	In addition, the phosphorylation of STAT3 was significantly downregulated by CBD and THC in THP-1 macrophages and HBECs, which was in turn attributed to the reduced phosphorylation of tyrosine kinase-2 (TYK2) by CBD and THC after LPS stimulation in these cells.	Cannabidiol	77-80	GLI family zinc finger 2	Homo sapiens	92-97
35443806-0	2022	Effects of Cannabidiol Interactions with CYP2R1, CYP27B1, CYP24A1, and Vitamin D3 Receptors on Spatial Memory, Pain, Inflammation, and Aging in Vitamin D3 Deficiency Diet-Induced Rats.	Cannabidiol	11-22	cytochrome P450, family 2, subfamily r, polypeptide 1	Rattus norvegicus	41-47
35563697-11	2022	In addition, the phosphorylation of STAT3 was significantly downregulated by CBD and THC in THP-1 macrophages and HBECs, which was in turn attributed to the reduced phosphorylation of tyrosine kinase-2 (TYK2) by CBD and THC after LPS stimulation in these cells.	Cannabidiol	77-80	tyrosine kinase 2	Homo sapiens	184-201
35563697-11	2022	In addition, the phosphorylation of STAT3 was significantly downregulated by CBD and THC in THP-1 macrophages and HBECs, which was in turn attributed to the reduced phosphorylation of tyrosine kinase-2 (TYK2) by CBD and THC after LPS stimulation in these cells.	Cannabidiol	77-80	tyrosine kinase 2	Homo sapiens	203-207
35563697-11	2022	In addition, the phosphorylation of STAT3 was significantly downregulated by CBD and THC in THP-1 macrophages and HBECs, which was in turn attributed to the reduced phosphorylation of tyrosine kinase-2 (TYK2) by CBD and THC after LPS stimulation in these cells.	Cannabidiol	212-215	signal transducer and activator of transcription 3	Homo sapiens	36-41
35563697-11	2022	In addition, the phosphorylation of STAT3 was significantly downregulated by CBD and THC in THP-1 macrophages and HBECs, which was in turn attributed to the reduced phosphorylation of tyrosine kinase-2 (TYK2) by CBD and THC after LPS stimulation in these cells.	Cannabidiol	212-215	tyrosine kinase 2	Homo sapiens	184-201
35563697-12	2022	Overall, CBD and THC were found to be effective in alleviating the LPS-induced cytokine storm in human macrophages and primary HBECs, at least via modulation of NLRP3 inflammasome and STAT3 signaling pathways.	Cannabidiol	9-12	NLR family pyrin domain containing 3	Homo sapiens	161-166
35563697-12	2022	Overall, CBD and THC were found to be effective in alleviating the LPS-induced cytokine storm in human macrophages and primary HBECs, at least via modulation of NLRP3 inflammasome and STAT3 signaling pathways.	Cannabidiol	9-12	signal transducer and activator of transcription 3	Homo sapiens	184-189
35443806-0	2022	Effects of Cannabidiol Interactions with CYP2R1, CYP27B1, CYP24A1, and Vitamin D3 Receptors on Spatial Memory, Pain, Inflammation, and Aging in Vitamin D3 Deficiency Diet-Induced Rats.	Cannabidiol	11-22	cytochrome P450, family 27, subfamily b, polypeptide 1	Rattus norvegicus	49-56
35443806-0	2022	Effects of Cannabidiol Interactions with CYP2R1, CYP27B1, CYP24A1, and Vitamin D3 Receptors on Spatial Memory, Pain, Inflammation, and Aging in Vitamin D3 Deficiency Diet-Induced Rats.	Cannabidiol	11-22	cytochrome P450, family 24, subfamily a, polypeptide 1	Rattus norvegicus	58-65
35441415-9	2022	In short, this study demonstrated the beneficial effects of CBD-IGF-1 in nerve regeneration.	Cannabidiol	60-63	insulin-like growth factor 1	Rattus norvegicus	64-69
35631322-0	2022	Antiseizure Effects of Cannabidiol Leading to Increased Peroxisome Proliferator-Activated Receptor Gamma Levels in the Hippocampal CA3 Subfield of Epileptic Rats.	Cannabidiol	23-34	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	56-104
35631322-0	2022	Antiseizure Effects of Cannabidiol Leading to Increased Peroxisome Proliferator-Activated Receptor Gamma Levels in the Hippocampal CA3 Subfield of Epileptic Rats.	Cannabidiol	23-34	carbonic anhydrase 3	Rattus norvegicus	131-134
35631322-8	2022	Overall, these results suggest that the antiseizure effects of CBD are associated with upregulation of PPARgamma in the hippocampal CA3 region.	Cannabidiol	63-66	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	103-112
35631322-8	2022	Overall, these results suggest that the antiseizure effects of CBD are associated with upregulation of PPARgamma in the hippocampal CA3 region.	Cannabidiol	63-66	carbonic anhydrase 3	Rattus norvegicus	132-135
35145212-8	2022	To determine if the unexpected effects of stress-NS and -CS resulted from THC + CBD altering conditioned stress, the effect of THC + CBD use on stress-NS/CS-induced coping behaviors and spine morphology was quantified.	Cannabidiol	133-136	citrate synthase	Rattus norvegicus	154-156
35455470-9	2022	CBD (10 and 20 mg/kg) showed anxiolytic and antidepressant actions in CD1 mice, being more effective at 20 mg/kg.	Cannabidiol	0-3	CD1 antigen complex	Mus musculus	70-73
35455470-13	2022	Real-time PCR studies revealed a significant reduction in Cnr1 and GABA(A)alpha2 and gamma2 gene expression in the HIPP and AMY of CD1 mice treated with CBD.	Cannabidiol	153-156	cannabinoid receptor 1 (brain)	Mus musculus	58-62
35455470-13	2022	Real-time PCR studies revealed a significant reduction in Cnr1 and GABA(A)alpha2 and gamma2 gene expression in the HIPP and AMY of CD1 mice treated with CBD.	Cannabidiol	153-156	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 2	Mus musculus	85-91
35455470-13	2022	Real-time PCR studies revealed a significant reduction in Cnr1 and GABA(A)alpha2 and gamma2 gene expression in the HIPP and AMY of CD1 mice treated with CBD.	Cannabidiol	153-156	CD1 antigen complex	Mus musculus	131-134
35455470-16	2022	CB1r appears to play a relevant role in modulating the anxiolytic actions of CBD.	Cannabidiol	77-80	cannabinoid receptor 1 (brain)	Mus musculus	0-4
35410608-0	2022	The NLRP3 inflammasome in stress response: another target for the promiscuous cannabidiol?	Cannabidiol	78-89	NLR family pyrin domain containing 3	Homo sapiens	4-9
35083862-1	2022	Cannabidiol (CBD) is an abundant non-psychoactive phytocannabinoid in Cannabis extracts which has high affinity on a series of receptors, including type 1 cannabinoid receptor (CB1), type 2 cannabinoid receptor (CB2), GPR55, transient receptor potential vanilloid (TRPV), and peroxisome proliferator-activated receptor gamma (PPARgamma).	Cannabidiol	0-11	cannabinoid receptor 1	Homo sapiens	177-180
35083862-1	2022	Cannabidiol (CBD) is an abundant non-psychoactive phytocannabinoid in Cannabis extracts which has high affinity on a series of receptors, including type 1 cannabinoid receptor (CB1), type 2 cannabinoid receptor (CB2), GPR55, transient receptor potential vanilloid (TRPV), and peroxisome proliferator-activated receptor gamma (PPARgamma).	Cannabidiol	0-11	cannabinoid receptor 2	Homo sapiens	212-215
35083862-1	2022	Cannabidiol (CBD) is an abundant non-psychoactive phytocannabinoid in Cannabis extracts which has high affinity on a series of receptors, including type 1 cannabinoid receptor (CB1), type 2 cannabinoid receptor (CB2), GPR55, transient receptor potential vanilloid (TRPV), and peroxisome proliferator-activated receptor gamma (PPARgamma).	Cannabidiol	0-11	G protein-coupled receptor 55	Homo sapiens	218-223
35083862-1	2022	Cannabidiol (CBD) is an abundant non-psychoactive phytocannabinoid in Cannabis extracts which has high affinity on a series of receptors, including type 1 cannabinoid receptor (CB1), type 2 cannabinoid receptor (CB2), GPR55, transient receptor potential vanilloid (TRPV), and peroxisome proliferator-activated receptor gamma (PPARgamma).	Cannabidiol	0-11	peroxisome proliferator activated receptor gamma	Homo sapiens	276-324
35083862-1	2022	Cannabidiol (CBD) is an abundant non-psychoactive phytocannabinoid in Cannabis extracts which has high affinity on a series of receptors, including type 1 cannabinoid receptor (CB1), type 2 cannabinoid receptor (CB2), GPR55, transient receptor potential vanilloid (TRPV), and peroxisome proliferator-activated receptor gamma (PPARgamma).	Cannabidiol	0-11	peroxisome proliferator activated receptor gamma	Homo sapiens	326-335
35083862-1	2022	Cannabidiol (CBD) is an abundant non-psychoactive phytocannabinoid in Cannabis extracts which has high affinity on a series of receptors, including type 1 cannabinoid receptor (CB1), type 2 cannabinoid receptor (CB2), GPR55, transient receptor potential vanilloid (TRPV), and peroxisome proliferator-activated receptor gamma (PPARgamma).	Cannabidiol	13-16	cannabinoid receptor 1	Homo sapiens	177-180
35083862-1	2022	Cannabidiol (CBD) is an abundant non-psychoactive phytocannabinoid in Cannabis extracts which has high affinity on a series of receptors, including type 1 cannabinoid receptor (CB1), type 2 cannabinoid receptor (CB2), GPR55, transient receptor potential vanilloid (TRPV), and peroxisome proliferator-activated receptor gamma (PPARgamma).	Cannabidiol	13-16	cannabinoid receptor 2	Homo sapiens	212-215
35083862-1	2022	Cannabidiol (CBD) is an abundant non-psychoactive phytocannabinoid in Cannabis extracts which has high affinity on a series of receptors, including type 1 cannabinoid receptor (CB1), type 2 cannabinoid receptor (CB2), GPR55, transient receptor potential vanilloid (TRPV), and peroxisome proliferator-activated receptor gamma (PPARgamma).	Cannabidiol	13-16	G protein-coupled receptor 55	Homo sapiens	218-223
35083862-1	2022	Cannabidiol (CBD) is an abundant non-psychoactive phytocannabinoid in Cannabis extracts which has high affinity on a series of receptors, including type 1 cannabinoid receptor (CB1), type 2 cannabinoid receptor (CB2), GPR55, transient receptor potential vanilloid (TRPV), and peroxisome proliferator-activated receptor gamma (PPARgamma).	Cannabidiol	13-16	peroxisome proliferator activated receptor gamma	Homo sapiens	276-324
35083862-1	2022	Cannabidiol (CBD) is an abundant non-psychoactive phytocannabinoid in Cannabis extracts which has high affinity on a series of receptors, including type 1 cannabinoid receptor (CB1), type 2 cannabinoid receptor (CB2), GPR55, transient receptor potential vanilloid (TRPV), and peroxisome proliferator-activated receptor gamma (PPARgamma).	Cannabidiol	13-16	peroxisome proliferator activated receptor gamma	Homo sapiens	326-335
35168076-6	2022	Moreover, we measured the alterations in expression of AMPAR subunits and ERK1/2 phosphorylation due to cannabidiol treatment or cocaine withdrawal.	Cannabidiol	104-115	mitogen-activated protein kinase 3	Mus musculus	74-80
35168076-8	2022	Cannabidiol also reduced GluA1/2 ratio and increased ERK1/2 phosphorylation in amygdala.	Cannabidiol	0-11	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	25-32
35168076-8	2022	Cannabidiol also reduced GluA1/2 ratio and increased ERK1/2 phosphorylation in amygdala.	Cannabidiol	0-11	mitogen-activated protein kinase 3	Mus musculus	53-59
35115300-1	2022	We previously reported the unbound reversible (IC50,u) and time-dependent (KI,u) inhibition potencies of cannabidiol (CBD), delta-9-tetrahydrocannabinol (THC), and THC metabolites (11-OH THC, 11-COOH THC) against the major cytochrome P450 (CYP) enzymes (1A2, 2C9, 2C19, 2D6, 3A).	Cannabidiol	105-116	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	223-238
35115300-1	2022	We previously reported the unbound reversible (IC50,u) and time-dependent (KI,u) inhibition potencies of cannabidiol (CBD), delta-9-tetrahydrocannabinol (THC), and THC metabolites (11-OH THC, 11-COOH THC) against the major cytochrome P450 (CYP) enzymes (1A2, 2C9, 2C19, 2D6, 3A).	Cannabidiol	105-116	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	240-243
35115300-1	2022	We previously reported the unbound reversible (IC50,u) and time-dependent (KI,u) inhibition potencies of cannabidiol (CBD), delta-9-tetrahydrocannabinol (THC), and THC metabolites (11-OH THC, 11-COOH THC) against the major cytochrome P450 (CYP) enzymes (1A2, 2C9, 2C19, 2D6, 3A).	Cannabidiol	118-121	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	223-238
35115300-1	2022	We previously reported the unbound reversible (IC50,u) and time-dependent (KI,u) inhibition potencies of cannabidiol (CBD), delta-9-tetrahydrocannabinol (THC), and THC metabolites (11-OH THC, 11-COOH THC) against the major cytochrome P450 (CYP) enzymes (1A2, 2C9, 2C19, 2D6, 3A).	Cannabidiol	118-121	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	240-243
35115300-3	2022	The IC50,u of CBD, 7-OH CBD, THC, and 11-OH THC against CYP2B6 was 0.05, 0.34, 0.40, and 0.38 microM, respectively and against CYP2C8 was 0.28, 1.02, 0.67, and 4.37 microM, respectively.	Cannabidiol	24-27	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	56-62
35115300-3	2022	The IC50,u of CBD, 7-OH CBD, THC, and 11-OH THC against CYP2B6 was 0.05, 0.34, 0.40, and 0.38 microM, respectively and against CYP2C8 was 0.28, 1.02, 0.67, and 4.37 microM, respectively.	Cannabidiol	24-27	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	127-133
35115300-10	2022	Significance Statement This study, combined with our previous findings, provides for the first time a comprehensive analysis of the potential for cannabidiol, delta-9-tetrahydrocannabinol, and their metabolites to inhibit cytochrome P450 enzymes in a reversible or time-dependent manner.	Cannabidiol	146-157	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	222-237
35217387-8	2022	Cannabidiol pre-treated rats showed a significant reduction in duration and severity of seizures, and IL-1beta levels, although the latency, incidence of seizures, and mortality rate remained unchanged as well the quantification of microglia in the selected areas.	Cannabidiol	0-11	interleukin 1 alpha	Rattus norvegicus	102-110
35145212-11	2022	Transient spine head expansion in nucleus accumbens core is necessary for cue-induced drug seeking, and THC + CBD self-administration prevented the increase in head diameter by stress-CS in control rats.	Cannabidiol	110-113	citrate synthase	Rattus norvegicus	184-186
35145212-12	2022	These data show THC + CBD self-administration altered the salience of environmental cues, causing neutral cues to promote active behavior (drug seeking and burying) and stress-CS to switch from active to passive behavior (inhibiting drug seeking and immobilization).	Cannabidiol	22-25	citrate synthase	Rattus norvegicus	176-178
35456540-4	2022	The aim of the present study is to investigate the in vitro effects of CBD and its inclusion complexes in randomly methylated beta-CD (RM-beta-CD) and 2-hyroxypropyl-beta-CD (HP-beta-CD).	Cannabidiol	71-74	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	138-145
35409142-7	2022	CIK cells showed a low level of intracellular phospho-p38 and, when stimulated with cannabidiol (CBD), a donor specific variability in phospho-CREB.	Cannabidiol	84-95	cAMP responsive element binding protein 1	Homo sapiens	143-147
35409142-7	2022	CIK cells showed a low level of intracellular phospho-p38 and, when stimulated with cannabidiol (CBD), a donor specific variability in phospho-CREB.	Cannabidiol	97-100	cAMP responsive element binding protein 1	Homo sapiens	143-147
35401543-1	2022	Cannabidiol (CBD) can prevent the inflammatory response of SARS-CoV-2 spike protein in Caco-2-cells.	Cannabidiol	0-11	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	70-75
35401543-1	2022	Cannabidiol (CBD) can prevent the inflammatory response of SARS-CoV-2 spike protein in Caco-2-cells.	Cannabidiol	13-16	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	70-75
35401543-7	2022	CBD exerts its activity through the interaction with PPARgamma in SARS-CoV-2 infection.	Cannabidiol	0-3	peroxisome proliferator activated receptor gamma	Homo sapiens	53-62
35401543-8	2022	Thus, we can hypothesize that CBD may counteract the inflammatory process of SARS-CoV-2 by its interactions with both ACE2 and the interplay between the WNT/beta-catenin pathway and PPARgamma.	Cannabidiol	30-33	angiotensin converting enzyme 2	Homo sapiens	118-122
35401543-8	2022	Thus, we can hypothesize that CBD may counteract the inflammatory process of SARS-CoV-2 by its interactions with both ACE2 and the interplay between the WNT/beta-catenin pathway and PPARgamma.	Cannabidiol	30-33	catenin beta 1	Homo sapiens	157-169
35401543-8	2022	Thus, we can hypothesize that CBD may counteract the inflammatory process of SARS-CoV-2 by its interactions with both ACE2 and the interplay between the WNT/beta-catenin pathway and PPARgamma.	Cannabidiol	30-33	peroxisome proliferator activated receptor gamma	Homo sapiens	182-191
35456540-4	2022	The aim of the present study is to investigate the in vitro effects of CBD and its inclusion complexes in randomly methylated beta-CD (RM-beta-CD) and 2-hyroxypropyl-beta-CD (HP-beta-CD).	Cannabidiol	71-74	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	178-185
35456540-5	2022	The enhanced solubility of CBD upon complexation with CDs was examined by phase solubility study, and the structure of the inclusion complexes of CBD in 2,6-di-O-methyl-beta-CD (DM-beta-CD) and 2,3,6-tri-O-methyl-beta-CD (TM-beta-CD) was determined by X-ray crystallography.	Cannabidiol	27-30	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	169-176
35456540-5	2022	The enhanced solubility of CBD upon complexation with CDs was examined by phase solubility study, and the structure of the inclusion complexes of CBD in 2,6-di-O-methyl-beta-CD (DM-beta-CD) and 2,3,6-tri-O-methyl-beta-CD (TM-beta-CD) was determined by X-ray crystallography.	Cannabidiol	27-30	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	181-188
35456540-5	2022	The enhanced solubility of CBD upon complexation with CDs was examined by phase solubility study, and the structure of the inclusion complexes of CBD in 2,6-di-O-methyl-beta-CD (DM-beta-CD) and 2,3,6-tri-O-methyl-beta-CD (TM-beta-CD) was determined by X-ray crystallography.	Cannabidiol	27-30	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	213-220
35456540-5	2022	The enhanced solubility of CBD upon complexation with CDs was examined by phase solubility study, and the structure of the inclusion complexes of CBD in 2,6-di-O-methyl-beta-CD (DM-beta-CD) and 2,3,6-tri-O-methyl-beta-CD (TM-beta-CD) was determined by X-ray crystallography.	Cannabidiol	27-30	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	225-232
35456540-5	2022	The enhanced solubility of CBD upon complexation with CDs was examined by phase solubility study, and the structure of the inclusion complexes of CBD in 2,6-di-O-methyl-beta-CD (DM-beta-CD) and 2,3,6-tri-O-methyl-beta-CD (TM-beta-CD) was determined by X-ray crystallography.	Cannabidiol	146-149	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	169-176
35456540-5	2022	The enhanced solubility of CBD upon complexation with CDs was examined by phase solubility study, and the structure of the inclusion complexes of CBD in 2,6-di-O-methyl-beta-CD (DM-beta-CD) and 2,3,6-tri-O-methyl-beta-CD (TM-beta-CD) was determined by X-ray crystallography.	Cannabidiol	146-149	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	181-188
35456540-5	2022	The enhanced solubility of CBD upon complexation with CDs was examined by phase solubility study, and the structure of the inclusion complexes of CBD in 2,6-di-O-methyl-beta-CD (DM-beta-CD) and 2,3,6-tri-O-methyl-beta-CD (TM-beta-CD) was determined by X-ray crystallography.	Cannabidiol	146-149	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	213-220
35456540-5	2022	The enhanced solubility of CBD upon complexation with CDs was examined by phase solubility study, and the structure of the inclusion complexes of CBD in 2,6-di-O-methyl-beta-CD (DM-beta-CD) and 2,3,6-tri-O-methyl-beta-CD (TM-beta-CD) was determined by X-ray crystallography.	Cannabidiol	146-149	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	225-232
35456540-7	2022	The cytotoxicity of CBD and its complexes with RM-beta-CD and HP-beta-CD was tested on two cell lines, the A172 glioblastoma and TE671 rhabdomyosarcoma cell lines.	Cannabidiol	20-23	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	50-57
35181336-8	2022	In addition, CBD treatment enhanced the worm resistance to oxidative stress, which was independent of the classical transcription factors DAF-16 and SKN-1.	Cannabidiol	13-16	Fork-head domain-containing protein;Forkhead box protein O	Caenorhabditis elegans	138-144
35325302-5	2022	Since the genetic signature of microglia offers many potential targets for drug discovery, molecular docking followed by molecular dynamics (MD) simulations of cluster of differentiation 40 ligand (CD40L) and colony-stimulating factor 1 receptor (CSF1R) kinase domain protein with some known neuro-immunomodulators (Curcumin, Cannabidiol, Ginsenoside Rg1, Resveratrol, and Sulforaphane) has been evaluated.	Cannabidiol	326-337	CD40 ligand	Homo sapiens	198-203
35325302-5	2022	Since the genetic signature of microglia offers many potential targets for drug discovery, molecular docking followed by molecular dynamics (MD) simulations of cluster of differentiation 40 ligand (CD40L) and colony-stimulating factor 1 receptor (CSF1R) kinase domain protein with some known neuro-immunomodulators (Curcumin, Cannabidiol, Ginsenoside Rg1, Resveratrol, and Sulforaphane) has been evaluated.	Cannabidiol	326-337	colony stimulating factor 1 receptor	Homo sapiens	209-245
35325302-6	2022	Curcumin and cannabidiol were observed likely to modulate CD40L and expression of cytokines and entry of inflammatory cells.	Cannabidiol	13-24	CD40 ligand	Homo sapiens	58-63
35181336-8	2022	In addition, CBD treatment enhanced the worm resistance to oxidative stress, which was independent of the classical transcription factors DAF-16 and SKN-1.	Cannabidiol	13-16	BZIP domain-containing protein;Protein skinhead-1	Caenorhabditis elegans	149-154
35335126-0	2022	Botanically-Derived Delta9-Tetrahydrocannabinol and Cannabidiol, and Their 1:1 Combination, Modulate Toll-like Receptor 3 and 4 Signalling in Immune Cells from People with Multiple Sclerosis.	Cannabidiol	52-63	toll like receptor 3	Homo sapiens	101-127
35277472-2	2022	Here, we show AKT serine/threonine kinase-dependent epigenetic control of ACE2 and TMPRSS2 expression by high-cannabidiol (CBD) cannabis extracts and their individual components.	Cannabidiol	123-126	AKT serine/threonine kinase 1	Homo sapiens	14-17
35277472-2	2022	Here, we show AKT serine/threonine kinase-dependent epigenetic control of ACE2 and TMPRSS2 expression by high-cannabidiol (CBD) cannabis extracts and their individual components.	Cannabidiol	123-126	angiotensin converting enzyme 2	Homo sapiens	74-78
35277472-2	2022	Here, we show AKT serine/threonine kinase-dependent epigenetic control of ACE2 and TMPRSS2 expression by high-cannabidiol (CBD) cannabis extracts and their individual components.	Cannabidiol	123-126	transmembrane serine protease 2	Homo sapiens	83-90
35277472-5	2022	CBD and terpene PTWT2.2 profoundly inhibited ACE2 and TMPRSS2 expression, both individually and in combination.	Cannabidiol	0-3	angiotensin converting enzyme 2	Homo sapiens	45-49
35277472-5	2022	CBD and terpene PTWT2.2 profoundly inhibited ACE2 and TMPRSS2 expression, both individually and in combination.	Cannabidiol	0-3	transmembrane serine protease 2	Homo sapiens	54-61
35335126-3	2022	Recent data from our laboratory reported that the plant-derived cannabinoids, Delta9-tetrahydrocannabinol (THC) and cannabidiol (CBD), regulate viral and bacterial inflammatory signalling pathways controlled by TLR3 and TLR4 in macrophages.	Cannabidiol	116-127	toll like receptor 3	Homo sapiens	211-215
35335126-3	2022	Recent data from our laboratory reported that the plant-derived cannabinoids, Delta9-tetrahydrocannabinol (THC) and cannabidiol (CBD), regulate viral and bacterial inflammatory signalling pathways controlled by TLR3 and TLR4 in macrophages.	Cannabidiol	116-127	toll like receptor 4	Homo sapiens	220-224
35335126-3	2022	Recent data from our laboratory reported that the plant-derived cannabinoids, Delta9-tetrahydrocannabinol (THC) and cannabidiol (CBD), regulate viral and bacterial inflammatory signalling pathways controlled by TLR3 and TLR4 in macrophages.	Cannabidiol	129-132	toll like receptor 3	Homo sapiens	211-215
35335126-3	2022	Recent data from our laboratory reported that the plant-derived cannabinoids, Delta9-tetrahydrocannabinol (THC) and cannabidiol (CBD), regulate viral and bacterial inflammatory signalling pathways controlled by TLR3 and TLR4 in macrophages.	Cannabidiol	129-132	toll like receptor 4	Homo sapiens	220-224
35335126-4	2022	The aim of this study was to assess the impact of THC and CBD, when delivered in isolation and in combination (1:1), on TLR3- and TLR4-dependent signalling in peripheral blood mononuclear cells (PBMCs) from people with MS (pwMS; n = 21) and healthy controls (HCs; n = 26).	Cannabidiol	58-61	toll like receptor 3	Homo sapiens	120-124
35335126-4	2022	The aim of this study was to assess the impact of THC and CBD, when delivered in isolation and in combination (1:1), on TLR3- and TLR4-dependent signalling in peripheral blood mononuclear cells (PBMCs) from people with MS (pwMS; n = 21) and healthy controls (HCs; n = 26).	Cannabidiol	58-61	toll like receptor 4	Homo sapiens	130-134
35335126-7	2022	THC and CBD (delivered in 1:1 combination at 10 muM) attenuated TLR3-induced CXCL10 and IFN-beta protein expression in PBMCs from pwMS and HCs, and this effect was not seen consistently when THC and CBD were delivered alone.	Cannabidiol	8-11	toll like receptor 3	Homo sapiens	64-68
35335126-7	2022	THC and CBD (delivered in 1:1 combination at 10 muM) attenuated TLR3-induced CXCL10 and IFN-beta protein expression in PBMCs from pwMS and HCs, and this effect was not seen consistently when THC and CBD were delivered alone.	Cannabidiol	8-11	C-X-C motif chemokine ligand 10	Homo sapiens	77-83
35335126-7	2022	THC and CBD (delivered in 1:1 combination at 10 muM) attenuated TLR3-induced CXCL10 and IFN-beta protein expression in PBMCs from pwMS and HCs, and this effect was not seen consistently when THC and CBD were delivered alone.	Cannabidiol	8-11	IFN1@	Homo sapiens	88-96
35335126-11	2022	Given their role in inflammation, TLRs are clinical targets, and data herein identify CBD and THC as TLR3 and TLR4 modulating drugs in primary immune cells in vitro.	Cannabidiol	86-89	toll like receptor 3	Homo sapiens	101-105
35335126-11	2022	Given their role in inflammation, TLRs are clinical targets, and data herein identify CBD and THC as TLR3 and TLR4 modulating drugs in primary immune cells in vitro.	Cannabidiol	86-89	toll like receptor 4	Homo sapiens	110-114
35229949-8	2022	Interestingly, CBD treatment significantly reduced these behavioural impairments and normalized gene expression of Cnr1 and Pomc in the NAcc and TH in the VTA of mice exposed to spontaneous heroin withdrawal.	Cannabidiol	15-18	cannabinoid receptor 1 (brain)	Mus musculus	115-119
35229949-8	2022	Interestingly, CBD treatment significantly reduced these behavioural impairments and normalized gene expression of Cnr1 and Pomc in the NAcc and TH in the VTA of mice exposed to spontaneous heroin withdrawal.	Cannabidiol	15-18	pro-opiomelanocortin-alpha	Mus musculus	124-128
35229949-9	2022	Also, CBD induced an up-regulation of Cnr2, whereas it did not change the increased gene expression of Oprm1 in the NAcc of abstinent animals.	Cannabidiol	6-9	cannabinoid receptor 2 (macrophage)	Mus musculus	38-42
35220282-0	2022	Cannabidiol Promotes Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells in the Inflammatory Microenvironment via the CB2-dependent p38 MAPK Signaling Pathway.	Cannabidiol	0-11	cannabinoid receptor 2 (macrophage)	Mus musculus	131-134
35220282-0	2022	Cannabidiol Promotes Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells in the Inflammatory Microenvironment via the CB2-dependent p38 MAPK Signaling Pathway.	Cannabidiol	0-11	mitogen-activated protein kinase 14	Mus musculus	145-153
35220282-10	2022	In addition, AM630 and SB530689, a selective p38 MAPK inhibitor, attenuated the enhancement of osteogenic markers expression levels by CBD in inflammatory microenvironment, respectively.	Cannabidiol	135-138	mitogen-activated protein kinase 14	Mus musculus	45-53
35216351-7	2022	The above reductions were accompanied by markedly diminished expressions of myocardial serine palmitoyltransferase 1 and 2 as well as ceramide synthase 5 and 6 in the HFD group with 2-week CBD treatment.	Cannabidiol	189-192	serine palmitoyltransferase, long chain base subunit 1	Rattus norvegicus	87-122
35217991-4	2022	Next-generation RNA sequencing revealed GADD45A, GADD45G, FASN, LOX, and integrin (i.e., -alpha5, -beta5) genes to be novelly altered by CBD in MDA-MB-231 cells.	Cannabidiol	137-140	growth arrest and DNA damage inducible alpha	Homo sapiens	40-47
35217991-4	2022	Next-generation RNA sequencing revealed GADD45A, GADD45G, FASN, LOX, and integrin (i.e., -alpha5, -beta5) genes to be novelly altered by CBD in MDA-MB-231 cells.	Cannabidiol	137-140	growth arrest and DNA damage inducible gamma	Homo sapiens	49-56
35217991-4	2022	Next-generation RNA sequencing revealed GADD45A, GADD45G, FASN, LOX, and integrin (i.e., -alpha5, -beta5) genes to be novelly altered by CBD in MDA-MB-231 cells.	Cannabidiol	137-140	fatty acid synthase	Homo sapiens	58-62
35217991-4	2022	Next-generation RNA sequencing revealed GADD45A, GADD45G, FASN, LOX, and integrin (i.e., -alpha5, -beta5) genes to be novelly altered by CBD in MDA-MB-231 cells.	Cannabidiol	137-140	lysyl oxidase	Homo sapiens	64-67
35217991-4	2022	Next-generation RNA sequencing revealed GADD45A, GADD45G, FASN, LOX, and integrin (i.e., -alpha5, -beta5) genes to be novelly altered by CBD in MDA-MB-231 cells.	Cannabidiol	137-140	immunoglobulin kappa variable 2D-26	Homo sapiens	87-104
35217991-6	2022	Western blotting, RT-qPCR, and immunocytochemistry revealed that CBD inhibited autophagy (decreased Beclin1, and ATG-5, -7, and -16) of TNBC cells.	Cannabidiol	65-68	beclin 1	Homo sapiens	100-107
35217991-6	2022	Western blotting, RT-qPCR, and immunocytochemistry revealed that CBD inhibited autophagy (decreased Beclin1, and ATG-5, -7, and -16) of TNBC cells.	Cannabidiol	65-68	autophagy related 5	Homo sapiens	113-131
35217991-8	2022	CBD pre-treatment accompanied by DOX treatment decreased LOX and integrin-alpha5, and increased caspase 9 protein respectively in MDA-MB-468 cells.	Cannabidiol	0-3	lysyl oxidase	Homo sapiens	57-60
35217991-8	2022	CBD pre-treatment accompanied by DOX treatment decreased LOX and integrin-alpha5, and increased caspase 9 protein respectively in MDA-MB-468 cells.	Cannabidiol	0-3	integrin subunit alpha 5	Homo sapiens	65-80
35217991-8	2022	CBD pre-treatment accompanied by DOX treatment decreased LOX and integrin-alpha5, and increased caspase 9 protein respectively in MDA-MB-468 cells.	Cannabidiol	0-3	caspase 9	Homo sapiens	96-105
35216351-7	2022	The above reductions were accompanied by markedly diminished expressions of myocardial serine palmitoyltransferase 1 and 2 as well as ceramide synthase 5 and 6 in the HFD group with 2-week CBD treatment.	Cannabidiol	189-192	ceramide synthase 5	Rattus norvegicus	134-159
35356807-0	2022	Cannabidiol inhibits RAD51 and sensitizes glioblastoma to temozolomide in multiple orthotopic tumor models.	Cannabidiol	0-11	RAD51 recombinase	Homo sapiens	21-26
35179483-3	2022	Patch-clamp recordings showed that CBD acts at submicromolar concentrations to shift the voltage dependence of Kv7.2/7.3 channels in the hyperpolarizing direction, producing a dramatic enhancement of current at voltages near -50 mV.	Cannabidiol	35-38	potassium voltage-gated channel subfamily Q member 2	Homo sapiens	111-118
35356807-7	2022	Results: CBD enhanced the activity of TMZ in U87 MG and U251 GBM cell lines and in patient-derived primary GBM163 cells leading to stimulation of ROS, activation of the ROS sensor AMP-activated protein kinase (AMPK), and upregulation of the autophagy marker LC3A.	Cannabidiol	9-12	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	180-208
35356807-7	2022	Results: CBD enhanced the activity of TMZ in U87 MG and U251 GBM cell lines and in patient-derived primary GBM163 cells leading to stimulation of ROS, activation of the ROS sensor AMP-activated protein kinase (AMPK), and upregulation of the autophagy marker LC3A.	Cannabidiol	9-12	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	210-214
35356807-7	2022	Results: CBD enhanced the activity of TMZ in U87 MG and U251 GBM cell lines and in patient-derived primary GBM163 cells leading to stimulation of ROS, activation of the ROS sensor AMP-activated protein kinase (AMPK), and upregulation of the autophagy marker LC3A.	Cannabidiol	9-12	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	258-262
35356807-11	2022	We further demonstrate that CBD inhibited RAD51 expression in MGMT-methylated models of GBM, providing a potential mechanism for tumor sensitization to TMZ by CBD.	Cannabidiol	28-31	RAD51 recombinase	Homo sapiens	42-47
35356807-11	2022	We further demonstrate that CBD inhibited RAD51 expression in MGMT-methylated models of GBM, providing a potential mechanism for tumor sensitization to TMZ by CBD.	Cannabidiol	28-31	O-6-methylguanine-DNA methyltransferase	Homo sapiens	62-66
35356807-11	2022	We further demonstrate that CBD inhibited RAD51 expression in MGMT-methylated models of GBM, providing a potential mechanism for tumor sensitization to TMZ by CBD.	Cannabidiol	159-162	RAD51 recombinase	Homo sapiens	42-47
35356807-11	2022	We further demonstrate that CBD inhibited RAD51 expression in MGMT-methylated models of GBM, providing a potential mechanism for tumor sensitization to TMZ by CBD.	Cannabidiol	159-162	O-6-methylguanine-DNA methyltransferase	Homo sapiens	62-66
35107862-6	2022	The results indicated that the cannabidiol (CBD)-rich extract inhibited cell proliferation of K562 cell line in a dose-dependent manner and induced apoptosis via caspase 3 and 7 activation.	Cannabidiol	31-42	caspase 3	Homo sapiens	162-171
35273722-0	2022	Cannabidiol promotes apoptosis of osteosarcoma cells in vitro and in vivo by activating the SP1-CBX2 axis.	Cannabidiol	0-11	chromobox 2	Homo sapiens	96-100
35273722-8	2022	The in vitro study also demonstrated that SP1 contributes to chromobox protein homolog 2 (CBX2) reduction in cannabidiol-treated MG63 and HOS cells, and that cannabidiol may recruit SP1 into the CBX2 promoter regions to downregulate CBX2 expression at the transcriptional level and promote osteosarcoma cell apoptosis.	Cannabidiol	109-120	chromobox 2	Homo sapiens	61-88
35273722-8	2022	The in vitro study also demonstrated that SP1 contributes to chromobox protein homolog 2 (CBX2) reduction in cannabidiol-treated MG63 and HOS cells, and that cannabidiol may recruit SP1 into the CBX2 promoter regions to downregulate CBX2 expression at the transcriptional level and promote osteosarcoma cell apoptosis.	Cannabidiol	109-120	chromobox 2	Homo sapiens	90-94
35273722-8	2022	The in vitro study also demonstrated that SP1 contributes to chromobox protein homolog 2 (CBX2) reduction in cannabidiol-treated MG63 and HOS cells, and that cannabidiol may recruit SP1 into the CBX2 promoter regions to downregulate CBX2 expression at the transcriptional level and promote osteosarcoma cell apoptosis.	Cannabidiol	109-120	chromobox 2	Homo sapiens	233-237
35273722-8	2022	The in vitro study also demonstrated that SP1 contributes to chromobox protein homolog 2 (CBX2) reduction in cannabidiol-treated MG63 and HOS cells, and that cannabidiol may recruit SP1 into the CBX2 promoter regions to downregulate CBX2 expression at the transcriptional level and promote osteosarcoma cell apoptosis.	Cannabidiol	158-169	chromobox 2	Homo sapiens	195-199
35273722-8	2022	The in vitro study also demonstrated that SP1 contributes to chromobox protein homolog 2 (CBX2) reduction in cannabidiol-treated MG63 and HOS cells, and that cannabidiol may recruit SP1 into the CBX2 promoter regions to downregulate CBX2 expression at the transcriptional level and promote osteosarcoma cell apoptosis.	Cannabidiol	158-169	chromobox 2	Homo sapiens	233-237
35273722-10	2022	In summary, cannabidiol effectively promoted the apoptosis of osteosarcoma cells in vitro and in vivo and suppressed tumor growth in a mouse xenograft model by regulating the SP1-CBX2 axis.	Cannabidiol	12-23	chromobox 2	Mus musculus	179-183
35107862-6	2022	The results indicated that the cannabidiol (CBD)-rich extract inhibited cell proliferation of K562 cell line in a dose-dependent manner and induced apoptosis via caspase 3 and 7 activation.	Cannabidiol	44-47	caspase 3	Homo sapiens	162-171
35056767-5	2022	Applying our novel algorithm toolset-MCCS, we docked three known AMs of CB2 including Ec2la (C-2), trans-beta-caryophyllene (TBC) and cannabidiol (CBD) to each site for further comparisons and quantified the potential binding residues in each allosteric binding site.	Cannabidiol	134-145	cannabinoid receptor 2	Homo sapiens	72-75
35153788-0	2022	Cannabidiol Increases Seizure Resistance and Improves Behavior in an Scn8a Mouse Model.	Cannabidiol	0-11	sodium channel, voltage-gated, type VIII, alpha	Mus musculus	69-74
35153788-4	2022	Cannabidiol (CBD) has been included as a component of treatment regimens for some SCN8A patients; however, to date, there are no clinical trials that have evaluated the therapeutic potential of CBD in patients with SCN8A mutations.	Cannabidiol	0-11	sodium voltage-gated channel alpha subunit 8	Homo sapiens	82-87
35153788-4	2022	Cannabidiol (CBD) has been included as a component of treatment regimens for some SCN8A patients; however, to date, there are no clinical trials that have evaluated the therapeutic potential of CBD in patients with SCN8A mutations.	Cannabidiol	13-16	sodium voltage-gated channel alpha subunit 8	Homo sapiens	82-87
35153788-5	2022	In the current manuscript, we demonstrated a dose-dependent increase in seizure resistance following CBD treatment in mice expressing the human SCN8A mutation R1620L (RL/+).	Cannabidiol	101-104	sodium voltage-gated channel alpha subunit 8	Homo sapiens	144-149
35202235-7	2022	In particular, the expression of PSD95 was reduced following incubation for 72 h with THC and was increased following incubation with CBD.	Cannabidiol	134-137	discs large MAGUK scaffold protein 4	Rattus norvegicus	33-38
35056767-5	2022	Applying our novel algorithm toolset-MCCS, we docked three known AMs of CB2 including Ec2la (C-2), trans-beta-caryophyllene (TBC) and cannabidiol (CBD) to each site for further comparisons and quantified the potential binding residues in each allosteric binding site.	Cannabidiol	147-150	cannabinoid receptor 2	Homo sapiens	72-75
2550010-3	1989	Repetitive CBD treatment, on the other hand, resulted in the restoration of cytochrome P-450 content as well as hexobarbital hydroxylase and erythromycin N-demethylase activities.	Cannabidiol	11-14	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	76-92
2550010-7	1989	Thus, it appears that CBD initially inactivates at least one cytochrome P-450 isozyme, but after repetitive CBD treatment, an isozyme is induced that is resistant to further re-inactivation by CBD.	Cannabidiol	22-25	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	61-77
2550010-7	1989	Thus, it appears that CBD initially inactivates at least one cytochrome P-450 isozyme, but after repetitive CBD treatment, an isozyme is induced that is resistant to further re-inactivation by CBD.	Cannabidiol	108-111	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	61-77
2550010-7	1989	Thus, it appears that CBD initially inactivates at least one cytochrome P-450 isozyme, but after repetitive CBD treatment, an isozyme is induced that is resistant to further re-inactivation by CBD.	Cannabidiol	108-111	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	61-77
3675599-5	1987	The derivatives of CBD modified in the resorcinol moiety, CBD-monomethyl- and dimethylethers, almost lost the effect on cytochrome P-450, whereas those modified in the terpene moiety, 8,9-dihydro- and 1,2,8,9-tetrahydro-CBDs exhibited some potency to inactivate cytochrome P-450.	Cannabidiol	58-61	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	120-136
2779523-0	1989	Purification and characterization of a mouse liver cytochrome P-450 induced by cannabidiol.	Cannabidiol	79-90	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	51-67
2779523-1	1989	A cytochrome P-450 isozyme (Mr = 51,600) was purified to apparent homogeneity from hepatic microsomes of mice pretreated with cannabidiol (CBD), a major constituent of marijuana.	Cannabidiol	126-137	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	2-18
2779523-1	1989	A cytochrome P-450 isozyme (Mr = 51,600) was purified to apparent homogeneity from hepatic microsomes of mice pretreated with cannabidiol (CBD), a major constituent of marijuana.	Cannabidiol	139-142	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	2-18
2779523-4	1989	Because of the many similarities between the CBD-induced isozyme and certain other isozymes previously purified from PB-pretreated animals, a cytochrome P-450 isozyme was purified from PB-pretreated mice by a chromatographic procedure similar to that employed for purification of the CBD-induced isozyme.	Cannabidiol	45-48	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	142-158
2779523-4	1989	Because of the many similarities between the CBD-induced isozyme and certain other isozymes previously purified from PB-pretreated animals, a cytochrome P-450 isozyme was purified from PB-pretreated mice by a chromatographic procedure similar to that employed for purification of the CBD-induced isozyme.	Cannabidiol	284-287	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	142-158
2779523-7	1989	Thus, CBD exposure results in the induction of an isozyme that is refractory to CBD-mediated inactivation, thereby apparently altering the cytochrome P-450 isozymal composition of mouse hepatic microsomes.	Cannabidiol	6-9	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	139-155
2852360-1	1988	The effect of naturally occurring cannabinoids, delta 9-tetrahydrocannabinol (THC), cannabinol (CBN) and cannabidiol (CBD), on the brain receptors for thyrotropin releasing hormone (TRH) was investigated.	Cannabidiol	105-116	thyrotropin releasing hormone	Rattus norvegicus	151-180
2852360-1	1988	The effect of naturally occurring cannabinoids, delta 9-tetrahydrocannabinol (THC), cannabinol (CBN) and cannabidiol (CBD), on the brain receptors for thyrotropin releasing hormone (TRH) was investigated.	Cannabidiol	105-116	thyrotropin releasing hormone	Rattus norvegicus	182-185
3675599-0	1987	Self-catalyzed inactivation of cytochrome P-450 during microsomal metabolism of cannabidiol.	Cannabidiol	80-91	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	31-47
3675599-1	1987	When cannabidiol (CBD) was incubated with hepatic microsomes of mice in the presence of an NADPH-generating system, a significant decrease of cytochrome P-450 content was observed by measuring its carbon monoxide difference spectra.	Cannabidiol	5-16	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	142-158
3675599-1	1987	When cannabidiol (CBD) was incubated with hepatic microsomes of mice in the presence of an NADPH-generating system, a significant decrease of cytochrome P-450 content was observed by measuring its carbon monoxide difference spectra.	Cannabidiol	18-21	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	142-158
3675599-5	1987	The derivatives of CBD modified in the resorcinol moiety, CBD-monomethyl- and dimethylethers, almost lost the effect on cytochrome P-450, whereas those modified in the terpene moiety, 8,9-dihydro- and 1,2,8,9-tetrahydro-CBDs exhibited some potency to inactivate cytochrome P-450.	Cannabidiol	19-22	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	120-136
3675599-5	1987	The derivatives of CBD modified in the resorcinol moiety, CBD-monomethyl- and dimethylethers, almost lost the effect on cytochrome P-450, whereas those modified in the terpene moiety, 8,9-dihydro- and 1,2,8,9-tetrahydro-CBDs exhibited some potency to inactivate cytochrome P-450.	Cannabidiol	19-22	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	262-278
3675599-6	1987	The inactivation of cytochrome P-450 by CBD and related compounds led to the inhibition of hepatic microsomal p-nitroanisole O-demethylase and aniline hydroxylase activities.	Cannabidiol	40-43	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	20-36
6311937-1	1983	This paper presents the synthetic route used and the identification of the precursors and reaction products in a clandestine laboratory manufacture of cannabidiol (CBD), delta 9-cis-tetrahydrocannabinol (delta 9-cis-THC), and delta 9-trans-tetrahydrocannabinol (delta 9-trans-THC).	Cannabidiol	151-162	WASP actin nucleation promoting factor	Homo sapiens	216-219
3803591-2	1987	Cannabinoids delta 1-tetrahydrocannabinol, cannabinol, cannabidiol and cannabigerol have been shown to affect directly the activity of phospholipase A2 in a cell-free assay.	Cannabidiol	55-66	phospholipase A2 group IB	Homo sapiens	135-151
3012058-1	1986	The effects of cannabidiol (CBD) and delta 9-tetrahydrocannabinol (delta 9-THC) on the synthesis and degradation of hepatic microsomal cytochrome P-450 were studied in mice.	Cannabidiol	15-26	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	135-151
3012058-1	1986	The effects of cannabidiol (CBD) and delta 9-tetrahydrocannabinol (delta 9-THC) on the synthesis and degradation of hepatic microsomal cytochrome P-450 were studied in mice.	Cannabidiol	28-31	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	135-151
3012058-12	1986	These results suggest that CBD metabolites rather than CBD itself, play some role in the decreasing effect on cytochrome P-450 content in the hepatic microsomes in vitro, and that the microsomal formation of reactive metabolite of CBD is increased by phenobarbital-treatment.	Cannabidiol	27-30	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	110-126
3159590-7	1985	When cells were challenged with substrata coated with various ratios of CBD and PF4, PF4 was found to be an effective inhibitor of CBD-mediated neurite extension.	Cannabidiol	72-75	platelet factor 4	Homo sapiens	85-88
6732800-0	1984	Stimulation of sphingomyelin hydrolysis by cannabidiol in fibroblasts from a Niemann-Pick patient.	Cannabidiol	43-54	protein interacting with PRKCA 1	Homo sapiens	85-89
6311937-1	1983	This paper presents the synthetic route used and the identification of the precursors and reaction products in a clandestine laboratory manufacture of cannabidiol (CBD), delta 9-cis-tetrahydrocannabinol (delta 9-cis-THC), and delta 9-trans-tetrahydrocannabinol (delta 9-trans-THC).	Cannabidiol	151-162	WASP actin nucleation promoting factor	Homo sapiens	276-279
6311937-1	1983	This paper presents the synthetic route used and the identification of the precursors and reaction products in a clandestine laboratory manufacture of cannabidiol (CBD), delta 9-cis-tetrahydrocannabinol (delta 9-cis-THC), and delta 9-trans-tetrahydrocannabinol (delta 9-trans-THC).	Cannabidiol	164-167	WASP actin nucleation promoting factor	Homo sapiens	276-279
6251493-1	1980	delta 9-Tetrahydrocannabinol (THC) and cannabidiol (CBD) caused a marked stimulation of phospholipase A2 when incubated with intact human platelets that were prelabeled with [14C] arachidonate.	Cannabidiol	39-50	phospholipase A2 group IB	Homo sapiens	88-104
6251493-1	1980	delta 9-Tetrahydrocannabinol (THC) and cannabidiol (CBD) caused a marked stimulation of phospholipase A2 when incubated with intact human platelets that were prelabeled with [14C] arachidonate.	Cannabidiol	52-55	phospholipase A2 group IB	Homo sapiens	88-104
6251493-7	1980	The multiple effects of THC and CBD on phospholipase A2 and arachidonate metabolism may mediate some of the pharmacological actions of these compounds, such as their anticonvulsant, anti-inflammatory, and hypotensive properties.	Cannabidiol	32-35	phospholipase A2 group IB	Homo sapiens	39-55
33862125-0	2021	Cannabidiol modulates the METH-induced conditioned place preference through D2-like dopamine receptors in the hippocampal CA1 region.	Cannabidiol	0-11	carbonic anhydrase 1	Rattus norvegicus	122-125
201449-1	1977	ACTH, cholera toxin, cyclic AMP but not pregnenolone-induced steroidogenesis in Y-1 functional mouse adrenal tumor cells was significantly inhibited by delta-9-tetrahydrocannabinol, cannabidiol, and cannabinol.	Cannabidiol	182-193	pro-opiomelanocortin-alpha	Mus musculus	0-4
17525-3	1977	Acute administration of THC or CBD, 10 mg/kg, evoked no detectable changes in cytochrome P-450 levels, but a significant decrease in those of cytochrome b5.	Cannabidiol	31-34	cytochrome b5 type A	Rattus norvegicus	142-155
17525-4	1977	Chronic administration of THC or CBD, 2 mg/kg, decreased levels of cytochrome P-450, whereas cytochrome b5 levels appeared normal.	Cannabidiol	33-36	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	67-83
33862125-10	2021	Intra-CA1 administration of sulpiride reversed the decreasing effects of cannabidiol on METH-induced CPP in both acquisition and expression phases but more prominent in the expression phase.	Cannabidiol	73-84	carbonic anhydrase 1	Rattus norvegicus	6-9
33852975-11	2021	C3D was more potent than C2D and C4D in inhibiting LPS-induced NO and mRNAs of iNOS and IL-1beta, which implies that the linker length is critical for CBD-DHA conjugates" anti-inflammatory activities.	Cannabidiol	151-154	secretoglobin, family 2B, member 26	Mus musculus	25-28
33887676-8	2021	Chronic seizures increased cannabinoid receptors type 1 (CB1R) immunostaining in the hippocampus and the BLA, while CBD administration prevented changes in CB1R expression induced by the AuK.	Cannabidiol	116-119	cannabinoid receptor 1	Homo sapiens	156-160
33887676-9	2021	The neuroethological analysis provided details about CBD"s protective effects against brainstem and limbic seizures associated with FosB expression.	Cannabidiol	53-56	FosB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	132-136
33887676-10	2021	Our results strongly suggest chronic CBD anticonvulsant and antiepileptogenic effects associated with reduced chronic neuronal activity and modulation of CB1R expression.	Cannabidiol	37-40	cannabinoid receptor 1	Homo sapiens	154-158
32440886-6	2021	Early treatment of EAE with oral CBD reduced clinical disease at the day 18 timepoint which correlated with a significant decrease in the percentage of MOG35-55 specific IFN-gamma producing CD8+ T cells in the spleen at day 10.	Cannabidiol	33-36	interferon gamma	Mus musculus	170-179
33722705-10	2021	On the other hand, AEA and CBD not only exhibited high anti-aromatase activity but also induced up-regulation of ERbeta.	Cannabidiol	27-30	estrogen receptor 1	Homo sapiens	113-119
33895057-0	2021	Corrigendum to "Cannabidiol inhibits febrile seizure by modulating AMPA receptor kinetics through its interaction with the N-terminal domain of GluA1/GluA2" [Pharmacol.	Cannabidiol	16-27	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	144-149
33895057-0	2021	Corrigendum to "Cannabidiol inhibits febrile seizure by modulating AMPA receptor kinetics through its interaction with the N-terminal domain of GluA1/GluA2" [Pharmacol.	Cannabidiol	16-27	glutamate ionotropic receptor AMPA type subunit 2	Homo sapiens	150-156
33635384-0	2021	Sleep-wake cycle disturbances and NeuN-altered expression in adult rats after cannabidiol treatments during adolescence.	Cannabidiol	78-89	RNA binding fox-1 homolog 3	Rattus norvegicus	34-38
33635384-9	2021	Finally, we determined how the chronic administrations of CBD during the adolescence affected in the adulthood the NeuN expression in the suprachiasmatic nucleus, a sleep-related brain region.	Cannabidiol	58-61	RNA binding fox-1 homolog 3	Rattus norvegicus	115-119
33955754-0	2021	Cannabidiol Protects Human Skin Keratinocytes from Hydrogen-Peroxide-Induced Oxidative Stress via Modulation of the Caspase-1-IL-1beta Axis.	Cannabidiol	0-11	caspase 1	Homo sapiens	116-125
33955754-0	2021	Cannabidiol Protects Human Skin Keratinocytes from Hydrogen-Peroxide-Induced Oxidative Stress via Modulation of the Caspase-1-IL-1beta Axis.	Cannabidiol	0-11	interleukin 1 alpha	Homo sapiens	126-134
33955754-5	2021	CBD treatment down-regulated the mRNA expression levels of CASP1 and IL1B (by 32.9 and 51.0%, respectively) and reduced IL-1beta level (by 16.2%) in H2O2-stimulated HaCaT cells.	Cannabidiol	0-3	caspase 1	Homo sapiens	59-64
33955754-5	2021	CBD treatment down-regulated the mRNA expression levels of CASP1 and IL1B (by 32.9 and 51.0%, respectively) and reduced IL-1beta level (by 16.2%) in H2O2-stimulated HaCaT cells.	Cannabidiol	0-3	interleukin 1 beta	Homo sapiens	69-73
33955754-5	2021	CBD treatment down-regulated the mRNA expression levels of CASP1 and IL1B (by 32.9 and 51.0%, respectively) and reduced IL-1beta level (by 16.2%) in H2O2-stimulated HaCaT cells.	Cannabidiol	0-3	interleukin 1 alpha	Homo sapiens	120-128
33955754-6	2021	Furthermore, CBD inhibited the activity of caspase-1 enzyme (by 15.7%) via direct binding to caspase-1 protein, which was supported by data from a biophysical binding assay (surface plasmon resonance) and a computational docking experiment.	Cannabidiol	13-16	caspase 1	Homo sapiens	43-52
33955754-6	2021	Furthermore, CBD inhibited the activity of caspase-1 enzyme (by 15.7%) via direct binding to caspase-1 protein, which was supported by data from a biophysical binding assay (surface plasmon resonance) and a computational docking experiment.	Cannabidiol	13-16	caspase 1	Homo sapiens	93-102
33955754-8	2021	The findings from the current study suggest that CBD exerts protective effects in human keratinocytes via the modulation of the caspase-1-IL-1beta axis, supporting its potential skin health applications.	Cannabidiol	49-52	caspase 1	Homo sapiens	128-137
33955754-8	2021	The findings from the current study suggest that CBD exerts protective effects in human keratinocytes via the modulation of the caspase-1-IL-1beta axis, supporting its potential skin health applications.	Cannabidiol	49-52	interleukin 1 alpha	Homo sapiens	138-146
34048863-0	2021	PPARgamma receptors are involved in the effects of cannabidiol on orofacial dyskinesia and cognitive dysfunction induced by typical antipsychotic in mice.	Cannabidiol	51-62	peroxisome proliferator activated receptor gamma	Mus musculus	0-9
34048863-4	2021	A previous study showed that cannabidiol (CBD), the major non-psychotomimetic compound of Cannabis sativa plant, prevents orofacial dyskinesia induced by typical antipsychotics by activating peroxisome proliferator-activated receptors gamma (PPARgamma).	Cannabidiol	29-40	peroxisome proliferator activated receptor gamma	Mus musculus	242-251
34048863-4	2021	A previous study showed that cannabidiol (CBD), the major non-psychotomimetic compound of Cannabis sativa plant, prevents orofacial dyskinesia induced by typical antipsychotics by activating peroxisome proliferator-activated receptors gamma (PPARgamma).	Cannabidiol	42-45	peroxisome proliferator activated receptor gamma	Mus musculus	242-251
34048863-11	2021	Pretreatment with the PPARgamma antagonist GW9662 (2 mg/kg/daily) blocked the behavioral effects of CBD.	Cannabidiol	100-103	peroxisome proliferator activated receptor gamma	Mus musculus	22-31
34019978-1	2021	Natural cannabidiol ((-)-CBD) and its derivatives have increased interest for medicinal applications due to their broad biological activity spectrum, including targeting of the cannabinoid receptors type 1 (CB1R) and type 2 (CB2R).	Cannabidiol	8-19	cannabinoid receptor 1 (brain)	Mus musculus	207-211
34019978-1	2021	Natural cannabidiol ((-)-CBD) and its derivatives have increased interest for medicinal applications due to their broad biological activity spectrum, including targeting of the cannabinoid receptors type 1 (CB1R) and type 2 (CB2R).	Cannabidiol	8-19	cannabinoid receptor 2 (macrophage)	Mus musculus	225-229
34019978-1	2021	Natural cannabidiol ((-)-CBD) and its derivatives have increased interest for medicinal applications due to their broad biological activity spectrum, including targeting of the cannabinoid receptors type 1 (CB1R) and type 2 (CB2R).	Cannabidiol	21-28	cannabinoid receptor 1 (brain)	Mus musculus	207-211
34019978-1	2021	Natural cannabidiol ((-)-CBD) and its derivatives have increased interest for medicinal applications due to their broad biological activity spectrum, including targeting of the cannabinoid receptors type 1 (CB1R) and type 2 (CB2R).	Cannabidiol	21-28	cannabinoid receptor 2 (macrophage)	Mus musculus	225-229
34019978-2	2021	Herein, we synthesized the (+)-enantiomer of CBD and its derivative (+)-CBD hydroxypentylester ((+)-CBD-HPE) that showed enhanced CB1R and CB2R binding and functional activities compared to their respective (-) enantiomers.	Cannabidiol	45-48	cannabinoid receptor 1 (brain)	Mus musculus	130-134
34019978-2	2021	Herein, we synthesized the (+)-enantiomer of CBD and its derivative (+)-CBD hydroxypentylester ((+)-CBD-HPE) that showed enhanced CB1R and CB2R binding and functional activities compared to their respective (-) enantiomers.	Cannabidiol	45-48	cannabinoid receptor 2 (macrophage)	Mus musculus	139-143
34019978-2	2021	Herein, we synthesized the (+)-enantiomer of CBD and its derivative (+)-CBD hydroxypentylester ((+)-CBD-HPE) that showed enhanced CB1R and CB2R binding and functional activities compared to their respective (-) enantiomers.	Cannabidiol	72-75	cannabinoid receptor 1 (brain)	Mus musculus	130-134
34019978-2	2021	Herein, we synthesized the (+)-enantiomer of CBD and its derivative (+)-CBD hydroxypentylester ((+)-CBD-HPE) that showed enhanced CB1R and CB2R binding and functional activities compared to their respective (-) enantiomers.	Cannabidiol	72-75	cannabinoid receptor 2 (macrophage)	Mus musculus	139-143
34019978-2	2021	Herein, we synthesized the (+)-enantiomer of CBD and its derivative (+)-CBD hydroxypentylester ((+)-CBD-HPE) that showed enhanced CB1R and CB2R binding and functional activities compared to their respective (-) enantiomers.	Cannabidiol	72-75	cannabinoid receptor 1 (brain)	Mus musculus	130-134
34019978-2	2021	Herein, we synthesized the (+)-enantiomer of CBD and its derivative (+)-CBD hydroxypentylester ((+)-CBD-HPE) that showed enhanced CB1R and CB2R binding and functional activities compared to their respective (-) enantiomers.	Cannabidiol	72-75	cannabinoid receptor 2 (macrophage)	Mus musculus	139-143
34019978-3	2021	(+)-CBD-HPE Ki values for CB1R and CB2R were 3.1 +- 1.1 and 0.8 +- 0.1nM respectively acting as CB1R antagonist and CB2R agonist.	Cannabidiol	4-7	cannabinoid receptor 1 (brain)	Mus musculus	26-30
34019978-3	2021	(+)-CBD-HPE Ki values for CB1R and CB2R were 3.1 +- 1.1 and 0.8 +- 0.1nM respectively acting as CB1R antagonist and CB2R agonist.	Cannabidiol	4-7	cannabinoid receptor 2 (macrophage)	Mus musculus	35-39
34019978-3	2021	(+)-CBD-HPE Ki values for CB1R and CB2R were 3.1 +- 1.1 and 0.8 +- 0.1nM respectively acting as CB1R antagonist and CB2R agonist.	Cannabidiol	4-7	cannabinoid receptor 1 (brain)	Mus musculus	96-100
34019978-3	2021	(+)-CBD-HPE Ki values for CB1R and CB2R were 3.1 +- 1.1 and 0.8 +- 0.1nM respectively acting as CB1R antagonist and CB2R agonist.	Cannabidiol	4-7	cannabinoid receptor 2 (macrophage)	Mus musculus	116-120
34019978-6	2021	(+)-CBD-HPE significantly reduced activation of NF-kappaB by phosphorylation by 15% compared to STZ-vehicle mice, and CD3+ T cell infiltration into the islets was avoided.	Cannabidiol	4-7	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	48-57
33993443-5	2021	To find out the impact of D1-like dopamine receptor antagonist, SCH23390, in the CA1 on the inhibitory influence of CBD on the acquisition of METH, the rats received intra-CA1 administration of SCH23390 (0.25, 1, and 4 microg/0.5 microl) following ICV treatment of CBD (10 microg/5 microl) over conditioning phase of METH.	Cannabidiol	116-119	carbonic anhydrase 1	Rattus norvegicus	81-84
33993443-7	2021	Intra-CA1 microinjection of SCH23390 abolished CBD"s suppressive impact on both METH-induced CPP phases without any side effect on the locomotion.	Cannabidiol	47-50	carbonic anhydrase 1	Rattus norvegicus	6-9
33993443-8	2021	The current research disclosed that CBD inhibited the rewarding characteristic of METH via D1-like dopamine receptors in the CA1 region of the hippocampus.	Cannabidiol	36-39	carbonic anhydrase 1	Rattus norvegicus	125-128
33984046-5	2021	We also investigated whether the effect of CBD on cytokine release is mediated by the G protein coupled receptor 3 (GPR3), which was recently identified as a novel receptor for CBD.	Cannabidiol	43-46	G-protein coupled receptor 3	Mus musculus	86-114
33984046-5	2021	We also investigated whether the effect of CBD on cytokine release is mediated by the G protein coupled receptor 3 (GPR3), which was recently identified as a novel receptor for CBD.	Cannabidiol	43-46	G-protein coupled receptor 3	Mus musculus	116-120
33984046-5	2021	We also investigated whether the effect of CBD on cytokine release is mediated by the G protein coupled receptor 3 (GPR3), which was recently identified as a novel receptor for CBD.	Cannabidiol	177-180	G-protein coupled receptor 3	Mus musculus	86-114
33984046-5	2021	We also investigated whether the effect of CBD on cytokine release is mediated by the G protein coupled receptor 3 (GPR3), which was recently identified as a novel receptor for CBD.	Cannabidiol	177-180	G-protein coupled receptor 3	Mus musculus	116-120
33984046-6	2021	Our results showed that CBD inhibited inflammatory responses of astrocytes and microglia stimulated with lipopolysaccharide (LPS), a Toll-like receptor 4 (TLR4) ligand in vitro and in vivo.	Cannabidiol	24-27	toll-like receptor 4	Mus musculus	133-153
33984046-6	2021	Our results showed that CBD inhibited inflammatory responses of astrocytes and microglia stimulated with lipopolysaccharide (LPS), a Toll-like receptor 4 (TLR4) ligand in vitro and in vivo.	Cannabidiol	24-27	toll-like receptor 4	Mus musculus	155-159
33951339-0	2021	A Phase 1 Open-Label, Fixed-Sequence Pharmacokinetic Drug Interaction Trial to Investigate the Effect of Cannabidiol on the CYP1A2 Probe Caffeine in Healthy Subjects.	Cannabidiol	105-116	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	124-130
33998900-7	2021	Results: Tumor necrosis factor alpha, interleukin (IL)-1beta, IL-6, and interferon gamma were the most commonly studied pro-inflammatory cytokines and their levels were consistently reduced after treatment with CBD, CBG, or CBD+THC, but not with THC alone.	Cannabidiol	224-227	tumor necrosis factor	Homo sapiens	9-36
33904801-11	2021	Within each CBD dose group, repeated administration increased total systemic exposure to CBD 1.6- to 3.3-fold.	Cannabidiol	12-15	defensin beta 1	Canis lupus familiaris	89-94
33022751-3	2021	Sixteen healthy adults were enrolled in a phase 1, open-label, fixed single-sequence drug-drug interaction trial to investigate the effect of repeated dose administration of CBD (1500 mg/day) on cytochrome P450 (CYP) 1A2 activity.	Cannabidiol	174-177	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	195-220
33658314-0	2021	CANNABIDIOL ENHANCES INTESTINAL CB2 RECEPTOR EXPRESSION AND ACTIVATION INCREASING REGULATORY T CELLS AND REDUCES MURINE ACUTE GRAFT-VERSUS-HOST DISEASE WITHOUT INTERFERING WITH THE GRAFT-VERSUS-LEUKEMIA RESPONSE.	Cannabidiol	0-11	cannabinoid receptor 2 (macrophage)	Mus musculus	32-35
33658314-5	2021	Analysis of the jejunum and ileum showed that CBD treatment reduced the levels of CCL2, CCL3, CCL5, TNF-alpha, and IFN-gamma.	Cannabidiol	46-49	chemokine (C-C motif) ligand 2	Mus musculus	82-86
33658314-5	2021	Analysis of the jejunum and ileum showed that CBD treatment reduced the levels of CCL2, CCL3, CCL5, TNF-alpha, and IFN-gamma.	Cannabidiol	46-49	chemokine (C-C motif) ligand 3	Mus musculus	88-92
33658314-5	2021	Analysis of the jejunum and ileum showed that CBD treatment reduced the levels of CCL2, CCL3, CCL5, TNF-alpha, and IFN-gamma.	Cannabidiol	46-49	chemokine (C-C motif) ligand 5	Mus musculus	94-98
33658314-5	2021	Analysis of the jejunum and ileum showed that CBD treatment reduced the levels of CCL2, CCL3, CCL5, TNF-alpha, and IFN-gamma.	Cannabidiol	46-49	tumor necrosis factor	Mus musculus	100-109
33658314-5	2021	Analysis of the jejunum and ileum showed that CBD treatment reduced the levels of CCL2, CCL3, CCL5, TNF-alpha, and IFN-gamma.	Cannabidiol	46-49	interferon gamma	Mus musculus	115-124
33658314-8	2021	Antagonists of the CB2 receptor reduced the survival rates of CBD-treated mice, suggesting the participation of this receptor in the effects of CBD.	Cannabidiol	62-65	cannabinoid receptor 2 (macrophage)	Mus musculus	19-22
33658314-8	2021	Antagonists of the CB2 receptor reduced the survival rates of CBD-treated mice, suggesting the participation of this receptor in the effects of CBD.	Cannabidiol	144-147	cannabinoid receptor 2 (macrophage)	Mus musculus	19-22
33521943-9	2021	Only cannabidiolic acid synthase (CBDAS) was expressed in CBD-type Cannabis, while both CBDAS and THCAS were expressed in a cultivar with an intermediate THC:CBD ratio.	Cannabidiol	34-37	cannabidiolic acid synthase	Cannabis sativa	5-32
33998900-7	2021	Results: Tumor necrosis factor alpha, interleukin (IL)-1beta, IL-6, and interferon gamma were the most commonly studied pro-inflammatory cytokines and their levels were consistently reduced after treatment with CBD, CBG, or CBD+THC, but not with THC alone.	Cannabidiol	211-214	tumor necrosis factor	Homo sapiens	9-36
33998900-7	2021	Results: Tumor necrosis factor alpha, interleukin (IL)-1beta, IL-6, and interferon gamma were the most commonly studied pro-inflammatory cytokines and their levels were consistently reduced after treatment with CBD, CBG, or CBD+THC, but not with THC alone.	Cannabidiol	211-214	interleukin 1 alpha	Homo sapiens	38-60
33998900-7	2021	Results: Tumor necrosis factor alpha, interleukin (IL)-1beta, IL-6, and interferon gamma were the most commonly studied pro-inflammatory cytokines and their levels were consistently reduced after treatment with CBD, CBG, or CBD+THC, but not with THC alone.	Cannabidiol	211-214	interleukin 6	Homo sapiens	62-66
33998900-7	2021	Results: Tumor necrosis factor alpha, interleukin (IL)-1beta, IL-6, and interferon gamma were the most commonly studied pro-inflammatory cytokines and their levels were consistently reduced after treatment with CBD, CBG, or CBD+THC, but not with THC alone.	Cannabidiol	211-214	interferon gamma	Homo sapiens	72-88
33998900-7	2021	Results: Tumor necrosis factor alpha, interleukin (IL)-1beta, IL-6, and interferon gamma were the most commonly studied pro-inflammatory cytokines and their levels were consistently reduced after treatment with CBD, CBG, or CBD+THC, but not with THC alone.	Cannabidiol	224-227	interleukin 1 alpha	Homo sapiens	38-60
33998900-7	2021	Results: Tumor necrosis factor alpha, interleukin (IL)-1beta, IL-6, and interferon gamma were the most commonly studied pro-inflammatory cytokines and their levels were consistently reduced after treatment with CBD, CBG, or CBD+THC, but not with THC alone.	Cannabidiol	224-227	interferon gamma	Homo sapiens	72-88
33571569-0	2021	Cannabidiol efficiently suppressed the acquisition and expression of methamphetamine-induced conditioned place preference in the rat.	Cannabidiol	0-11	MET proto-oncogene, receptor tyrosine kinase	Rattus norvegicus	69-84
33922473-9	2021	We have also found that the presence of a complete N-terminal domain is essential for a stable binding of CBD in the allosteric site of CB1R as well as for the allosteric-orthosteric coupling mechanism.	Cannabidiol	106-109	cannabinoid receptor 1	Homo sapiens	136-140
33892503-7	2021	Conversely, the cnr1-/- larvae were more resistant to CBD-induced malformations, mortality, and behavioral alteration implicating Cnr1 in CBD-mediated toxicity.	Cannabidiol	54-57	cannabinoid receptor 1	Danio rerio	16-20
33892503-7	2021	Conversely, the cnr1-/- larvae were more resistant to CBD-induced malformations, mortality, and behavioral alteration implicating Cnr1 in CBD-mediated toxicity.	Cannabidiol	54-57	cannabinoid receptor 1	Danio rerio	130-134
33892503-7	2021	Conversely, the cnr1-/- larvae were more resistant to CBD-induced malformations, mortality, and behavioral alteration implicating Cnr1 in CBD-mediated toxicity.	Cannabidiol	138-141	cannabinoid receptor 1	Danio rerio	16-20
33892503-7	2021	Conversely, the cnr1-/- larvae were more resistant to CBD-induced malformations, mortality, and behavioral alteration implicating Cnr1 in CBD-mediated toxicity.	Cannabidiol	138-141	cannabinoid receptor 1	Danio rerio	130-134
33892503-9	2021	Co-exposure to the PPARgamma inhibitor GW9662 and CBD in cnr+/+ and cnr2-/- strains caused more adverse outcomes compared to CBD alone, but not in the cnr1-/- fish, suggesting that PPARgamma plays a role in CBD metabolism downstream of Cnr1.	Cannabidiol	50-53	cannabinoid receptor 2	Danio rerio	68-72
33892503-9	2021	Co-exposure to the PPARgamma inhibitor GW9662 and CBD in cnr+/+ and cnr2-/- strains caused more adverse outcomes compared to CBD alone, but not in the cnr1-/- fish, suggesting that PPARgamma plays a role in CBD metabolism downstream of Cnr1.	Cannabidiol	50-53	cannabinoid receptor 1	Danio rerio	236-240
33864076-0	2021	Cannabidiol converts NFkappaB into a tumor suppressor in glioblastoma with defined antioxidative properties.	Cannabidiol	0-11	nuclear factor kappa B subunit 1	Homo sapiens	21-29
33864076-3	2021	METHODS: In a pharmacogenomics study with a panel of transgenic glioma cells we observed that NFkappaB can be converted into a tumor suppressor by the non-psychotropic cannabinoid Cannabidiol (CBD).	Cannabidiol	180-191	nuclear factor kappa B subunit 1	Homo sapiens	94-102
33864076-3	2021	METHODS: In a pharmacogenomics study with a panel of transgenic glioma cells we observed that NFkappaB can be converted into a tumor suppressor by the non-psychotropic cannabinoid Cannabidiol (CBD).	Cannabidiol	193-196	nuclear factor kappa B subunit 1	Homo sapiens	94-102
33864076-7	2021	RESULTS: We found that CBD promotes DNA binding of the NFkappaB subunit RELA and simultaneously prevents RELA-phosphorylation on serine-311, a key residue which permits genetic transactivation.	Cannabidiol	23-26	nuclear factor kappa B subunit 1	Homo sapiens	55-63
33872753-11	2021	RT-PCR revealed CBD-induced increased the expression of angiogenic and odontogenic genes, such as DSPP, DMP-1, OPN, ALP, Runx2, VEGFR1 and ICAM-1.	Cannabidiol	16-19	dentin sialophosphoprotein	Homo sapiens	98-102
33872753-11	2021	RT-PCR revealed CBD-induced increased the expression of angiogenic and odontogenic genes, such as DSPP, DMP-1, OPN, ALP, Runx2, VEGFR1 and ICAM-1.	Cannabidiol	16-19	dentin matrix acidic phosphoprotein 1	Homo sapiens	104-109
33872753-11	2021	RT-PCR revealed CBD-induced increased the expression of angiogenic and odontogenic genes, such as DSPP, DMP-1, OPN, ALP, Runx2, VEGFR1 and ICAM-1.	Cannabidiol	16-19	secreted phosphoprotein 1	Homo sapiens	111-114
33872753-11	2021	RT-PCR revealed CBD-induced increased the expression of angiogenic and odontogenic genes, such as DSPP, DMP-1, OPN, ALP, Runx2, VEGFR1 and ICAM-1.	Cannabidiol	16-19	ATHS	Homo sapiens	116-119
33872753-11	2021	RT-PCR revealed CBD-induced increased the expression of angiogenic and odontogenic genes, such as DSPP, DMP-1, OPN, ALP, Runx2, VEGFR1 and ICAM-1.	Cannabidiol	16-19	RUNX family transcription factor 2	Homo sapiens	121-126
33872753-11	2021	RT-PCR revealed CBD-induced increased the expression of angiogenic and odontogenic genes, such as DSPP, DMP-1, OPN, ALP, Runx2, VEGFR1 and ICAM-1.	Cannabidiol	16-19	fms related receptor tyrosine kinase 1	Homo sapiens	128-134
33872753-11	2021	RT-PCR revealed CBD-induced increased the expression of angiogenic and odontogenic genes, such as DSPP, DMP-1, OPN, ALP, Runx2, VEGFR1 and ICAM-1.	Cannabidiol	16-19	intercellular adhesion molecule 1	Homo sapiens	139-145
33854029-3	2021	CASE REPORT We present a 20-year-old patient who worked at a cannabidiol (CBD) manufacturing facility with a history of e-cigarette use and polysubstance abuse in remission who presented with respiratory and gastrointestinal symptoms accompanied by 50-pound weight loss over 6 months.	Cannabidiol	61-72	immunoglobulin kappa variable 1-27	Homo sapiens	23-27
33854029-3	2021	CASE REPORT We present a 20-year-old patient who worked at a cannabidiol (CBD) manufacturing facility with a history of e-cigarette use and polysubstance abuse in remission who presented with respiratory and gastrointestinal symptoms accompanied by 50-pound weight loss over 6 months.	Cannabidiol	74-77	immunoglobulin kappa variable 1-27	Homo sapiens	23-27
33912679-1	2021	Background: We previously reported that cannabidiol (CBD), a cannabinoid with a low toxicity profile, downregulated the expression of the prometastatic gene inhibitor of DNA binding 1 (ID1) in cancer cells, leading to inhibition of tumor progression in vivo.	Cannabidiol	40-51	inhibitor of DNA binding 1, HLH protein	Homo sapiens	185-188
33912679-1	2021	Background: We previously reported that cannabidiol (CBD), a cannabinoid with a low toxicity profile, downregulated the expression of the prometastatic gene inhibitor of DNA binding 1 (ID1) in cancer cells, leading to inhibition of tumor progression in vivo.	Cannabidiol	53-56	inhibitor of DNA binding 1, HLH protein	Homo sapiens	185-188
33477086-12	2021	The VIP plots of all models demonstrated that the THC and CBD distinctive band regions bared the highest importance for predicting the content of the molecules of interest in the respected PLS models.	Cannabidiol	58-61	vasoactive intestinal peptide	Homo sapiens	4-7
33477086-14	2021	Taking into account the presented results, ATR-MIR should be considered as a promising PAT tool for THC and CBD content estimation, in terms of critical material and quality parameters for Cannabis flowers and extracts.	Cannabidiol	108-111	ATR serine/threonine kinase	Homo sapiens	43-46
33848261-0	2021	Potential role of cannabidiol in Parkinson"s disease by targeting the WNT/beta-catenin pathway, oxidative stress and inflammation.	Cannabidiol	18-29	catenin beta 1	Homo sapiens	74-86
33927630-12	2021	The possible interventions by curcumin, resveratrol, cannabidiol, ginsenosides, flavonoids and sulforaphane on microglia specific protein Iba1 suggest possibility of natural products mediated regulation of microglia phenotypes and its functions to control redox imbalance and neuroinflammation in management of Alzheimer"s, Parkinson"s and Multiple Sclerosis for microglia-mediated therapeutics.	Cannabidiol	53-64	allograft inflammatory factor 1	Homo sapiens	138-142
33837269-0	2022	Possible actions of cannabidiol in obsessive-compulsive disorder by targeting the WNT/beta-catenin pathway.	Cannabidiol	20-31	catenin beta 1	Homo sapiens	86-98
33595947-8	2021	METHODS: PTH(7-33)-CBD (1000 microg/kg, subcutaneous) or vehicle was administered 24 h prior to MDA-MB-231 breast cancer cell inoculation into the tibia marrow.	Cannabidiol	19-22	parathyroid hormone	Homo sapiens	9-12
33464458-12	2021	The previous treatment with the antagonists - 5-HT1A, CB1, or CB2 - blocked the CBD-induced antidepressant-like effect whereas only the blockade of 5-HT1A or CB1 receptors was able to inhibit the CBD-induced anxiolytic-like effect.	Cannabidiol	80-83	5-hydroxytryptamine receptor 1A	Rattus norvegicus	46-52
33464458-12	2021	The previous treatment with the antagonists - 5-HT1A, CB1, or CB2 - blocked the CBD-induced antidepressant-like effect whereas only the blockade of 5-HT1A or CB1 receptors was able to inhibit the CBD-induced anxiolytic-like effect.	Cannabidiol	80-83	cannabinoid receptor 1	Rattus norvegicus	54-57
33464458-12	2021	The previous treatment with the antagonists - 5-HT1A, CB1, or CB2 - blocked the CBD-induced antidepressant-like effect whereas only the blockade of 5-HT1A or CB1 receptors was able to inhibit the CBD-induced anxiolytic-like effect.	Cannabidiol	80-83	cannabinoid receptor 2	Rattus norvegicus	62-65
33464458-12	2021	The previous treatment with the antagonists - 5-HT1A, CB1, or CB2 - blocked the CBD-induced antidepressant-like effect whereas only the blockade of 5-HT1A or CB1 receptors was able to inhibit the CBD-induced anxiolytic-like effect.	Cannabidiol	80-83	cannabinoid receptor 1	Rattus norvegicus	158-161
33464458-12	2021	The previous treatment with the antagonists - 5-HT1A, CB1, or CB2 - blocked the CBD-induced antidepressant-like effect whereas only the blockade of 5-HT1A or CB1 receptors was able to inhibit the CBD-induced anxiolytic-like effect.	Cannabidiol	196-199	5-hydroxytryptamine receptor 1A	Rattus norvegicus	46-52
33464458-12	2021	The previous treatment with the antagonists - 5-HT1A, CB1, or CB2 - blocked the CBD-induced antidepressant-like effect whereas only the blockade of 5-HT1A or CB1 receptors was able to inhibit the CBD-induced anxiolytic-like effect.	Cannabidiol	196-199	cannabinoid receptor 1	Rattus norvegicus	54-57
33464458-12	2021	The previous treatment with the antagonists - 5-HT1A, CB1, or CB2 - blocked the CBD-induced antidepressant-like effect whereas only the blockade of 5-HT1A or CB1 receptors was able to inhibit the CBD-induced anxiolytic-like effect.	Cannabidiol	196-199	cannabinoid receptor 2	Rattus norvegicus	62-65
33464458-12	2021	The previous treatment with the antagonists - 5-HT1A, CB1, or CB2 - blocked the CBD-induced antidepressant-like effect whereas only the blockade of 5-HT1A or CB1 receptors was able to inhibit the CBD-induced anxiolytic-like effect.	Cannabidiol	196-199	5-hydroxytryptamine receptor 1A	Rattus norvegicus	148-154
33464458-12	2021	The previous treatment with the antagonists - 5-HT1A, CB1, or CB2 - blocked the CBD-induced antidepressant-like effect whereas only the blockade of 5-HT1A or CB1 receptors was able to inhibit the CBD-induced anxiolytic-like effect.	Cannabidiol	196-199	cannabinoid receptor 1	Rattus norvegicus	158-161
33464458-13	2021	Regarding glycemic control, only the blockade of CB2 was able to inhibit the beneficial effect of CBD in reducing the glycemia of diabetic animals.	Cannabidiol	98-101	cannabinoid receptor 2	Rattus norvegicus	49-52
33998893-5	2021	Relative to the LPS-activated and untreated control (M[LPS]), both 25 muM CBD and 10 muM Dex reduced expression of pro-inflammatory markers-tumor necrosis factor alpha, interleukin 1 beta, and regulated on activation, normal T cell expressed and secreted (RANTES)-as well as the pleiotropic marker interleukin-6 (IL-6).	Cannabidiol	74-77	tumor necrosis factor	Homo sapiens	140-167
33859553-0	2021	Cannabidiol Induces Autophagy to Protects Neural Cells From Mitochondrial Dysfunction by Upregulating SIRT1 to Inhibits NF-kappaB and NOTCH Pathways.	Cannabidiol	0-11	sirtuin 1	Homo sapiens	102-107
33859553-8	2021	Cannabidiol alleviated loss of TH expression and cytotoxicity in the MPP+-induced SH-SY5Y cells.	Cannabidiol	0-11	tyrosine hydroxylase	Homo sapiens	31-33
33859553-9	2021	Further mechanistic investigation showed that Cannabidiol induced SH-SY5Y cells autophagy to protects cells from mitochondrial dysfunction by upregulating SIRT1 to Inhibits NF-kappaB and NOTCH Pathways.	Cannabidiol	46-57	sirtuin 1	Homo sapiens	155-160
33998893-5	2021	Relative to the LPS-activated and untreated control (M[LPS]), both 25 muM CBD and 10 muM Dex reduced expression of pro-inflammatory markers-tumor necrosis factor alpha, interleukin 1 beta, and regulated on activation, normal T cell expressed and secreted (RANTES)-as well as the pleiotropic marker interleukin-6 (IL-6).	Cannabidiol	74-77	interleukin 1 beta	Homo sapiens	169-187
33998893-5	2021	Relative to the LPS-activated and untreated control (M[LPS]), both 25 muM CBD and 10 muM Dex reduced expression of pro-inflammatory markers-tumor necrosis factor alpha, interleukin 1 beta, and regulated on activation, normal T cell expressed and secreted (RANTES)-as well as the pleiotropic marker interleukin-6 (IL-6).	Cannabidiol	74-77	C-C motif chemokine ligand 5	Homo sapiens	256-262
33998893-5	2021	Relative to the LPS-activated and untreated control (M[LPS]), both 25 muM CBD and 10 muM Dex reduced expression of pro-inflammatory markers-tumor necrosis factor alpha, interleukin 1 beta, and regulated on activation, normal T cell expressed and secreted (RANTES)-as well as the pleiotropic marker interleukin-6 (IL-6).	Cannabidiol	74-77	interleukin 6	Homo sapiens	298-311
33998893-5	2021	Relative to the LPS-activated and untreated control (M[LPS]), both 25 muM CBD and 10 muM Dex reduced expression of pro-inflammatory markers-tumor necrosis factor alpha, interleukin 1 beta, and regulated on activation, normal T cell expressed and secreted (RANTES)-as well as the pleiotropic marker interleukin-6 (IL-6).	Cannabidiol	74-77	interleukin 6	Homo sapiens	313-317
33998893-8	2021	The anti-inflammatory capacity of 25 muM CBD was concurrent with reduction in levels of phosphorylated mammalian target of rapamycin Ser 2448, endothelial nitric oxide synthase, and induction of cyclooxygenase 2 relative to M(LPS).	Cannabidiol	41-44	nitric oxide synthase 3	Homo sapiens	143-176
33998893-8	2021	The anti-inflammatory capacity of 25 muM CBD was concurrent with reduction in levels of phosphorylated mammalian target of rapamycin Ser 2448, endothelial nitric oxide synthase, and induction of cyclooxygenase 2 relative to M(LPS).	Cannabidiol	41-44	prostaglandin-endoperoxide synthase 2	Homo sapiens	195-211
33754154-10	2022	Moreover, we were able to quantify CBD-gluc and showed that 7-CBD-COOH, 7-hydroxy-CBD and CBD-gluc are the major CBD metabolites in human plasma.	Cannabidiol	35-38	glucosylceramidase beta 3 (gene/pseudogene)	Homo sapiens	39-43
33686185-0	2021	Cannabidiol induces autophagy via ERK1/2 activation in neural cells.	Cannabidiol	0-11	mitogen-activated protein kinase 3	Homo sapiens	34-40
33754154-3	2022	METHODS: CBD-glucuronide (CBD-gluc) standard was produced in-house by isolation of CBD-gluc from urine of patients using pure CBD oil.	Cannabidiol	9-12	glucosylceramidase beta 3 (gene/pseudogene)	Homo sapiens	13-17
33754154-3	2022	METHODS: CBD-glucuronide (CBD-gluc) standard was produced in-house by isolation of CBD-gluc from urine of patients using pure CBD oil.	Cannabidiol	9-12	glucosylceramidase beta 3 (gene/pseudogene)	Homo sapiens	30-34
33657198-8	2021	Anticancer effects of CBD/Mg-GA include a significant increase in ROS production and a reduction in anti-inflammatory responses as reflected by a significant decrease in TNF-alpha expression levels.	Cannabidiol	22-25	tumor necrosis factor	Homo sapiens	170-179
33686185-6	2021	We found that CBD-induced autophagy was substantially reduced in the presence of CB1, CB2 and TRPV1 receptor antagonists, AM 251, AM 630 and capsazepine, respectively.	Cannabidiol	14-17	cannabinoid receptor 1	Homo sapiens	81-84
33686185-6	2021	We found that CBD-induced autophagy was substantially reduced in the presence of CB1, CB2 and TRPV1 receptor antagonists, AM 251, AM 630 and capsazepine, respectively.	Cannabidiol	14-17	cannabinoid receptor 2	Homo sapiens	86-89
33686185-6	2021	We found that CBD-induced autophagy was substantially reduced in the presence of CB1, CB2 and TRPV1 receptor antagonists, AM 251, AM 630 and capsazepine, respectively.	Cannabidiol	14-17	transient receptor potential cation channel subfamily V member 1	Homo sapiens	94-99
33686185-8	2021	Additionally, we demonstrated that CBD activates autophagy through ERK1/2 activation and AKT suppression.	Cannabidiol	35-38	mitogen-activated protein kinase 3	Homo sapiens	67-73
33686185-8	2021	Additionally, we demonstrated that CBD activates autophagy through ERK1/2 activation and AKT suppression.	Cannabidiol	35-38	AKT serine/threonine kinase 1	Homo sapiens	89-92
33686185-9	2021	Interestingly, CBD-mediated autophagy activation is dependent on the autophagy initiator ULK1, but mTORC1 independent.	Cannabidiol	15-18	unc-51 like autophagy activating kinase 1	Homo sapiens	89-93
33686185-11	2021	Our findings collectively provide evidence that CBD stimulates autophagy signal transduction via crosstalk between the ERK1/2 and AKT kinases, which represent putative regulators of cell proliferation and survival.	Cannabidiol	48-51	mitogen-activated protein kinase 3	Homo sapiens	119-125
33686185-11	2021	Our findings collectively provide evidence that CBD stimulates autophagy signal transduction via crosstalk between the ERK1/2 and AKT kinases, which represent putative regulators of cell proliferation and survival.	Cannabidiol	48-51	AKT serine/threonine kinase 1	Homo sapiens	130-133
33513342-12	2021	Our results demonstrate that CBD produced antidepressant-like effects in the LPS neuroinflammatory model, associated to a reduction in the kynurenine pathway activation, IL-6 levels and NF-kB activation.	Cannabidiol	29-32	interleukin 6	Mus musculus	170-174
33347604-1	2021	BACKGROUND AND PURPOSE: Cannabidiol (CBD) has been shown to differentially regulate the mechanistic target of rapamycin complex 1 (mTORC1) in preclinical models of disease, where it reduces activity in models of epilepsies and cancer and increases it in models of multiple sclerosis (MS) and psychosis.	Cannabidiol	24-35	CREB regulated transcription coactivator 1	Mus musculus	131-137
33347604-1	2021	BACKGROUND AND PURPOSE: Cannabidiol (CBD) has been shown to differentially regulate the mechanistic target of rapamycin complex 1 (mTORC1) in preclinical models of disease, where it reduces activity in models of epilepsies and cancer and increases it in models of multiple sclerosis (MS) and psychosis.	Cannabidiol	37-40	CREB regulated transcription coactivator 1	Mus musculus	131-137
33347604-6	2021	KEY RESULTS: Both CBD and the more abundant cannabigerol (CBG) enhance mTORC1 activity in D. discoideum.	Cannabidiol	18-21	CREB regulated transcription coactivator 1	Mus musculus	71-77
33347604-9	2021	Clinical relevance of this effect was shown in primary human peripheral blood mononuclear cells, where CBD and CBG treatment increased mTORC1 activity in cells derived from healthy individuals and decreased mTORC1 activity in cells derived from pwMS.	Cannabidiol	103-106	CREB regulated transcription coactivator 1	Mus musculus	135-141
33347604-9	2021	Clinical relevance of this effect was shown in primary human peripheral blood mononuclear cells, where CBD and CBG treatment increased mTORC1 activity in cells derived from healthy individuals and decreased mTORC1 activity in cells derived from pwMS.	Cannabidiol	103-106	CREB regulated transcription coactivator 1	Mus musculus	207-213
33347604-10	2021	CONCLUSION AND IMPLICATIONS: Our findings suggest that both CBD and the abundant CBG differentially regulate mTORC1 signalling through a mechanism dependent on the activity of the upstream IPMK signalling pathway, with potential relevance to the treatment of mTOR-related disorders, including MS.	Cannabidiol	60-63	CREB regulated transcription coactivator 1	Mus musculus	109-115
33347604-10	2021	CONCLUSION AND IMPLICATIONS: Our findings suggest that both CBD and the abundant CBG differentially regulate mTORC1 signalling through a mechanism dependent on the activity of the upstream IPMK signalling pathway, with potential relevance to the treatment of mTOR-related disorders, including MS.	Cannabidiol	60-63	inositol polyphosphate multikinase	Homo sapiens	189-193
33347604-10	2021	CONCLUSION AND IMPLICATIONS: Our findings suggest that both CBD and the abundant CBG differentially regulate mTORC1 signalling through a mechanism dependent on the activity of the upstream IPMK signalling pathway, with potential relevance to the treatment of mTOR-related disorders, including MS.	Cannabidiol	60-63	mechanistic target of rapamycin kinase	Homo sapiens	109-113
33522084-7	2021	The anxiolytic-like effects of CBD in BCCAO mice were attenuated by CB1 , CB2 , 5-HT1A , and PPAR-gamma receptor antagonists.	Cannabidiol	31-34	cannabinoid receptor 1 (brain)	Mus musculus	68-71
33522084-7	2021	The anxiolytic-like effects of CBD in BCCAO mice were attenuated by CB1 , CB2 , 5-HT1A , and PPAR-gamma receptor antagonists.	Cannabidiol	31-34	cannabinoid receptor 2 (macrophage)	Mus musculus	74-77
33522084-7	2021	The anxiolytic-like effects of CBD in BCCAO mice were attenuated by CB1 , CB2 , 5-HT1A , and PPAR-gamma receptor antagonists.	Cannabidiol	31-34	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	80-86
33522084-7	2021	The anxiolytic-like effects of CBD in BCCAO mice were attenuated by CB1 , CB2 , 5-HT1A , and PPAR-gamma receptor antagonists.	Cannabidiol	31-34	peroxisome proliferator activated receptor gamma	Mus musculus	93-103
33522084-9	2021	Together, these findings indicate the involvement of CB1 , CB2 , 5-HT1A, and PPAR-gamma receptors in the functional recovery induced by CBD in BCCAO mice.	Cannabidiol	136-139	cannabinoid receptor 1 (brain)	Mus musculus	53-56
33522084-9	2021	Together, these findings indicate the involvement of CB1 , CB2 , 5-HT1A, and PPAR-gamma receptors in the functional recovery induced by CBD in BCCAO mice.	Cannabidiol	136-139	cannabinoid receptor 2 (macrophage)	Mus musculus	59-62
33522084-9	2021	Together, these findings indicate the involvement of CB1 , CB2 , 5-HT1A, and PPAR-gamma receptors in the functional recovery induced by CBD in BCCAO mice.	Cannabidiol	136-139	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	65-71
33522084-9	2021	Together, these findings indicate the involvement of CB1 , CB2 , 5-HT1A, and PPAR-gamma receptors in the functional recovery induced by CBD in BCCAO mice.	Cannabidiol	136-139	peroxisome proliferator activated receptor gamma	Mus musculus	77-87
33629929-6	2021	Mechanistically, calcium flux induced by CBD through TRPV4 (transient receptor potential cation channel subfamily V member 4) activation played a key role in mitophagy initiation.	Cannabidiol	41-44	transient receptor potential cation channel subfamily V member 4	Homo sapiens	53-58
33629929-0	2021	Cannabidiol inhibits human glioma by induction of lethal mitophagy through activating TRPV4.	Cannabidiol	0-11	transient receptor potential cation channel subfamily V member 4	Homo sapiens	86-91
33604949-8	2022	This study proposed that cannabidiol (CBD) mechanism that occurred through the influx of Ca2+ via the TRPV1 receptor, and increasing ROS production affects protein folding and induces ER stress.	Cannabidiol	25-36	transient receptor potential cation channel subfamily V member 1	Homo sapiens	102-107
33604949-8	2022	This study proposed that cannabidiol (CBD) mechanism that occurred through the influx of Ca2+ via the TRPV1 receptor, and increasing ROS production affects protein folding and induces ER stress.	Cannabidiol	38-41	transient receptor potential cation channel subfamily V member 1	Homo sapiens	102-107
33629929-6	2021	Mechanistically, calcium flux induced by CBD through TRPV4 (transient receptor potential cation channel subfamily V member 4) activation played a key role in mitophagy initiation.	Cannabidiol	41-44	transient receptor potential cation channel subfamily V member 4	Homo sapiens	60-124
33629929-8	2021	Transcriptome analysis and other results demonstrated that ER stress and the ATF4-DDIT3-TRIB3-AKT-MTOR axis downstream of TRPV4 were involved in CBD-induced mitophagy in glioma cells.	Cannabidiol	145-148	activating transcription factor 4	Homo sapiens	77-81
33629929-8	2021	Transcriptome analysis and other results demonstrated that ER stress and the ATF4-DDIT3-TRIB3-AKT-MTOR axis downstream of TRPV4 were involved in CBD-induced mitophagy in glioma cells.	Cannabidiol	145-148	DNA damage inducible transcript 3	Homo sapiens	82-87
33629929-8	2021	Transcriptome analysis and other results demonstrated that ER stress and the ATF4-DDIT3-TRIB3-AKT-MTOR axis downstream of TRPV4 were involved in CBD-induced mitophagy in glioma cells.	Cannabidiol	145-148	tribbles pseudokinase 3	Homo sapiens	88-93
33629929-8	2021	Transcriptome analysis and other results demonstrated that ER stress and the ATF4-DDIT3-TRIB3-AKT-MTOR axis downstream of TRPV4 were involved in CBD-induced mitophagy in glioma cells.	Cannabidiol	145-148	AKT serine/threonine kinase 1	Homo sapiens	94-97
33629929-8	2021	Transcriptome analysis and other results demonstrated that ER stress and the ATF4-DDIT3-TRIB3-AKT-MTOR axis downstream of TRPV4 were involved in CBD-induced mitophagy in glioma cells.	Cannabidiol	145-148	mechanistic target of rapamycin kinase	Homo sapiens	98-102
33629929-8	2021	Transcriptome analysis and other results demonstrated that ER stress and the ATF4-DDIT3-TRIB3-AKT-MTOR axis downstream of TRPV4 were involved in CBD-induced mitophagy in glioma cells.	Cannabidiol	145-148	transient receptor potential cation channel subfamily V member 4	Homo sapiens	122-127
33629929-10	2021	Altogether, these findings showed for the first time that the antitumor effect of CBD in glioma is caused by lethal mitophagy and identified TRPV4 as a molecular target and potential biomarker of CBD in glioma.	Cannabidiol	82-85	transient receptor potential cation channel, subfamily V, member 4	Mus musculus	141-146
33629929-10	2021	Altogether, these findings showed for the first time that the antitumor effect of CBD in glioma is caused by lethal mitophagy and identified TRPV4 as a molecular target and potential biomarker of CBD in glioma.	Cannabidiol	196-199	transient receptor potential cation channel, subfamily V, member 4	Mus musculus	141-146
33465546-4	2021	Cannabidiol (CBD) is a modulator of CB1 receptor and CB1 agonists can reduce tremors in experimental models.	Cannabidiol	0-11	cannabinoid receptor 1	Homo sapiens	36-39
33614948-7	2021	Pre-clinical studies reveal the molecular targets of CBD in these indications as the cannabinoid receptor type 1 and cannabinoid receptor type 2 (mainly in fear memory processing), serotonin 1A receptor (mainly in anxiolysis) and peroxisome proliferator-activated receptor gamma (mainly in the underpinning anti-inflammatory/antioxidant effects).	Cannabidiol	53-56	peroxisome proliferator activated receptor gamma	Homo sapiens	230-278
33559194-7	2021	There was a strong interest to see if, highly purified Cannabidiol Isolate (>99% purity) might function to control release of active Caspase-1 by testing of NHEKs using the previously described models.	Cannabidiol	55-66	caspase 1	Homo sapiens	133-142
33559194-11	2021	CONCLUSIONS: Data presented suggests that if Cannabidiol functions as an anti-inflammatory, it does so through pathways not associated with either the NLRP inflammasome-mediated expression of Caspase-1 or through the more commonly known expression of interleukin or prostaglandin inflammatory pathways.	Cannabidiol	45-56	caspase 1	Homo sapiens	192-201
33613284-7	2020	Likewise, some of the molecular targets proposed for CBD actions are f expressed in glial cells, including pharmacological receptors such as CB1, CB2, PPAR-gamma, and 5-HT1A.	Cannabidiol	53-56	cannabinoid receptor 1	Homo sapiens	141-144
33613284-7	2020	Likewise, some of the molecular targets proposed for CBD actions are f expressed in glial cells, including pharmacological receptors such as CB1, CB2, PPAR-gamma, and 5-HT1A.	Cannabidiol	53-56	cannabinoid receptor 2	Homo sapiens	146-149
33613284-7	2020	Likewise, some of the molecular targets proposed for CBD actions are f expressed in glial cells, including pharmacological receptors such as CB1, CB2, PPAR-gamma, and 5-HT1A.	Cannabidiol	53-56	peroxisome proliferator activated receptor gamma	Homo sapiens	151-161
33613284-7	2020	Likewise, some of the molecular targets proposed for CBD actions are f expressed in glial cells, including pharmacological receptors such as CB1, CB2, PPAR-gamma, and 5-HT1A.	Cannabidiol	53-56	5-hydroxytryptamine receptor 1A	Homo sapiens	167-173
32950556-6	2021	Moreover, KET induced regionally-dependent alterations in NR1 and NR2B expression and ERK phosphorylation that were reversed by CBD pre-administration.	Cannabidiol	128-131	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	58-61
32950556-6	2021	Moreover, KET induced regionally-dependent alterations in NR1 and NR2B expression and ERK phosphorylation that were reversed by CBD pre-administration.	Cannabidiol	128-131	glutamate ionotropic receptor NMDA type subunit 2B	Homo sapiens	66-70
32950556-6	2021	Moreover, KET induced regionally-dependent alterations in NR1 and NR2B expression and ERK phosphorylation that were reversed by CBD pre-administration.	Cannabidiol	128-131	mitogen-activated protein kinase 1	Homo sapiens	86-89
33465546-4	2021	Cannabidiol (CBD) is a modulator of CB1 receptor and CB1 agonists can reduce tremors in experimental models.	Cannabidiol	13-16	cannabinoid receptor 1	Homo sapiens	36-39
33519674-9	2020	Additionally, we identify functional changes in oligodendrocytes reflected by myelin basic protein abnormalities upon CBD-tau inoculation.	Cannabidiol	118-121	myelin basic protein	Mus musculus	78-98
33388355-10	2021	Similarly, the chronic administration of CBD 30 mg/kg and CBD 100 mg/kg significantly decreased nuclear factor kappa B (NF-kappaB) expression in the HPC.	Cannabidiol	41-44	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	96-118
33388355-10	2021	Similarly, the chronic administration of CBD 30 mg/kg and CBD 100 mg/kg significantly decreased nuclear factor kappa B (NF-kappaB) expression in the HPC.	Cannabidiol	41-44	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	120-129
33388355-10	2021	Similarly, the chronic administration of CBD 30 mg/kg and CBD 100 mg/kg significantly decreased nuclear factor kappa B (NF-kappaB) expression in the HPC.	Cannabidiol	58-61	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	96-118
33388355-10	2021	Similarly, the chronic administration of CBD 30 mg/kg and CBD 100 mg/kg significantly decreased nuclear factor kappa B (NF-kappaB) expression in the HPC.	Cannabidiol	58-61	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	120-129
33497073-0	2021	The Quality of Online Resources Available to Patients Regarding Cannabidiol for Symptomatic Relief of Hip or Knee Arthritis is Poor.	Cannabidiol	64-75	hedgehog interacting protein	Homo sapiens	102-105
33275960-0	2021	Cannabidiol selectively inhibits the contraction of rat small resistance arteries: possible role for CGRP and voltage-gated calcium channels.	Cannabidiol	0-11	calcitonin-related polypeptide alpha	Rattus norvegicus	101-105
33275960-7	2021	Cannabidiol 1-3 muM significantly inhibited the contraction of small resistance arteries to all tested agents through a combination of mechanisms that include CGRP and L-type calcium channels.	Cannabidiol	0-11	calcitonin-related polypeptide alpha	Rattus norvegicus	159-163
33519674-9	2020	Additionally, we identify functional changes in oligodendrocytes reflected by myelin basic protein abnormalities upon CBD-tau inoculation.	Cannabidiol	118-121	microtubule associated protein tau	Homo sapiens	122-125
33255796-7	2020	CBD applied to the skin of UV-irradiated rats down-regulated LPC, up-regulated PE and phosphatidylserines (PS) and reduced PLA2 activity.	Cannabidiol	0-3	phospholipase A2 group IB	Rattus norvegicus	123-127
33510643-5	2020	Treatment with the phytocannabinoid cannabidiol and the transient receptor potential vanilloid-1 (TRPV-1) channel antagonist capsazepine diminished LID intensity and decreased TNF-alpha levels without impacting other inflammation markers.	Cannabidiol	36-47	tumor necrosis factor	Mus musculus	176-185
33510643-9	2020	Of interest, the antidyskinetic treatment with cannabidiol + capsazepine reduced TNF-alpha release in glutamate-activated astrocytes.	Cannabidiol	47-58	tumor necrosis factor	Mus musculus	81-90
32623021-10	2021	Moreover, THC induced robust phosphorylation of ERK1/2 that was prevented by CBD, while CBD decreased phosphorylation of p70S6K, independently of THC.	Cannabidiol	77-80	mitogen activated protein kinase 3	Rattus norvegicus	48-54
33086172-6	2021	UVA/UVB radiation significantly increased the expression and biological effectiveness of the nuclear factor associated with erythroid factor 2 (Nrf2) and cytoprotective proteins being products of its transcriptional activity, including superoxide dismutase (Cu,Zn-SOD) and the inflammatory response (nuclear receptor coactivator-3 and paralemmin-3), while CBD treatment counteracted and partially eliminated these changes.	Cannabidiol	356-359	NFE2 like bZIP transcription factor 2	Rattus norvegicus	144-148
33086172-7	2021	Moreover, cannabidiol reversed changes in the UV-induced apoptotic pathways by modifying anti-apoptotic and pro-apoptotic factors (apoptosis regulator Bcl-2 and transforming growth factor-beta).	Cannabidiol	10-21	BCL2, apoptosis regulator	Rattus norvegicus	131-156
33332002-10	2021	CBD acts as a noncompetitive negative allosteric modulator of the CB1 receptor, as an inverse agonist of the CB2 receptor, and as an inhibitor of the reuptake of the endocannabinoid anandamide.	Cannabidiol	0-3	cannabinoid receptor 2	Homo sapiens	109-112
33332002-11	2021	Moreover, CBD also activates 5-HT1A serotonergic receptors and vanilloid receptors.	Cannabidiol	10-13	5-hydroxytryptamine receptor 1A	Homo sapiens	29-35
33612548-0	2021	Cannabidiol Ameliorates Cognitive Function via Regulation of IL-33 and TREM2 Upregulation in a Murine Model of Alzheimer"s Disease.	Cannabidiol	0-11	interleukin 33	Mus musculus	61-66
33612548-0	2021	Cannabidiol Ameliorates Cognitive Function via Regulation of IL-33 and TREM2 Upregulation in a Murine Model of Alzheimer"s Disease.	Cannabidiol	0-11	triggering receptor expressed on myeloid cells 2	Mus musculus	71-76
33612548-5	2021	Our findings suggest that CBD treatment enhanced IL-33 and TREM2 expression, ameliorated the symptoms of AD, and retarded cognitive decline.	Cannabidiol	26-29	interleukin 33	Mus musculus	49-54
33612548-5	2021	Our findings suggest that CBD treatment enhanced IL-33 and TREM2 expression, ameliorated the symptoms of AD, and retarded cognitive decline.	Cannabidiol	26-29	triggering receptor expressed on myeloid cells 2	Mus musculus	59-64
33096116-0	2021	Cannabidiol (CBD) enhanced the hippocampal immune response and autophagy of APP/PS1 Alzheimer"s mice uncovered by RNA-seq.	Cannabidiol	0-11	presenilin 1	Mus musculus	80-83
33096116-0	2021	Cannabidiol (CBD) enhanced the hippocampal immune response and autophagy of APP/PS1 Alzheimer"s mice uncovered by RNA-seq.	Cannabidiol	13-16	presenilin 1	Mus musculus	80-83
33096116-5	2021	We performed transcriptome sequence in the hippocampus of 6 month old APP/PS1 mice chronically treated with CBD for one month or 30 days.	Cannabidiol	108-111	presenilin 1	Mus musculus	74-77
33096116-10	2021	Finally, the autophagy of hippocampal neurons in APP/PS1 mice treated with CBD was significantly enhanced by transmission electron microscopy.	Cannabidiol	75-78	presenilin 1	Mus musculus	53-56
33230690-9	2021	Moreover, the administration of CBD blocked the increase of DAT and TH gene expression in mice exposed to the cocaine withdrawal, regulated the decrease of CNR1 and induced an additional upregulation of CNR2 gene expression.	Cannabidiol	32-35	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	60-63
33230690-9	2021	Moreover, the administration of CBD blocked the increase of DAT and TH gene expression in mice exposed to the cocaine withdrawal, regulated the decrease of CNR1 and induced an additional upregulation of CNR2 gene expression.	Cannabidiol	32-35	tyrosine hydroxylase	Mus musculus	68-70
33230690-9	2021	Moreover, the administration of CBD blocked the increase of DAT and TH gene expression in mice exposed to the cocaine withdrawal, regulated the decrease of CNR1 and induced an additional upregulation of CNR2 gene expression.	Cannabidiol	32-35	cannabinoid receptor 1 (brain)	Mus musculus	156-160
33230690-9	2021	Moreover, the administration of CBD blocked the increase of DAT and TH gene expression in mice exposed to the cocaine withdrawal, regulated the decrease of CNR1 and induced an additional upregulation of CNR2 gene expression.	Cannabidiol	32-35	cannabinoid receptor 2 (macrophage)	Mus musculus	203-207
33374481-7	2020	Both in vivo and in vitro receptor mechanism studies indicate that CBD may act as a negative allosteric modulator of type 1 cannabinoid (CB1) receptor and an agonist of type 2 cannabinoid (CB2), transient receptor potential vanilloid 1 (TRPV1), and serotonin 5-HT1A receptors.	Cannabidiol	67-70	cannabinoid receptor 2	Homo sapiens	189-192
33374481-7	2020	Both in vivo and in vitro receptor mechanism studies indicate that CBD may act as a negative allosteric modulator of type 1 cannabinoid (CB1) receptor and an agonist of type 2 cannabinoid (CB2), transient receptor potential vanilloid 1 (TRPV1), and serotonin 5-HT1A receptors.	Cannabidiol	67-70	transient receptor potential cation channel subfamily V member 1	Homo sapiens	195-235
33374481-7	2020	Both in vivo and in vitro receptor mechanism studies indicate that CBD may act as a negative allosteric modulator of type 1 cannabinoid (CB1) receptor and an agonist of type 2 cannabinoid (CB2), transient receptor potential vanilloid 1 (TRPV1), and serotonin 5-HT1A receptors.	Cannabidiol	67-70	transient receptor potential cation channel subfamily V member 1	Homo sapiens	237-242
33998876-0	2022	Cannabidiol Interferes with Establishment of Delta9-Tetrahydrocannabinol-Induced Nausea Through a 5-HT1A Mechanism.	Cannabidiol	0-11	5-hydroxytryptamine receptor 1A	Rattus norvegicus	98-104
33097185-4	2020	Knockout of DOP-3, the dopamine D2-like receptor critical for locomotor behavior, eliminated the paralysis induced by dopamine, CBD, and CBDV.	Cannabidiol	128-131	Dopamine receptor 3	Caenorhabditis elegans	12-17
33097185-5	2020	In contrast, both CBD and CBDV caused paralysis in animals lacking CAT-2, an enzyme necessary for dopamine synthesis.	Cannabidiol	18-21	BH4_AAA_HYDROXYL_2 domain-containing protein;Tyrosine 3-hydroxylase;Tyrosine 3-monooxygenase	Caenorhabditis elegans	67-72
33381645-0	2020	Nonlinear Disposition and Metabolic Interactions of Cannabidiol Through CYP3A Inhibition In Vivo in Rats.	Cannabidiol	52-63	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	72-77
33381645-3	2020	Therefore, we investigated the saturability of CBD metabolism and CBD-drug interactions through inhibition of CYP3A in vivo.	Cannabidiol	47-50	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	110-115
33384591-1	2020	Experimental evidence indicates that cannabidiol (CBD) induces anxiolytic and antiepileptic effects through the activation of 5-HT1A receptors.	Cannabidiol	37-48	5-hydroxytryptamine receptor 1A	Homo sapiens	126-132
33384591-1	2020	Experimental evidence indicates that cannabidiol (CBD) induces anxiolytic and antiepileptic effects through the activation of 5-HT1A receptors.	Cannabidiol	50-53	5-hydroxytryptamine receptor 1A	Homo sapiens	126-132
33384591-6	2020	The [3H]-8-OH-DPAT binding assay was used to determine the pharmacological interaction of CBD with 5-HT1A receptors.	Cannabidiol	90-93	5-hydroxytryptamine receptor 1A	Homo sapiens	99-105
33384591-13	2020	However, at high concentrations, CBD acts as an inverse agonist of 5-HT1A receptors.	Cannabidiol	33-36	5-hydroxytryptamine receptor 1A	Homo sapiens	67-73
33384602-10	2020	Although the CBD-induced neuroprotection observed in animal models of PD has been attributed to the activation of the CB1 receptor, recent research conducted at a molecular level has proposed that CBD is capable of activating other receptors, such as CB2 and the TRPV-1 receptor, both of which are expressed in the dopaminergic neurons of the nigro-striatal pathway.	Cannabidiol	13-16	cannabinoid receptor 2	Homo sapiens	251-254
33384602-10	2020	Although the CBD-induced neuroprotection observed in animal models of PD has been attributed to the activation of the CB1 receptor, recent research conducted at a molecular level has proposed that CBD is capable of activating other receptors, such as CB2 and the TRPV-1 receptor, both of which are expressed in the dopaminergic neurons of the nigro-striatal pathway.	Cannabidiol	197-200	cannabinoid receptor 2	Homo sapiens	251-254
33384602-12	2020	Cannabidiol activates the PPARgamma, GPR55, GPR3, GPR6, GPR12, and GPR18 receptors, causing a variety of biochemical, molecular, and behavioral effects due to the broad range of receptors it activates in the CNS.	Cannabidiol	0-11	peroxisome proliferator activated receptor gamma	Homo sapiens	26-35
33384602-12	2020	Cannabidiol activates the PPARgamma, GPR55, GPR3, GPR6, GPR12, and GPR18 receptors, causing a variety of biochemical, molecular, and behavioral effects due to the broad range of receptors it activates in the CNS.	Cannabidiol	0-11	G protein-coupled receptor 55	Homo sapiens	37-42
33384602-12	2020	Cannabidiol activates the PPARgamma, GPR55, GPR3, GPR6, GPR12, and GPR18 receptors, causing a variety of biochemical, molecular, and behavioral effects due to the broad range of receptors it activates in the CNS.	Cannabidiol	0-11	G protein-coupled receptor 3	Homo sapiens	44-48
33384602-12	2020	Cannabidiol activates the PPARgamma, GPR55, GPR3, GPR6, GPR12, and GPR18 receptors, causing a variety of biochemical, molecular, and behavioral effects due to the broad range of receptors it activates in the CNS.	Cannabidiol	0-11	G protein-coupled receptor 6	Homo sapiens	50-54
33384602-12	2020	Cannabidiol activates the PPARgamma, GPR55, GPR3, GPR6, GPR12, and GPR18 receptors, causing a variety of biochemical, molecular, and behavioral effects due to the broad range of receptors it activates in the CNS.	Cannabidiol	0-11	G protein-coupled receptor 12	Homo sapiens	56-61
33384602-12	2020	Cannabidiol activates the PPARgamma, GPR55, GPR3, GPR6, GPR12, and GPR18 receptors, causing a variety of biochemical, molecular, and behavioral effects due to the broad range of receptors it activates in the CNS.	Cannabidiol	0-11	G protein-coupled receptor 18	Homo sapiens	67-72
33362478-3	2020	A recently published cryo-EM structure showed the putative binding location of a well-known cannabinoid ligand, cannabidiol (CBD), in TRPV2, a channel that has been implicated in inflammation and chronic pain.	Cannabidiol	112-123	transient receptor potential cation channel subfamily V member 2	Homo sapiens	134-139
33362478-3	2020	A recently published cryo-EM structure showed the putative binding location of a well-known cannabinoid ligand, cannabidiol (CBD), in TRPV2, a channel that has been implicated in inflammation and chronic pain.	Cannabidiol	125-128	transient receptor potential cation channel subfamily V member 2	Homo sapiens	134-139
33113429-8	2020	The different distinctive plant-derived cannabinoids were discovered like cannabidiol (CBD), cannabinol (CBN), cannabichromene (CBC), and cannabidiol (CBG).	Cannabidiol	138-149	glucosylceramidase beta 3 (gene/pseudogene)	Homo sapiens	151-154
32656944-0	2020	Cannabidiol induces osteoblast differentiation via angiopoietin1 and p38 MAPK.	Cannabidiol	0-11	angiopoietin 1	Homo sapiens	51-64
32656944-2	2020	Cannabidiol increased the expression of Angiopoietin1 and the enzyme activity of alkaline phosphatase in U2OS and MG-63.	Cannabidiol	0-11	angiopoietin 1	Homo sapiens	40-53
32656944-4	2020	Western blotting analysis showed that the expression of tight junction related proteins such as Claudin1, Claudin4, Occuludin1, and ZO1 was increased by cannabidiol in U2OS and MG-63.	Cannabidiol	153-164	claudin 1	Homo sapiens	96-104
32656944-4	2020	Western blotting analysis showed that the expression of tight junction related proteins such as Claudin1, Claudin4, Occuludin1, and ZO1 was increased by cannabidiol in U2OS and MG-63.	Cannabidiol	153-164	claudin 4	Homo sapiens	106-114
32656944-4	2020	Western blotting analysis showed that the expression of tight junction related proteins such as Claudin1, Claudin4, Occuludin1, and ZO1 was increased by cannabidiol in U2OS and MG-63.	Cannabidiol	153-164	tight junction protein 1	Homo sapiens	132-135
32656944-7	2020	Mechanistically, cannabidiol-regulated osteoblastic differentiation in U2OS and MG-63 by strengthen the protein-protein interaction among RUNX2, OSX, or the phosphorylated p38 mitogen-activated protein kinase (MAPK).	Cannabidiol	17-28	RUNX family transcription factor 2	Homo sapiens	138-143
32656944-7	2020	Mechanistically, cannabidiol-regulated osteoblastic differentiation in U2OS and MG-63 by strengthen the protein-protein interaction among RUNX2, OSX, or the phosphorylated p38 mitogen-activated protein kinase (MAPK).	Cannabidiol	17-28	Sp7 transcription factor	Homo sapiens	145-148
32656944-7	2020	Mechanistically, cannabidiol-regulated osteoblastic differentiation in U2OS and MG-63 by strengthen the protein-protein interaction among RUNX2, OSX, or the phosphorylated p38 mitogen-activated protein kinase (MAPK).	Cannabidiol	17-28	mitogen-activated protein kinase 14	Homo sapiens	172-208
32656944-8	2020	In conclusion, cannabidiol increased Angiopoietin1 expression and p38 MAPK activation for osteoblastic differentiation in U2OS and MG-63 suggesting that cannabidiol might provide a novel therapeutic option for the bone regeneration.	Cannabidiol	15-26	angiopoietin 1	Homo sapiens	37-50
32656944-8	2020	In conclusion, cannabidiol increased Angiopoietin1 expression and p38 MAPK activation for osteoblastic differentiation in U2OS and MG-63 suggesting that cannabidiol might provide a novel therapeutic option for the bone regeneration.	Cannabidiol	153-164	angiopoietin 1	Homo sapiens	37-50
32215966-0	2020	Cannabidiol alleviates hemorrhagic shock-induced neural apoptosis in rats by inducing autophagy through activation of the PI3K/AKT pathway.	Cannabidiol	0-11	AKT serine/threonine kinase 1	Rattus norvegicus	127-130
33635755-3	2020	THC and CBD bind with cannabinoid receptors (CB1 and CB2), which are present in the brain and many organs.	Cannabidiol	8-11	cannabinoid receptor 1	Homo sapiens	45-48
33635755-3	2020	THC and CBD bind with cannabinoid receptors (CB1 and CB2), which are present in the brain and many organs.	Cannabidiol	8-11	cannabinoid receptor 2	Homo sapiens	53-56
33635755-14	2020	CBD is hydroxylated to 7-OH-CBD and 7-COOH-CBD by cytochrome P450 enzymes CYP3A4 and CYP2C9 in the liver and is excreted mainly in feces and less in urine.	Cannabidiol	0-3	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	74-80
33635755-14	2020	CBD is hydroxylated to 7-OH-CBD and 7-COOH-CBD by cytochrome P450 enzymes CYP3A4 and CYP2C9 in the liver and is excreted mainly in feces and less in urine.	Cannabidiol	0-3	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
33998871-0	2021	Effect of Cannabidiol on the Long-Term Toxicity and Lifespan in the Preclinical Model Caenorhabditis elegans.	Cannabidiol	10-21	Protein lon-1;SCP domain-containing protein	Caenorhabditis elegans	29-33
33998871-3	2021	In this study, we examined both acute and long-term exposure studies of CBD at physiologically relevant concentrations.	Cannabidiol	72-75	Protein lon-1;SCP domain-containing protein	Caenorhabditis elegans	42-46
33998871-6	2021	Long-term toxicity was assessed by exposing day 1 adults to 10, 40, and 100 muM CBD until all animals perished.	Cannabidiol	80-83	Protein lon-1;SCP domain-containing protein	Caenorhabditis elegans	0-4
33191836-0	2022	Reduction in Tamoxifen Metabolites Endoxifen and N-desmethyltamoxifen With Chronic Administration of Low Dose Cannabidiol: A CYP3A4 and CYP2D6 Drug Interaction.	Cannabidiol	110-121	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	125-131
33228239-6	2020	In addition, certain key targets have been related with these CBD pharmacological actions, including cannabinoid receptors (CB1r and CB2r), 5-HT1A receptor and neurogenesis factors.	Cannabidiol	62-65	cannabinoid receptor 1	Homo sapiens	124-128
33228239-6	2020	In addition, certain key targets have been related with these CBD pharmacological actions, including cannabinoid receptors (CB1r and CB2r), 5-HT1A receptor and neurogenesis factors.	Cannabidiol	62-65	5-hydroxytryptamine receptor 1A	Homo sapiens	140-155
33191836-0	2022	Reduction in Tamoxifen Metabolites Endoxifen and N-desmethyltamoxifen With Chronic Administration of Low Dose Cannabidiol: A CYP3A4 and CYP2D6 Drug Interaction.	Cannabidiol	110-121	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	136-142
33191836-8	2022	CONCLUSION: CBD at a low dose of 40 mg/day resulted in the potential inhibition of CYP3A4 and/or CYP2D6.	Cannabidiol	12-15	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	83-89
33191836-8	2022	CONCLUSION: CBD at a low dose of 40 mg/day resulted in the potential inhibition of CYP3A4 and/or CYP2D6.	Cannabidiol	12-15	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	97-103
33171772-6	2020	CBD exerts its neuroprotective effects through three G protein coupled-receptors (adenosine receptor subtype 2A, serotonin receptor subtype 1A and G protein-coupled receptor 55), one ligand-gated ion channel (transient receptor potential vanilloid channel-1) and one nuclear factor (peroxisome proliferator-activated receptor gamma).	Cannabidiol	0-3	G protein-coupled receptor 55	Homo sapiens	113-176
33171772-6	2020	CBD exerts its neuroprotective effects through three G protein coupled-receptors (adenosine receptor subtype 2A, serotonin receptor subtype 1A and G protein-coupled receptor 55), one ligand-gated ion channel (transient receptor potential vanilloid channel-1) and one nuclear factor (peroxisome proliferator-activated receptor gamma).	Cannabidiol	0-3	peroxisome proliferator activated receptor gamma	Homo sapiens	283-331
32910945-4	2020	We found that CBD inhibits with comparable micromolar potencies the peak and late components of the NaV1.5 sodium current, the CaV1.2 mediated L-type calcium current, as well as all the repolarizing potassium currents examined except Kir2.1.	Cannabidiol	14-17	sodium voltage-gated channel alpha subunit 5	Homo sapiens	100-106
32910945-4	2020	We found that CBD inhibits with comparable micromolar potencies the peak and late components of the NaV1.5 sodium current, the CaV1.2 mediated L-type calcium current, as well as all the repolarizing potassium currents examined except Kir2.1.	Cannabidiol	14-17	calcium voltage-gated channel subunit alpha1 C	Homo sapiens	127-133
32910945-4	2020	We found that CBD inhibits with comparable micromolar potencies the peak and late components of the NaV1.5 sodium current, the CaV1.2 mediated L-type calcium current, as well as all the repolarizing potassium currents examined except Kir2.1.	Cannabidiol	14-17	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	234-240
33058425-2	2020	In a follow-up study to our recent findings indicating the potential of Cannabidiol (CBD) in the treatment of acute respiratory distress syndrome (ARDS), here we show for the first time that CBD may ameliorate the symptoms of ARDS through up-regulation of apelin, a peptide with significant role in the central and peripheral regulation of immunity, CNS, metabolic and cardiovascular system.	Cannabidiol	72-83	apelin	Homo sapiens	256-262
33058425-2	2020	In a follow-up study to our recent findings indicating the potential of Cannabidiol (CBD) in the treatment of acute respiratory distress syndrome (ARDS), here we show for the first time that CBD may ameliorate the symptoms of ARDS through up-regulation of apelin, a peptide with significant role in the central and peripheral regulation of immunity, CNS, metabolic and cardiovascular system.	Cannabidiol	191-194	apelin	Homo sapiens	256-262
33058425-5	2020	Importantly, CBD treatment increased the apelin expression significantly, suggesting a potential crosstalk between apelinergic system and CBD may be the therapeutic target in the treatment of inflammatory diseases such as COVID-19 and many other pathologic conditions.	Cannabidiol	13-16	apelin	Mus musculus	41-47
33058425-5	2020	Importantly, CBD treatment increased the apelin expression significantly, suggesting a potential crosstalk between apelinergic system and CBD may be the therapeutic target in the treatment of inflammatory diseases such as COVID-19 and many other pathologic conditions.	Cannabidiol	138-141	apelin	Mus musculus	41-47
33126623-6	2020	Furthermore, CBD and/or THC reduced the expression of PD-L1 by either PC or PSC cells.	Cannabidiol	13-16	CD274 antigen	Mus musculus	54-59
32965166-0	2020	Cannabidiol activation of vagal afferent neurons requires TRPA1.	Cannabidiol	0-11	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	58-63
32965166-5	2020	CBD produced strong excitatory effects in neurons expressing TRPA1.	Cannabidiol	0-3	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	61-66
32965166-7	2020	These pharmacological experiments were confirmed using genetic knockouts where TRPA1 KO mice lacked CBD responses while TRPV1 KO mice exhibited CBD-induced activation.	Cannabidiol	144-147	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	120-125
32965166-8	2020	We also characterized CBD-provoked inward currents at resting potentials in vagal afferents expressing TRPA1 that were absent in TRPA1 KO mice, but persisted in TRPV1 KO mice.	Cannabidiol	22-25	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	103-108
32965166-8	2020	We also characterized CBD-provoked inward currents at resting potentials in vagal afferents expressing TRPA1 that were absent in TRPA1 KO mice, but persisted in TRPV1 KO mice.	Cannabidiol	22-25	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	129-134
32965166-8	2020	We also characterized CBD-provoked inward currents at resting potentials in vagal afferents expressing TRPA1 that were absent in TRPA1 KO mice, but persisted in TRPV1 KO mice.	Cannabidiol	22-25	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	161-166
32965166-11	2020	Cannabis exposure reduced the magnitude of CBD responses likely due to a loss of TRPA1 signaling.	Cannabidiol	43-46	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	81-86
32965166-12	2020	Together these findings detail a novel excitatory action of CBD at vagal afferent neurons which requires TRPA1 and may contribute to the vagal mimetic effects of CBD and adaptation following chronic cannabis use.	Cannabidiol	60-63	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	105-110
32805354-0	2020	Cannabidiol inhibits febrile seizure by modulating AMPA receptor kinetics through its interaction with the N-terminal domain of GluA1/GluA2.	Cannabidiol	0-11	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	128-133
32805354-0	2020	Cannabidiol inhibits febrile seizure by modulating AMPA receptor kinetics through its interaction with the N-terminal domain of GluA1/GluA2.	Cannabidiol	0-11	glutamate ionotropic receptor AMPA type subunit 2	Homo sapiens	134-139
32805354-11	2020	The inhibitory effects of CBD on AMPAR depended on its interaction with the distal N-terminal domain of GluA1/GluA2.	Cannabidiol	26-29	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	104-109
32805354-11	2020	The inhibitory effects of CBD on AMPAR depended on its interaction with the distal N-terminal domain of GluA1/GluA2.	Cannabidiol	26-29	glutamate ionotropic receptor AMPA type subunit 2	Homo sapiens	110-115
33126623-7	2020	Knockout of p-21 activated kinase 1 (PAK1, activated by KRas) in PC and PSC cells and, in mice, dramatically decreased or blocked these inhibitory effects of CBD and/or THC.	Cannabidiol	158-161	p21 (RAC1) activated kinase 1	Mus musculus	12-35
33126623-7	2020	Knockout of p-21 activated kinase 1 (PAK1, activated by KRas) in PC and PSC cells and, in mice, dramatically decreased or blocked these inhibitory effects of CBD and/or THC.	Cannabidiol	158-161	p21 (RAC1) activated kinase 1	Mus musculus	37-41
33126623-8	2020	These results indicated that CBD and THC exerted their inhibitions on PC and PSC via a p-21 activated kinase 1 (PAK1)-dependent pathway, suggesting that CBD and THC suppress Kras activated pathway by targeting PAK1.	Cannabidiol	29-32	p21 (RAC1) activated kinase 1	Mus musculus	87-110
33126623-8	2020	These results indicated that CBD and THC exerted their inhibitions on PC and PSC via a p-21 activated kinase 1 (PAK1)-dependent pathway, suggesting that CBD and THC suppress Kras activated pathway by targeting PAK1.	Cannabidiol	29-32	p21 (RAC1) activated kinase 1	Mus musculus	112-116
33126623-8	2020	These results indicated that CBD and THC exerted their inhibitions on PC and PSC via a p-21 activated kinase 1 (PAK1)-dependent pathway, suggesting that CBD and THC suppress Kras activated pathway by targeting PAK1.	Cannabidiol	29-32	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	174-178
33126623-8	2020	These results indicated that CBD and THC exerted their inhibitions on PC and PSC via a p-21 activated kinase 1 (PAK1)-dependent pathway, suggesting that CBD and THC suppress Kras activated pathway by targeting PAK1.	Cannabidiol	29-32	p21 (RAC1) activated kinase 1	Mus musculus	210-214
33126623-8	2020	These results indicated that CBD and THC exerted their inhibitions on PC and PSC via a p-21 activated kinase 1 (PAK1)-dependent pathway, suggesting that CBD and THC suppress Kras activated pathway by targeting PAK1.	Cannabidiol	153-156	p21 (RAC1) activated kinase 1	Mus musculus	87-110
33126623-8	2020	These results indicated that CBD and THC exerted their inhibitions on PC and PSC via a p-21 activated kinase 1 (PAK1)-dependent pathway, suggesting that CBD and THC suppress Kras activated pathway by targeting PAK1.	Cannabidiol	153-156	p21 (RAC1) activated kinase 1	Mus musculus	112-116
33126623-8	2020	These results indicated that CBD and THC exerted their inhibitions on PC and PSC via a p-21 activated kinase 1 (PAK1)-dependent pathway, suggesting that CBD and THC suppress Kras activated pathway by targeting PAK1.	Cannabidiol	153-156	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	174-178
33126623-8	2020	These results indicated that CBD and THC exerted their inhibitions on PC and PSC via a p-21 activated kinase 1 (PAK1)-dependent pathway, suggesting that CBD and THC suppress Kras activated pathway by targeting PAK1.	Cannabidiol	153-156	p21 (RAC1) activated kinase 1	Mus musculus	210-214
33108021-7	2022	Interestingly, activation of PPARgamma and PPARalpha with selective agonists has been shown to decrease mesocorticolimbic DA activity and block neuropsychiatric symptoms similar to CBD and omega-3s, raising the possibility that CBD and omega-3s produce their effects through PPAR signaling.	Cannabidiol	181-184	peroxisome proliferator activated receptor gamma	Homo sapiens	29-38
33108021-7	2022	Interestingly, activation of PPARgamma and PPARalpha with selective agonists has been shown to decrease mesocorticolimbic DA activity and block neuropsychiatric symptoms similar to CBD and omega-3s, raising the possibility that CBD and omega-3s produce their effects through PPAR signaling.	Cannabidiol	181-184	peroxisome proliferator activated receptor alpha	Homo sapiens	43-52
33108021-7	2022	Interestingly, activation of PPARgamma and PPARalpha with selective agonists has been shown to decrease mesocorticolimbic DA activity and block neuropsychiatric symptoms similar to CBD and omega-3s, raising the possibility that CBD and omega-3s produce their effects through PPAR signaling.	Cannabidiol	181-184	peroxisome proliferator activated receptor alpha	Homo sapiens	29-33
33108021-7	2022	Interestingly, activation of PPARgamma and PPARalpha with selective agonists has been shown to decrease mesocorticolimbic DA activity and block neuropsychiatric symptoms similar to CBD and omega-3s, raising the possibility that CBD and omega-3s produce their effects through PPAR signaling.	Cannabidiol	228-231	peroxisome proliferator activated receptor gamma	Homo sapiens	29-38
33108021-7	2022	Interestingly, activation of PPARgamma and PPARalpha with selective agonists has been shown to decrease mesocorticolimbic DA activity and block neuropsychiatric symptoms similar to CBD and omega-3s, raising the possibility that CBD and omega-3s produce their effects through PPAR signaling.	Cannabidiol	228-231	peroxisome proliferator activated receptor alpha	Homo sapiens	43-52
33108021-7	2022	Interestingly, activation of PPARgamma and PPARalpha with selective agonists has been shown to decrease mesocorticolimbic DA activity and block neuropsychiatric symptoms similar to CBD and omega-3s, raising the possibility that CBD and omega-3s produce their effects through PPAR signaling.	Cannabidiol	228-231	peroxisome proliferator activated receptor alpha	Homo sapiens	29-33
33076330-4	2020	At a concentration of 3 microM, CBD induced an upregulation of HO-1 mRNA and protein within 6 h, whereas for MA only a late and comparatively lower increase in the HO-1 protein could be detected after 48 h. In addition, both cannabinoids induced time- and concentration-dependent increases in LC3A/B-II protein, a marker of autophagy, and in metabolic activity.	Cannabidiol	32-35	heme oxygenase 1	Homo sapiens	63-67
33001729-0	2020	Crowdfunding Cannabidiol (CBD) for Cancer: Hype and Misinformation on GoFundMe.	Cannabidiol	26-29	FIC domain protein adenylyltransferase	Homo sapiens	43-47
32863231-5	2020	The phytocannabinoid cannabidiol (CBD) inhibits BACH1 but lacks significant NRF2 activating properties.	Cannabidiol	21-32	BTB domain and CNC homolog 1	Homo sapiens	48-53
32654189-7	2020	Tissue NLRP3 levels were 80% higher in the DCD-WT group compared to the CBD-WT group.	Cannabidiol	72-75	NLR family, pyrin domain containing 3	Mus musculus	7-12
32587099-9	2020	A combined (reversible inhibition and TDI) mechanistic static model populated with these data predicted a moderate to strong pharmacokinetic interaction risk between orally administered CBD and drugs extensively metabolized by CYP1A2/2C9/2C19/2D6/3A and between orally administered THC and drugs extensively metabolized by CYP1A2/2C9/3A.	Cannabidiol	186-189	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	227-233
32587099-9	2020	A combined (reversible inhibition and TDI) mechanistic static model populated with these data predicted a moderate to strong pharmacokinetic interaction risk between orally administered CBD and drugs extensively metabolized by CYP1A2/2C9/2C19/2D6/3A and between orally administered THC and drugs extensively metabolized by CYP1A2/2C9/3A.	Cannabidiol	186-189	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	323-336
32424477-2	2020	Cannabidiol (CBD) is a potent inhibitor of the CYP3A family.	Cannabidiol	0-11	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	47-52
32424477-2	2020	Cannabidiol (CBD) is a potent inhibitor of the CYP3A family.	Cannabidiol	13-16	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	47-52
32424477-14	2020	When CBD has been administered as a single dose, the effect is believed to be mainly caused by the inhibition of CBZ metabolism through CYP3A.	Cannabidiol	5-8	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	136-141
32863231-5	2020	The phytocannabinoid cannabidiol (CBD) inhibits BACH1 but lacks significant NRF2 activating properties.	Cannabidiol	34-37	BTB domain and CNC homolog 1	Homo sapiens	48-53
32863231-6	2020	Based on this scaffold, we have developed a novel CBD derivative that is highly effective at both inhibiting BACH1 and activating NRF2.	Cannabidiol	50-53	BTB domain and CNC homolog 1	Homo sapiens	109-114
32863231-6	2020	Based on this scaffold, we have developed a novel CBD derivative that is highly effective at both inhibiting BACH1 and activating NRF2.	Cannabidiol	50-53	NFE2 like bZIP transcription factor 2	Homo sapiens	130-134
32999428-0	2020	The electrophysiological effect of cannabidiol on hERG current and in guinea-pig and rabbit cardiac preparations.	Cannabidiol	35-46	ETS transcription factor ERG	Homo sapiens	50-54
32999428-6	2020	CBD inhibited hERG potassium channels with an IC50 value of 2.07 microM at room temperature and delayed rectifier potassium current with 6.5 microM at 37  C, respectively.	Cannabidiol	0-3	ETS transcription factor ERG	Homo sapiens	14-18
33998860-12	2020	Tweed Argyle also inhibited ABCB11 transporter function with an IC50 value of 11.9 muM for CBD and 7.7 muM for Delta9-THC.	Cannabidiol	91-94	ATP binding cassette subfamily B member 11	Homo sapiens	28-34
32982390-3	2020	Hence, we conducted in vitro studies, to elucidate the efficacy and mechanisms of CBD for inhibiting neuronal hypersensitivity in cultured rat sensory neurons, following activation of TRPV1.	Cannabidiol	82-85	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	184-189
32574650-0	2020	Cannabidiol anticonvulsant effect is mediated by the PI3Kgamma pathway.	Cannabidiol	0-11	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma	Homo sapiens	53-62
32574650-3	2020	This work aims to investigate if the anticonvulsant and neuroprotective effects of cannabidiol (CBD) are mediated by PI3Kgamma.	Cannabidiol	83-94	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma	Homo sapiens	117-126
32574650-3	2020	This work aims to investigate if the anticonvulsant and neuroprotective effects of cannabidiol (CBD) are mediated by PI3Kgamma.	Cannabidiol	96-99	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma	Homo sapiens	117-126
32574650-9	2020	CBD in vivo effects were abolished by pharmacological inhibition of cannabinoid receptor or mTOR.	Cannabidiol	0-3	mechanistic target of rapamycin kinase	Homo sapiens	92-96
32574650-11	2020	Thus, we suggest that the modulation of PI3K/mTOR signaling pathway is involved in the anticonvulsant and neuroprotective effects of CBD.	Cannabidiol	133-136	mechanistic target of rapamycin kinase	Homo sapiens	45-49
33162767-8	2020	Cannabidiol, which mainly acts on CB1 and CB2 receptors, is currently being tested in patients with alcohol use disorder and opioid use disorder.	Cannabidiol	0-11	cannabinoid receptor 1	Homo sapiens	34-37
33162767-8	2020	Cannabidiol, which mainly acts on CB1 and CB2 receptors, is currently being tested in patients with alcohol use disorder and opioid use disorder.	Cannabidiol	0-11	cannabinoid receptor 2	Homo sapiens	42-45
32918835-5	2020	Induction of CYP3A4 and CYP2C19 led to small reductions in exposure to CBD and its major metabolites.	Cannabidiol	71-74	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	13-19
32918835-5	2020	Induction of CYP3A4 and CYP2C19 led to small reductions in exposure to CBD and its major metabolites.	Cannabidiol	71-74	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
32918835-6	2020	Inhibition of CYP3A4 activity did not affect CBD exposure and caused small increases in exposure to CBD metabolites.	Cannabidiol	100-103	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	14-20
32918835-7	2020	Inhibition of CYP2C19 activity led to a small increase in exposure to CBD and small decreases in exposure to CBD metabolites.	Cannabidiol	70-73	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	14-21
32918835-7	2020	Inhibition of CYP2C19 activity led to a small increase in exposure to CBD and small decreases in exposure to CBD metabolites.	Cannabidiol	109-112	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	14-21
32553926-6	2020	KEY FINDINGS: Upon the treatment of aged pancreatic islets cells with cannabidiol and tetrahydrocannabinol, the expression of p53, p38, p21 and the activity of beta-galactosidase were reduced.	Cannabidiol	70-81	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	126-129
32553926-6	2020	KEY FINDINGS: Upon the treatment of aged pancreatic islets cells with cannabidiol and tetrahydrocannabinol, the expression of p53, p38, p21 and the activity of beta-galactosidase were reduced.	Cannabidiol	70-81	mitogen activated protein kinase 14	Rattus norvegicus	131-134
32553926-6	2020	KEY FINDINGS: Upon the treatment of aged pancreatic islets cells with cannabidiol and tetrahydrocannabinol, the expression of p53, p38, p21 and the activity of beta-galactosidase were reduced.	Cannabidiol	70-81	KRAS proto-oncogene, GTPase	Rattus norvegicus	136-139
32553926-7	2020	Cannabidiol and tetrahydrocannabinol increase insulin release, Pdx1, Glut2, and thiol molecules expression, while the oxidative stress parameters were decreased.	Cannabidiol	0-11	pancreatic and duodenal homeobox 1	Rattus norvegicus	63-67
32553926-7	2020	Cannabidiol and tetrahydrocannabinol increase insulin release, Pdx1, Glut2, and thiol molecules expression, while the oxidative stress parameters were decreased.	Cannabidiol	0-11	solute carrier family 2 member 2	Rattus norvegicus	69-74
32599064-3	2020	VCE-004.8 is a multitarget synthetic cannabidiol (CBD) derivative acting as a dual Peroxisome proliferator-activated receptor-gamma/Cannabinoid receptor type 2 (PPARgamma/CB2) ligand agonist that also activates the Hypoxia-inducible factor (HIF) pathway.	Cannabidiol	50-53	peroxisome proliferator activated receptor gamma	Mus musculus	161-170
32599064-3	2020	VCE-004.8 is a multitarget synthetic cannabidiol (CBD) derivative acting as a dual Peroxisome proliferator-activated receptor-gamma/Cannabinoid receptor type 2 (PPARgamma/CB2) ligand agonist that also activates the Hypoxia-inducible factor (HIF) pathway.	Cannabidiol	50-53	cannabinoid receptor 2 (macrophage)	Mus musculus	171-174
32345916-5	2020	In vitro and in mouse models, CBD significantly attenuated the production of pro-inflammatory cytokines IL-6 and TNF-alpha while elevating levels of anti-inflammatory IL-10.	Cannabidiol	30-33	interleukin 6	Mus musculus	104-108
32345916-5	2020	In vitro and in mouse models, CBD significantly attenuated the production of pro-inflammatory cytokines IL-6 and TNF-alpha while elevating levels of anti-inflammatory IL-10.	Cannabidiol	30-33	tumor necrosis factor	Mus musculus	113-122
32345916-5	2020	In vitro and in mouse models, CBD significantly attenuated the production of pro-inflammatory cytokines IL-6 and TNF-alpha while elevating levels of anti-inflammatory IL-10.	Cannabidiol	30-33	interleukin 10	Mus musculus	167-172
32982390-14	2020	Conclusion: CBD at low doses corresponding to plasma concentrations observed physiologically inhibits or desensitizes neuronal TRPV1 signalling by inhibiting the adenylyl cyclase - cAMP pathway, which is essential for maintaining TRPV1 phosphorylation and sensitization.	Cannabidiol	12-15	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	127-132
32982390-14	2020	Conclusion: CBD at low doses corresponding to plasma concentrations observed physiologically inhibits or desensitizes neuronal TRPV1 signalling by inhibiting the adenylyl cyclase - cAMP pathway, which is essential for maintaining TRPV1 phosphorylation and sensitization.	Cannabidiol	12-15	cathelicidin antimicrobial peptide	Rattus norvegicus	181-185
32982390-14	2020	Conclusion: CBD at low doses corresponding to plasma concentrations observed physiologically inhibits or desensitizes neuronal TRPV1 signalling by inhibiting the adenylyl cyclase - cAMP pathway, which is essential for maintaining TRPV1 phosphorylation and sensitization.	Cannabidiol	12-15	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	230-235
32562718-3	2020	Cannabidiol (CBD), a non-toxic constituent of the Cannabis sativa plant, has been shown to prevent and reverse cognitive deficits in Abeta transgenic mouse models of AD.	Cannabidiol	0-11	amyloid beta (A4) precursor protein	Mus musculus	133-138
32562718-3	2020	Cannabidiol (CBD), a non-toxic constituent of the Cannabis sativa plant, has been shown to prevent and reverse cognitive deficits in Abeta transgenic mouse models of AD.	Cannabidiol	13-16	amyloid beta (A4) precursor protein	Mus musculus	133-138
32903924-3	2020	Studies have observed that the antagonists of CB1 and CB2 receptors and transient receptor potential vanilloid 1 reverse the immunomodulatory effects of CBD.	Cannabidiol	153-156	cannabinoid receptor 1	Homo sapiens	46-49
32903924-3	2020	Studies have observed that the antagonists of CB1 and CB2 receptors and transient receptor potential vanilloid 1 reverse the immunomodulatory effects of CBD.	Cannabidiol	153-156	cannabinoid receptor 2	Homo sapiens	54-57
32690657-5	2020	In contrast, anti-inflammatory cannabinoids such as cannabidiol or delta-9-tetrahydrocannabinol decreased the expression of AW112010 in T cells.	Cannabidiol	52-63	expressed sequence AW112010	Mus musculus	124-132
32330591-8	2020	Exposure of these cells to tetrahydrocannabinol (THC) or cannabidiol (CBD) reduced the immunological response of the P2X7 receptor, which was dependent on the identified genetic variant.	Cannabidiol	57-68	purinergic receptor P2X 7	Homo sapiens	117-130
32470563-0	2020	Pharmacological data of cannabidiol- and cannabigerol-type phytocannabinoids acting on cannabinoid CB1, CB2 and CB1/CB2 heteromer receptors.	Cannabidiol	24-35	cannabinoid receptor 1	Homo sapiens	99-102
32470563-0	2020	Pharmacological data of cannabidiol- and cannabigerol-type phytocannabinoids acting on cannabinoid CB1, CB2 and CB1/CB2 heteromer receptors.	Cannabidiol	24-35	cannabinoid receptor 2	Homo sapiens	104-107
32470563-0	2020	Pharmacological data of cannabidiol- and cannabigerol-type phytocannabinoids acting on cannabinoid CB1, CB2 and CB1/CB2 heteromer receptors.	Cannabidiol	24-35	cannabinoid receptor 1	Homo sapiens	112-115
32470563-0	2020	Pharmacological data of cannabidiol- and cannabigerol-type phytocannabinoids acting on cannabinoid CB1, CB2 and CB1/CB2 heteromer receptors.	Cannabidiol	24-35	cannabinoid receptor 2	Homo sapiens	116-119
32330591-8	2020	Exposure of these cells to tetrahydrocannabinol (THC) or cannabidiol (CBD) reduced the immunological response of the P2X7 receptor, which was dependent on the identified genetic variant.	Cannabidiol	70-73	purinergic receptor P2X 7	Homo sapiens	117-130
31215752-5	2020	CBD appeared to be more efficacious in CB1-/- mice than in WT mice.	Cannabidiol	0-3	cannabinoid receptor 1 (brain)	Mus musculus	39-42
32752303-6	2020	The activities of glutathione reductase and glutathione peroxidase were significantly increased in cells exposed to THC and significantly decreased in those treated with CBD.	Cannabidiol	170-173	glutathione-disulfide reductase	Homo sapiens	18-39
32752303-9	2020	The Annexin V-Propidium Iodide assay showed a significantly increased percentage of cells apoptotic after CB83 exposition and necrotic cells after CBD and THC exposition.	Cannabidiol	147-150	annexin A5	Homo sapiens	4-13
32751388-1	2020	Several studies support, both in vitro and in vivo, the anti-cancer effects of cannabidiol (CBD), a transient receptor potential vanilloid 2 (TRPV2) ligand.	Cannabidiol	79-90	transient receptor potential cation channel subfamily V member 2	Homo sapiens	100-140
32751388-1	2020	Several studies support, both in vitro and in vivo, the anti-cancer effects of cannabidiol (CBD), a transient receptor potential vanilloid 2 (TRPV2) ligand.	Cannabidiol	79-90	transient receptor potential cation channel subfamily V member 2	Homo sapiens	142-147
32751388-1	2020	Several studies support, both in vitro and in vivo, the anti-cancer effects of cannabidiol (CBD), a transient receptor potential vanilloid 2 (TRPV2) ligand.	Cannabidiol	92-95	transient receptor potential cation channel subfamily V member 2	Homo sapiens	100-140
32751388-1	2020	Several studies support, both in vitro and in vivo, the anti-cancer effects of cannabidiol (CBD), a transient receptor potential vanilloid 2 (TRPV2) ligand.	Cannabidiol	92-95	transient receptor potential cation channel subfamily V member 2	Homo sapiens	142-147
32708634-0	2020	Cannabidiol Promotes Endothelial Cell Survival by Heme Oxygenase-1-Mediated Autophagy.	Cannabidiol	0-11	heme oxygenase 1	Homo sapiens	50-66
32708634-2	2020	This study investigated the influence of CBD on the expression of heme oxygenase-1 (HO-1) and its functional role in regulating metabolic, autophagic, and apoptotic processes of human umbilical vein endothelial cells (HUVEC).	Cannabidiol	41-44	heme oxygenase 1	Homo sapiens	66-82
32708634-2	2020	This study investigated the influence of CBD on the expression of heme oxygenase-1 (HO-1) and its functional role in regulating metabolic, autophagic, and apoptotic processes of human umbilical vein endothelial cells (HUVEC).	Cannabidiol	41-44	heme oxygenase 1	Homo sapiens	84-88
32708634-3	2020	Concentrations up to 10 microM CBD showed a concentration-dependent increase of HO-1 mRNA and protein and an increase of the HO-1-regulating transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2).	Cannabidiol	31-34	heme oxygenase 1	Homo sapiens	80-84
32708634-3	2020	Concentrations up to 10 microM CBD showed a concentration-dependent increase of HO-1 mRNA and protein and an increase of the HO-1-regulating transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2).	Cannabidiol	31-34	heme oxygenase 1	Homo sapiens	125-129
32708634-3	2020	Concentrations up to 10 microM CBD showed a concentration-dependent increase of HO-1 mRNA and protein and an increase of the HO-1-regulating transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2).	Cannabidiol	31-34	NFE2 like bZIP transcription factor 2	Homo sapiens	162-205
32708634-3	2020	Concentrations up to 10 microM CBD showed a concentration-dependent increase of HO-1 mRNA and protein and an increase of the HO-1-regulating transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2).	Cannabidiol	31-34	NFE2 like bZIP transcription factor 2	Homo sapiens	207-211
32708634-4	2020	CBD-induced HO-1 expression was not decreased by antagonists of cannabinoid-activated receptors (CB1, CB2, transient receptor potential vanilloid 1), but by the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC).	Cannabidiol	0-3	heme oxygenase 1	Homo sapiens	12-16
32708634-4	2020	CBD-induced HO-1 expression was not decreased by antagonists of cannabinoid-activated receptors (CB1, CB2, transient receptor potential vanilloid 1), but by the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC).	Cannabidiol	0-3	cannabinoid receptor 1	Homo sapiens	97-100
32708634-4	2020	CBD-induced HO-1 expression was not decreased by antagonists of cannabinoid-activated receptors (CB1, CB2, transient receptor potential vanilloid 1), but by the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC).	Cannabidiol	0-3	cannabinoid receptor 2	Homo sapiens	102-105
32708634-5	2020	The incubation of HUVEC with 6 microM CBD resulted in increased metabolic activity, while 10 microM CBD caused decreased metabolic activity and an induction of apoptosis, as demonstrated by enhanced caspase-3 cleavage.	Cannabidiol	100-103	caspase 3	Homo sapiens	199-208
32708634-9	2020	On the other hand, the inhibition of HO-1 activity with tin protoporphyrin IX (SnPPIX) or knockdown of HO-1 expression by Nrf2 siRNA was associated with a decrease in CBD-mediated autophagy and apoptosis.	Cannabidiol	167-170	heme oxygenase 1	Homo sapiens	37-41
32708634-9	2020	On the other hand, the inhibition of HO-1 activity with tin protoporphyrin IX (SnPPIX) or knockdown of HO-1 expression by Nrf2 siRNA was associated with a decrease in CBD-mediated autophagy and apoptosis.	Cannabidiol	167-170	heme oxygenase 1	Homo sapiens	103-107
32708634-9	2020	On the other hand, the inhibition of HO-1 activity with tin protoporphyrin IX (SnPPIX) or knockdown of HO-1 expression by Nrf2 siRNA was associated with a decrease in CBD-mediated autophagy and apoptosis.	Cannabidiol	167-170	NFE2 like bZIP transcription factor 2	Homo sapiens	122-126
32708634-10	2020	In summary, our data show for the first time ROS-mediated HO-1 expression in endothelial cells as a mechanism by which CBD mediates protective autophagy, which at higher CBD concentrations, however, can no longer prevent cell death inducing apoptosis.	Cannabidiol	119-122	heme oxygenase 1	Homo sapiens	58-62
32708634-10	2020	In summary, our data show for the first time ROS-mediated HO-1 expression in endothelial cells as a mechanism by which CBD mediates protective autophagy, which at higher CBD concentrations, however, can no longer prevent cell death inducing apoptosis.	Cannabidiol	170-173	heme oxygenase 1	Homo sapiens	58-62
31162770-6	2020	Our results show that a 6-day repeated temozolomide treatment (25 mg/kg/day), a chemotherapy drug that blocks hippocampal neurogenesis, prevented cannabidiol-induced increment in the early stages of neuronal maturation and differentiation, without altering the basal levels of BrdU/NeuN and doublecortin immunostaining.	Cannabidiol	146-157	RNA binding protein, fox-1 homolog (C. elegans) 3	Mus musculus	282-286
31215752-0	2020	Cannabidiol inhibits sucrose self-administration by CB1 and CB2 receptor mechanisms in rodents.	Cannabidiol	0-11	cannabinoid receptor 1 (brain)	Mus musculus	52-55
31215752-0	2020	Cannabidiol inhibits sucrose self-administration by CB1 and CB2 receptor mechanisms in rodents.	Cannabidiol	0-11	cannabinoid receptor 2 (macrophage)	Mus musculus	60-63
31215752-4	2020	Systemic administration of CBD (10, 20, and 40 mg/kg, ip) produced a dose-dependent reduction in sucrose self-administration in rats and in wild-type (WT) and CB1-/- mice but not in CB2-/- mice.	Cannabidiol	27-30	cannabinoid receptor 1	Rattus norvegicus	159-162
31215752-6	2020	Similarly, pretreatment with AM251, a CB1R antagonist, potentiated, while AM630, a selective CB2R antagonist, blocked CBD-induced reduction in sucrose self-administration, suggesting the involvement of CB1 and CB2 receptors.	Cannabidiol	118-121	cannabinoid receptor 2 (macrophage)	Mus musculus	93-97
31215752-6	2020	Similarly, pretreatment with AM251, a CB1R antagonist, potentiated, while AM630, a selective CB2R antagonist, blocked CBD-induced reduction in sucrose self-administration, suggesting the involvement of CB1 and CB2 receptors.	Cannabidiol	118-121	cannabinoid receptor 2 (macrophage)	Mus musculus	93-96
31215752-8	2020	Pretreatment with AM251 enhanced, while AM630 blocked JWH133-induced reduction in sucrose self-administration in WT mice, suggesting that CBD inhibits sucrose self-administration likely by CB1 receptor antagonism and CB2 receptor agonism.	Cannabidiol	138-141	cannabinoid receptor 1 (brain)	Mus musculus	189-192
31215752-8	2020	Pretreatment with AM251 enhanced, while AM630 blocked JWH133-induced reduction in sucrose self-administration in WT mice, suggesting that CBD inhibits sucrose self-administration likely by CB1 receptor antagonism and CB2 receptor agonism.	Cannabidiol	138-141	cannabinoid receptor 2 (macrophage)	Mus musculus	217-220
32360362-0	2020	Altered dopamine D3 receptor gene expression in MAM model of schizophrenia is reversed by peripubertal cannabidiol treatment.	Cannabidiol	103-114	dopamine receptor D3	Rattus norvegicus	8-28
32360362-4	2020	Peripubertal treatment with the non-euphoric phytocannabinoid cannabidiol (30 mg/kg) from postnatal day (PND) 19 to PND 39 was able to reverse in MAM exposed rats: i) the up-regulation of the dopamine D3 receptor mRNA (only partially prevented by haloperidol 0.6 mg/kg/day); and ii) the regional blood flow changes in MAM exposed rats.	Cannabidiol	62-73	dopamine receptor D3	Rattus norvegicus	192-212
32360362-5	2020	Molecular modelling predicted that cannabidiol could bind preferentially to dopamine D3 receptor, where it may act as a partial agonist according to conformation of ionic-lock, which is highly conserved in GPCRs.	Cannabidiol	35-46	dopamine receptor D3	Rattus norvegicus	76-96
32077098-4	2020	We further hypothesized that cannabidiol (CBD), one of the main constituents of Cannabis sativa, through its effects on Nav1.5, could protect against high glucose elicited oxidative stress and cytotoxicity.	Cannabidiol	29-40	sodium voltage-gated channel alpha subunit 5	Homo sapiens	120-126
32077098-4	2020	We further hypothesized that cannabidiol (CBD), one of the main constituents of Cannabis sativa, through its effects on Nav1.5, could protect against high glucose elicited oxidative stress and cytotoxicity.	Cannabidiol	42-45	sodium voltage-gated channel alpha subunit 5	Homo sapiens	120-126
32374168-0	2020	Inhibitory Effect of Cannabidiol on the Activation of NLRP3 Inflammasome Is Associated with Its Modulation of the P2X7 Receptor in Human Monocytes.	Cannabidiol	21-32	NLR family pyrin domain containing 3	Homo sapiens	54-59
32913957-0	2020	Add-on cannabidiol significantly decreases seizures in 3 patients with SYNGAP1 developmental and epileptic encephalopathy.	Cannabidiol	7-18	synaptic Ras GTPase activating protein 1	Homo sapiens	71-78
32913957-3	2020	In a prospective study of add-on cannabidiol (CBD), we identified three patients with SYNGAP1 mutations: two boys and one girl.	Cannabidiol	33-44	synaptic Ras GTPase activating protein 1	Homo sapiens	86-93
32913957-3	2020	In a prospective study of add-on cannabidiol (CBD), we identified three patients with SYNGAP1 mutations: two boys and one girl.	Cannabidiol	46-49	synaptic Ras GTPase activating protein 1	Homo sapiens	86-93
32913957-11	2020	CBD showed efficacy in patients with drug-resistant epilepsy due to SYNGAP1 mutations.	Cannabidiol	0-3	synaptic Ras GTPase activating protein 1	Homo sapiens	68-75
32409220-3	2020	Recent preclinical studies have suggested cannabidiol (CBD) may mediate the mTOR pathway, however, its exact effects are unclear.	Cannabidiol	42-53	mechanistic target of rapamycin kinase	Homo sapiens	76-80
32409220-3	2020	Recent preclinical studies have suggested cannabidiol (CBD) may mediate the mTOR pathway, however, its exact effects are unclear.	Cannabidiol	55-58	mechanistic target of rapamycin kinase	Homo sapiens	76-80
32374168-0	2020	Inhibitory Effect of Cannabidiol on the Activation of NLRP3 Inflammasome Is Associated with Its Modulation of the P2X7 Receptor in Human Monocytes.	Cannabidiol	21-32	purinergic receptor P2X 7	Homo sapiens	114-127
32374168-1	2020	Cannabidiol (CBD), a phytocannabinoid, has been reported to have anti-inflammatory effects associated with NLRP3 inflammasome activation, but its mechanism of anti-inflammasome action remains unclear.	Cannabidiol	0-11	NLR family pyrin domain containing 3	Homo sapiens	107-112
32374168-1	2020	Cannabidiol (CBD), a phytocannabinoid, has been reported to have anti-inflammatory effects associated with NLRP3 inflammasome activation, but its mechanism of anti-inflammasome action remains unclear.	Cannabidiol	13-16	NLR family pyrin domain containing 3	Homo sapiens	107-112
32374168-2	2020	Herein, we report CBD"s effect on NLRP3 inflammasome activation and its modulation of P2X7, an inflammasome activation-related receptor, in human THP-1 monocytes.	Cannabidiol	18-21	NLR family pyrin domain containing 3	Homo sapiens	34-39
32374168-2	2020	Herein, we report CBD"s effect on NLRP3 inflammasome activation and its modulation of P2X7, an inflammasome activation-related receptor, in human THP-1 monocytes.	Cannabidiol	18-21	purinergic receptor P2X 7	Homo sapiens	86-90
32374168-2	2020	Herein, we report CBD"s effect on NLRP3 inflammasome activation and its modulation of P2X7, an inflammasome activation-related receptor, in human THP-1 monocytes.	Cannabidiol	18-21	GLI family zinc finger 2	Homo sapiens	146-151
32374168-4	2020	CBD (10 muM) decreased nigericin-alone- and nigericin-lipopolysaccharide-induced potassium efflux by 13.7% and 13.0%, respectively, in THP-1 monocytes, strongly suggesting P2X7 receptor modulation.	Cannabidiol	0-3	GLI family zinc finger 2	Homo sapiens	135-140
32374168-4	2020	CBD (10 muM) decreased nigericin-alone- and nigericin-lipopolysaccharide-induced potassium efflux by 13.7% and 13.0%, respectively, in THP-1 monocytes, strongly suggesting P2X7 receptor modulation.	Cannabidiol	0-3	purinergic receptor P2X 7	Homo sapiens	172-185
32374168-5	2020	Computational docking data supported the potential for CBD binding to the P2X7 receptor via interaction with GLU 172 and VAL 173 residues.	Cannabidiol	55-58	purinergic receptor P2X 7	Homo sapiens	74-87
32374168-7	2020	CBD inhibitory effects on the NLRP3 inflammasome may contribute to the overall anti-inflammatory effects reported for this phytocannabinoid.	Cannabidiol	0-3	NLR family pyrin domain containing 3	Homo sapiens	30-35
32905152-0	2020	Erratum to: Cannabidiol attenuates methamphetamine-induced conditioned place preference via the Sigma1R/AKT/GSK-3beta/CREB signaling pathway in rats.	Cannabidiol	12-23	sigma non-opioid intracellular receptor 1	Rattus norvegicus	96-103
32905152-0	2020	Erratum to: Cannabidiol attenuates methamphetamine-induced conditioned place preference via the Sigma1R/AKT/GSK-3beta/CREB signaling pathway in rats.	Cannabidiol	12-23	AKT serine/threonine kinase 1	Rattus norvegicus	104-107
32905152-0	2020	Erratum to: Cannabidiol attenuates methamphetamine-induced conditioned place preference via the Sigma1R/AKT/GSK-3beta/CREB signaling pathway in rats.	Cannabidiol	12-23	glycogen synthase kinase 3 alpha	Rattus norvegicus	108-117
32905152-0	2020	Erratum to: Cannabidiol attenuates methamphetamine-induced conditioned place preference via the Sigma1R/AKT/GSK-3beta/CREB signaling pathway in rats.	Cannabidiol	12-23	cAMP responsive element binding protein 1	Rattus norvegicus	118-122
33463166-12	2020	This study demonstrates that CBD-mediated LL37 tethering is a viable strategy to reduce LL37 toxicity, and how substrate composition plays a crucial role in modulating the antimicrobial activity of tethered AMPs.	Cannabidiol	29-32	cathelicidin antimicrobial peptide	Homo sapiens	42-46
33463166-12	2020	This study demonstrates that CBD-mediated LL37 tethering is a viable strategy to reduce LL37 toxicity, and how substrate composition plays a crucial role in modulating the antimicrobial activity of tethered AMPs.	Cannabidiol	29-32	cathelicidin antimicrobial peptide	Homo sapiens	88-92
32656346-0	2020	Anticonvulsive Properties of Cannabidiol in a Model of Generalized Seizure Are Transient Receptor Potential Vanilloid 1 Dependent.	Cannabidiol	29-40	transient receptor potential cation channel subfamily V member 1	Homo sapiens	79-119
32656346-6	2020	Results: At 50 and 100 mg/kg, CBD significantly (p<0.0001) increased seizure threshold in wildtype mice compared with TRPV1 knockout and vehicle controls.	Cannabidiol	30-33	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	118-123
32656346-7	2020	This effect was observed only at 100 mg/kg in TRPV1 knockout mice compared with knockout vehicle mice, in which gene deletion partially attenuated the CBD-increased seizure threshold.	Cannabidiol	151-154	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	46-51
32656346-10	2020	Conclusion: These data strongly implicate TRPV1 in the potential mechanisms of action for the anticonvulsive effects of CBD.	Cannabidiol	120-123	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	42-47
32656346-11	2020	The partial inhibition of the anticonvulsive effect of high-dose CBD in TRPV1 knockout mice may indicate the involvement of targets other than TRPV1.	Cannabidiol	65-68	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	72-77
32656346-12	2020	Further characterization of TRPV1 in the anticonvulsive effect of CBD in validated models of seizure is warranted, as is pharmacological investigation of the molecular interaction between CBD and TRPV1.	Cannabidiol	66-69	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	28-33
32656347-3	2020	Materials and Methods: We tested whether a natural cannabis extract highly enriched in cannabidiol (CBD) might be effective in curbing the pathological phenotype of malin knockout (KO) mice as an animal model of LD.	Cannabidiol	87-98	NHL repeat containing 1	Mus musculus	165-170
32656347-3	2020	Materials and Methods: We tested whether a natural cannabis extract highly enriched in cannabidiol (CBD) might be effective in curbing the pathological phenotype of malin knockout (KO) mice as an animal model of LD.	Cannabidiol	100-103	NHL repeat containing 1	Mus musculus	165-170
32656347-4	2020	Results: Our results reveal for the first time that alterations in the ECS occur during the evolution of LD, mainly at the level of CB1, CB2, and G protein-coupled receptor 55 (GPR55) receptor expression, and that a CBD-enriched extract (CBDext) is able to reduce the cognitive impairment exhibited by malin KO mice.	Cannabidiol	216-219	G protein-coupled receptor 55	Mus musculus	146-175
32656347-4	2020	Results: Our results reveal for the first time that alterations in the ECS occur during the evolution of LD, mainly at the level of CB1, CB2, and G protein-coupled receptor 55 (GPR55) receptor expression, and that a CBD-enriched extract (CBDext) is able to reduce the cognitive impairment exhibited by malin KO mice.	Cannabidiol	216-219	NHL repeat containing 1	Mus musculus	302-307
32452532-1	2020	OBJECTIVE: To evaluate the potential impact of concomitant clobazam (CLB) use on the efficacy of cannabidiol (CBD) treatment in patients with Dravet syndrome and Lennox-Gastaut syndrome using meta-analytical techniques.	Cannabidiol	97-108	citramalyl-CoA lyase	Homo sapiens	69-72
32321192-7	2020	KEY RESULTS: In Scn1a-/- mice, cannabidiol increased survival and delayed worsening of neonatal welfare.	Cannabidiol	31-42	sodium channel, voltage-gated, type I, alpha	Mus musculus	16-21
32321192-8	2020	In Scn1a+/- mice, chronic cannabidiol administration did not show any adverse effect on motor function and gait, reduced premature mortality, improved social behaviour and memory function, and reduced anxiety-like and depressive-like behaviours.	Cannabidiol	26-37	sodium channel, voltage-gated, type I, alpha	Mus musculus	3-8
32147492-0	2020	The effect of delta-9-tetrahydrocannabinol and cannabidiol on p50 of the oxygen haemoglobin dissociation curve.	Cannabidiol	47-58	nuclear factor kappa B subunit 1	Homo sapiens	62-65
32147492-7	2020	The results indicate that there is a decrease in P50 with increasing concentrations of both THC and CBD separately and in combination.	Cannabidiol	100-103	nuclear factor kappa B subunit 1	Homo sapiens	49-52
32147492-8	2020	The decrease in P50 was significant (p < .05) at all concentrations of THC and CBD.	Cannabidiol	79-82	nuclear factor kappa B subunit 1	Homo sapiens	16-19
32184097-0	2020	Cannabidiol exerts protective effects in an in vitro model of Parkinson"s disease activating AKT/mTOR pathway.	Cannabidiol	0-11	AKT serine/threonine kinase 1	Homo sapiens	93-96
32184097-0	2020	Cannabidiol exerts protective effects in an in vitro model of Parkinson"s disease activating AKT/mTOR pathway.	Cannabidiol	0-11	mechanistic target of rapamycin kinase	Homo sapiens	97-101
32184097-5	2020	CBD counteracted the loss of cell viability caused by MPP+, reducing apoptosis as demonstrated by the reduction of Bax and caspase 3.	Cannabidiol	0-3	BCL2 associated X, apoptosis regulator	Homo sapiens	115-118
32184097-5	2020	CBD counteracted the loss of cell viability caused by MPP+, reducing apoptosis as demonstrated by the reduction of Bax and caspase 3.	Cannabidiol	0-3	caspase 3	Homo sapiens	123-132
32151683-0	2020	Cannabidiol attenuates behavioral changes in a rodent model of schizophrenia through 5-HT1A, but not CB1 and CB2 receptors.	Cannabidiol	0-11	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	85-91
32151683-8	2020	These data suggest that CBD induces antipsychotic-like effects by activating 5-HT1A receptors and indicate that this compound could be an interesting alternative for the treatment of negative and cognitive symptoms of schizophrenia.	Cannabidiol	24-27	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	77-83
32444381-8	2020	Cannabidiol inhibits CYP3A4 and CYP2C19, both of which are involved in the metabolism of methadone.	Cannabidiol	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	21-27
32444381-8	2020	Cannabidiol inhibits CYP3A4 and CYP2C19, both of which are involved in the metabolism of methadone.	Cannabidiol	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-39
32452532-6	2020	Among CBD-treated patients, 240 (55.9%) were taking concomitant CLB (CLB-On) and 189 (44.1%) were not taking concomitant CLB (CLB-Off); in placebo-treated patients, 158 (55.4%) were CLB-On and 127 (44.6%) CLB-Off.	Cannabidiol	6-9	citramalyl-CoA lyase	Homo sapiens	64-67
32452532-6	2020	Among CBD-treated patients, 240 (55.9%) were taking concomitant CLB (CLB-On) and 189 (44.1%) were not taking concomitant CLB (CLB-Off); in placebo-treated patients, 158 (55.4%) were CLB-On and 127 (44.6%) CLB-Off.	Cannabidiol	6-9	citramalyl-CoA lyase	Homo sapiens	205-212
32452532-8	2020	Among CBL-On patients, the >=50% reduction in seizure frequency was found in 52.9% and 27.8% in the CBD and placebo groups, respectively (RR = 1.85, 95% CI = 1.40-2.44, P < .001).	Cannabidiol	100-103	Cbl proto-oncogene	Homo sapiens	6-9
32670551-0	2020	Cannabidiol attenuates methamphetamine-induced conditioned place preference via the Sigma1R/AKT/GSK-3beta/CREB signaling pathway in rats.	Cannabidiol	0-11	sigma non-opioid intracellular receptor 1	Rattus norvegicus	84-91
32670551-0	2020	Cannabidiol attenuates methamphetamine-induced conditioned place preference via the Sigma1R/AKT/GSK-3beta/CREB signaling pathway in rats.	Cannabidiol	0-11	AKT serine/threonine kinase 1	Rattus norvegicus	92-95
32670551-0	2020	Cannabidiol attenuates methamphetamine-induced conditioned place preference via the Sigma1R/AKT/GSK-3beta/CREB signaling pathway in rats.	Cannabidiol	0-11	glycogen synthase kinase 3 alpha	Rattus norvegicus	96-105
32670551-0	2020	Cannabidiol attenuates methamphetamine-induced conditioned place preference via the Sigma1R/AKT/GSK-3beta/CREB signaling pathway in rats.	Cannabidiol	0-11	cAMP responsive element binding protein 1	Rattus norvegicus	106-110
32670551-4	2020	The present study examines whether CBD has a protective effect on METH-induced conditioned place preference (CPP) in rats by regulating the Sigma1R and AKT-GSK3beta-CREB signaling pathway.	Cannabidiol	35-38	sigma non-opioid intracellular receptor 1	Rattus norvegicus	140-147
32670551-4	2020	The present study examines whether CBD has a protective effect on METH-induced conditioned place preference (CPP) in rats by regulating the Sigma1R and AKT-GSK3beta-CREB signaling pathway.	Cannabidiol	35-38	AKT serine/threonine kinase 1	Rattus norvegicus	152-155
32670551-4	2020	The present study examines whether CBD has a protective effect on METH-induced conditioned place preference (CPP) in rats by regulating the Sigma1R and AKT-GSK3beta-CREB signaling pathway.	Cannabidiol	35-38	glycogen synthase kinase 3 alpha	Rattus norvegicus	156-164
32670551-4	2020	The present study examines whether CBD has a protective effect on METH-induced conditioned place preference (CPP) in rats by regulating the Sigma1R and AKT-GSK3beta-CREB signaling pathway.	Cannabidiol	35-38	cAMP responsive element binding protein 1	Rattus norvegicus	165-169
32670551-11	2020	Treatment involving different doses of CBD caused differential inhibitory responses in the cellular protein abundance of Sigma1R, p-AKT, p-GSK3beta, and p-CREB across various brain regions.	Cannabidiol	39-42	sigma non-opioid intracellular receptor 1	Rattus norvegicus	121-128
32670551-11	2020	Treatment involving different doses of CBD caused differential inhibitory responses in the cellular protein abundance of Sigma1R, p-AKT, p-GSK3beta, and p-CREB across various brain regions.	Cannabidiol	39-42	AKT serine/threonine kinase 1	Rattus norvegicus	132-135
32670551-11	2020	Treatment involving different doses of CBD caused differential inhibitory responses in the cellular protein abundance of Sigma1R, p-AKT, p-GSK3beta, and p-CREB across various brain regions.	Cannabidiol	39-42	glycogen synthase kinase 3 alpha	Rattus norvegicus	139-147
32670551-11	2020	Treatment involving different doses of CBD caused differential inhibitory responses in the cellular protein abundance of Sigma1R, p-AKT, p-GSK3beta, and p-CREB across various brain regions.	Cannabidiol	39-42	cAMP responsive element binding protein 1	Rattus norvegicus	155-159
32457622-6	2020	Exogenously, GPR12 is a target for the phytocannabinoid cannabidiol (CBD).	Cannabidiol	56-67	G protein-coupled receptor 12	Homo sapiens	13-18
32457622-6	2020	Exogenously, GPR12 is a target for the phytocannabinoid cannabidiol (CBD).	Cannabidiol	69-72	G protein-coupled receptor 12	Homo sapiens	13-18
31013550-7	2020	Results indicated that CNR1 rs1049353 GG carriers showed increased state satiety after THC/THC + CBD administration in comparison with placebo and reduced the salience of appetitive cues after THC in comparison with CBD administration; A carriers did not vary on either of these measures indicative of a vulnerability to CUD.	Cannabidiol	97-100	cannabinoid receptor 1	Homo sapiens	23-27
31013550-7	2020	Results indicated that CNR1 rs1049353 GG carriers showed increased state satiety after THC/THC + CBD administration in comparison with placebo and reduced the salience of appetitive cues after THC in comparison with CBD administration; A carriers did not vary on either of these measures indicative of a vulnerability to CUD.	Cannabidiol	216-219	cannabinoid receptor 1	Homo sapiens	23-27
31074060-10	2020	Repeated administration with CBD (60 mg/kg) significantly reduced TH and OPRM1 in males.	Cannabidiol	29-32	opioid receptor, mu 1	Mus musculus	73-78
31074060-11	2020	In addition, CBD (30 and 60 mg/kg) significantly reduced CB1 r in males.	Cannabidiol	13-16	cannabinoid receptor 1 (brain)	Mus musculus	57-62
31800399-9	2020	CONCLUSION: The CBD-induced relaxation in hPAs that was reduced in hypertensive, obese and hypercholesteremic patients was endothelium-dependent and mediated via KCa and IP, EP4, TRPV1 receptors.	Cannabidiol	16-19	prostaglandin E receptor 4	Homo sapiens	174-177
31437433-0	2020	Cannabidiol attenuates the rewarding effects of cocaine in rats by CB2, 5-TH1A and TRPV1 receptor mechanisms.	Cannabidiol	0-11	cannabinoid receptor 2	Rattus norvegicus	67-70
31437433-0	2020	Cannabidiol attenuates the rewarding effects of cocaine in rats by CB2, 5-TH1A and TRPV1 receptor mechanisms.	Cannabidiol	0-11	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	83-88
31800399-9	2020	CONCLUSION: The CBD-induced relaxation in hPAs that was reduced in hypertensive, obese and hypercholesteremic patients was endothelium-dependent and mediated via KCa and IP, EP4, TRPV1 receptors.	Cannabidiol	16-19	transient receptor potential cation channel subfamily V member 1	Homo sapiens	179-184
31800399-10	2020	The CBD effect in rats was CB1-sensitive and dependent on the hypertension model.	Cannabidiol	4-7	cannabinoid receptor 1	Rattus norvegicus	27-30
32244818-0	2020	Differential Inhibition of Human Nav1.2 Resurgent and Persistent Sodium Currents by Cannabidiol and GS967.	Cannabidiol	84-95	sodium voltage-gated channel alpha subunit 2	Homo sapiens	33-39
31724188-8	2020	Cannabidiol inhibits CYP2C19, an isoenzyme responsible for the transformation of clopidogrel to its active thiol metabolite.	Cannabidiol	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-28
31919563-0	2020	Cannabidiol-induced panicolytic-like effects and fear-induced antinociception impairment: the role of the CB1 receptor in the ventromedial hypothalamus.	Cannabidiol	0-11	cannabinoid receptor 1	Rattus norvegicus	106-109
31919563-6	2020	In addition, the most effective dose of CBD was used after pre-treatment with the CB1 receptor selective antagonist AM251, followed by NMDA microinjections in the VMH.	Cannabidiol	40-43	cannabinoid receptor 1	Rattus norvegicus	82-85
31919563-10	2020	CONCLUSION: These findings suggest that CBD causes panicolytic-like effects and reduces unconditioned fear-induced antinociception when administered in the VMH, and these effects are mediated by the CB1 receptor-endocannabinoid signalling mechanism in VMH.	Cannabidiol	40-43	cannabinoid receptor 1	Rattus norvegicus	199-202
31953017-6	2020	We also show that CBD prevents the increase on transcript levels of CYP19A1 gene and the elevation of E2 levels that are observed in differentiating ESCs.	Cannabidiol	18-21	cytochrome P450 family 19 subfamily A member 1	Homo sapiens	68-75
32244518-6	2020	Cannabidiol reestablished the epithelial organization lost by dispersion of the cells and re-localized E-cadherin and beta-catenin at the adherens junctions.	Cannabidiol	0-11	cadherin 1	Homo sapiens	103-113
32410828-10	2020	Numerous drugs were found exerting their anti-tumor function through Id1-related signaling pathways, such as fucoidan, berberine, tetramethylpyrazine, crizotinib, cannabidiol and vinblastine.	Cannabidiol	163-174	inhibitor of DNA binding 1, HLH protein	Homo sapiens	69-72
32244518-6	2020	Cannabidiol reestablished the epithelial organization lost by dispersion of the cells and re-localized E-cadherin and beta-catenin at the adherens junctions.	Cannabidiol	0-11	catenin beta 1	Homo sapiens	118-130
32244518-8	2020	Cannabidiol inhibited the protein kinase B (AKT) activation, a crucial effector in the IL-1beta/IL-1RI/beta-catenin pathway, indicating that at this point there is crosstalk between IL-1beta and CBD signaling which results in phenotype reversion.	Cannabidiol	0-11	protein tyrosine kinase 2 beta	Homo sapiens	26-42
32244518-8	2020	Cannabidiol inhibited the protein kinase B (AKT) activation, a crucial effector in the IL-1beta/IL-1RI/beta-catenin pathway, indicating that at this point there is crosstalk between IL-1beta and CBD signaling which results in phenotype reversion.	Cannabidiol	0-11	AKT serine/threonine kinase 1	Homo sapiens	44-47
32244518-8	2020	Cannabidiol inhibited the protein kinase B (AKT) activation, a crucial effector in the IL-1beta/IL-1RI/beta-catenin pathway, indicating that at this point there is crosstalk between IL-1beta and CBD signaling which results in phenotype reversion.	Cannabidiol	0-11	interleukin 1 alpha	Homo sapiens	87-95
32244518-8	2020	Cannabidiol inhibited the protein kinase B (AKT) activation, a crucial effector in the IL-1beta/IL-1RI/beta-catenin pathway, indicating that at this point there is crosstalk between IL-1beta and CBD signaling which results in phenotype reversion.	Cannabidiol	0-11	interleukin 1 receptor type 1	Homo sapiens	96-102
32244518-8	2020	Cannabidiol inhibited the protein kinase B (AKT) activation, a crucial effector in the IL-1beta/IL-1RI/beta-catenin pathway, indicating that at this point there is crosstalk between IL-1beta and CBD signaling which results in phenotype reversion.	Cannabidiol	0-11	catenin beta 1	Homo sapiens	103-115
32244518-8	2020	Cannabidiol inhibited the protein kinase B (AKT) activation, a crucial effector in the IL-1beta/IL-1RI/beta-catenin pathway, indicating that at this point there is crosstalk between IL-1beta and CBD signaling which results in phenotype reversion.	Cannabidiol	0-11	interleukin 1 alpha	Homo sapiens	182-190
31647138-0	2020	Cannabidiol prevents LPS-induced microglial inflammation by inhibiting ROS/NF-kappaB-dependent signaling and glucose consumption.	Cannabidiol	0-11	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	75-84
32256321-4	2020	Here, we have employed astrocytes and vascular endothelial cell cultures subjected to hypoxia, to test the effect of cannabidiol (CBD) on the P-gp-dependent Rhodamine-123 (Rho-123) efflux.	Cannabidiol	117-128	ATP binding cassette subfamily B member 1	Homo sapiens	142-146
32256321-4	2020	Here, we have employed astrocytes and vascular endothelial cell cultures subjected to hypoxia, to test the effect of cannabidiol (CBD) on the P-gp-dependent Rhodamine-123 (Rho-123) efflux.	Cannabidiol	130-133	ATP binding cassette subfamily B member 1	Homo sapiens	142-146
32256321-7	2020	Additionally, docking studies predicted that CBD could behave as a P-gp substrate by the interaction with several residues in the alpha-helix of the P-gp transmembrane domain.	Cannabidiol	45-48	ATP binding cassette subfamily B member 1	Homo sapiens	67-71
32256321-7	2020	Additionally, docking studies predicted that CBD could behave as a P-gp substrate by the interaction with several residues in the alpha-helix of the P-gp transmembrane domain.	Cannabidiol	45-48	ATP binding cassette subfamily B member 1	Homo sapiens	149-153
32256440-7	2020	Nabiximols (a combination of THC and CBD oromucosal spray) interact with both CB1 and CB2 receptors.	Cannabidiol	37-40	cannabinoid receptor 1	Homo sapiens	78-81
32256440-7	2020	Nabiximols (a combination of THC and CBD oromucosal spray) interact with both CB1 and CB2 receptors.	Cannabidiol	37-40	cannabinoid receptor 2	Homo sapiens	86-89
30793820-6	2020	The aim of this study was to assess whether CBD prevents reinstatement of METH through change of gene expression of cytokines such as interleukin-1beta, interleukin-6, interleukin-10, and tumor necrosis factor alpha (TNF-alpha) in extinguished rats.	Cannabidiol	44-47	interleukin 1 beta	Rattus norvegicus	134-151
30793820-6	2020	The aim of this study was to assess whether CBD prevents reinstatement of METH through change of gene expression of cytokines such as interleukin-1beta, interleukin-6, interleukin-10, and tumor necrosis factor alpha (TNF-alpha) in extinguished rats.	Cannabidiol	44-47	interleukin 6	Rattus norvegicus	153-166
30793820-6	2020	The aim of this study was to assess whether CBD prevents reinstatement of METH through change of gene expression of cytokines such as interleukin-1beta, interleukin-6, interleukin-10, and tumor necrosis factor alpha (TNF-alpha) in extinguished rats.	Cannabidiol	44-47	interleukin 10	Rattus norvegicus	168-182
30793820-6	2020	The aim of this study was to assess whether CBD prevents reinstatement of METH through change of gene expression of cytokines such as interleukin-1beta, interleukin-6, interleukin-10, and tumor necrosis factor alpha (TNF-alpha) in extinguished rats.	Cannabidiol	44-47	tumor necrosis factor	Rattus norvegicus	188-215
30793820-6	2020	The aim of this study was to assess whether CBD prevents reinstatement of METH through change of gene expression of cytokines such as interleukin-1beta, interleukin-6, interleukin-10, and tumor necrosis factor alpha (TNF-alpha) in extinguished rats.	Cannabidiol	44-47	tumor necrosis factor	Rattus norvegicus	217-226
31647138-2	2020	Under LPS stimulation, CBD (1-10 muM) potently inhibited the release of prototypical proinflammatory cytokines (TNF-alpha and IL-1beta) and that of glutamate, a noncytokine mediator of inflammation.	Cannabidiol	23-26	tumor necrosis factor	Mus musculus	112-121
31647138-2	2020	Under LPS stimulation, CBD (1-10 muM) potently inhibited the release of prototypical proinflammatory cytokines (TNF-alpha and IL-1beta) and that of glutamate, a noncytokine mediator of inflammation.	Cannabidiol	23-26	interleukin 1 alpha	Mus musculus	126-134
31647138-3	2020	The effects of CBD were predominantly receptor-independent and only marginally blunted by blockade of CB2 receptors.	Cannabidiol	15-18	cannabinoid receptor 2 (macrophage)	Mus musculus	102-105
31647138-4	2020	We established that CBD inhibited a mechanism involving, sequentially, NADPH oxidase-mediated ROS production and NF-kappaB-dependent signaling events.	Cannabidiol	20-23	2,4-dienoyl CoA reductase 1, mitochondrial	Mus musculus	71-76
31647138-4	2020	We established that CBD inhibited a mechanism involving, sequentially, NADPH oxidase-mediated ROS production and NF-kappaB-dependent signaling events.	Cannabidiol	20-23	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	113-122
31647138-6	2020	Of interest, CBD also prevented the rise in glucose uptake observed in microglial cells challenged with LPS, as did the inhibitor of NADPH oxidase apocynin and the inhibitor of IkappaB kinase-2, TPCA-1.	Cannabidiol	13-16	2,4-dienoyl CoA reductase 1, mitochondrial	Mus musculus	133-138
31647138-9	2020	Interestingly, CBD and 2-DG, as well as apocynin and TPCA-1 caused a reduction in glucose-derived NADPH, a cofactor required for NADPH oxidase activation and ROS generation.	Cannabidiol	15-18	2,4-dienoyl CoA reductase 1, mitochondrial	Mus musculus	98-103
31647138-9	2020	Interestingly, CBD and 2-DG, as well as apocynin and TPCA-1 caused a reduction in glucose-derived NADPH, a cofactor required for NADPH oxidase activation and ROS generation.	Cannabidiol	15-18	2,4-dienoyl CoA reductase 1, mitochondrial	Mus musculus	129-134
31647138-10	2020	These different observations suggest that CBD exerts its anti-inflammatory effects towards microglia through an intrinsic antioxidant effect, which is amplified through inhibition of glucose-dependent NADPH synthesis.	Cannabidiol	42-45	2,4-dienoyl CoA reductase 1, mitochondrial	Mus musculus	201-206
31802588-9	2020	O-1602 and CBD each lowered MPO and IL-6 levels remarkably in TNBS colitis, while TNF-alpha levels experienced no change.	Cannabidiol	11-14	myeloperoxidase	Rattus norvegicus	28-31
31802588-9	2020	O-1602 and CBD each lowered MPO and IL-6 levels remarkably in TNBS colitis, while TNF-alpha levels experienced no change.	Cannabidiol	11-14	interleukin 6	Rattus norvegicus	36-40
32121131-14	2020	The UV- and psoriasis-induced activity of transmembrane transporters (Multidrug-Resistance (MDR) and breast cancer resistance protein (BCRP)) is normalized after CBD treatment.	Cannabidiol	162-165	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	101-133
32121131-14	2020	The UV- and psoriasis-induced activity of transmembrane transporters (Multidrug-Resistance (MDR) and breast cancer resistance protein (BCRP)) is normalized after CBD treatment.	Cannabidiol	162-165	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	135-139
32185239-8	2020	While TAT-GILZ treatment did not significantly affect cells positive for cannabinoid receptors subtype 2 (CB2+), cannabidiol treatment increased frequency of both CB2+ and GILZ-positive (GILZ+) cells of IRI kidneys.	Cannabidiol	113-124	cannabinoid receptor 2 (macrophage)	Mus musculus	163-166
32185239-8	2020	While TAT-GILZ treatment did not significantly affect cells positive for cannabinoid receptors subtype 2 (CB2+), cannabidiol treatment increased frequency of both CB2+ and GILZ-positive (GILZ+) cells of IRI kidneys.	Cannabidiol	113-124	TSC22 domain family, member 3	Mus musculus	172-176
32185239-8	2020	While TAT-GILZ treatment did not significantly affect cells positive for cannabinoid receptors subtype 2 (CB2+), cannabidiol treatment increased frequency of both CB2+ and GILZ-positive (GILZ+) cells of IRI kidneys.	Cannabidiol	113-124	TSC22 domain family, member 3	Mus musculus	172-176
32185239-10	2020	Treatment with cannabidiol increased frequencies of each subset of GILZ+ ILCs, but the effect was more marked for ILC2s.	Cannabidiol	15-26	TSC22 domain family, member 3	Mus musculus	67-71
32185239-11	2020	Indeed, cannabidiol treatment increased CB2+ GILZ+ ILC2s.	Cannabidiol	8-19	cannabinoid receptor 2 (macrophage)	Mus musculus	40-43
32185239-11	2020	Indeed, cannabidiol treatment increased CB2+ GILZ+ ILC2s.	Cannabidiol	8-19	TSC22 domain family, member 3	Mus musculus	45-49
31986271-8	2020	For both CBD and Delta9-THC, in-tube SPME/UHPLC-MS/MS presented linear range from 10 to 300 ng mL-1, precision with coefficient of variation (CV) values ranging from 0.2% to 19.1% (LLOQ), and accuracy with relative standard deviation (RSD) values spanning from -9.3% to 19.6% (LLOQ).	Cannabidiol	9-12	L1 cell adhesion molecule	Mus musculus	95-99
32075117-5	2020	In the respective normotensive control rats, CBD increased lipid peroxidation, free fatty acid levels and FAAH activity.	Cannabidiol	45-48	fatty-acid amide hydrolase-like	Rattus norvegicus	106-110
32060308-8	2020	Furthermore, CBD enhanced the pro-apoptotic activities of JNK1/2 and MAPK p38 signaling cascades while partially downregulated the pro-survival PI3K-AKT cascade, thereby changing a balance between cell death and survival.	Cannabidiol	13-16	mitogen-activated protein kinase 8	Homo sapiens	58-64
32060308-9	2020	Suppression of JNK activation partially reduced CBD-induced cell death in 3D GBM cultures.	Cannabidiol	48-51	mitogen-activated protein kinase 8	Homo sapiens	15-18
32060308-10	2020	In contrast, co-treatment of CBD-targeted cells with inhibitors of PI3K-AKT-NF-kappaB, IKK-NF-kappaB or JAK2-STAT3 pathways killed surviving GBM cells in both 2D and 3D cultures, potentially improving the therapeutic ratio of GBM.	Cannabidiol	29-32	nuclear factor kappa B subunit 1	Homo sapiens	76-85
32060308-10	2020	In contrast, co-treatment of CBD-targeted cells with inhibitors of PI3K-AKT-NF-kappaB, IKK-NF-kappaB or JAK2-STAT3 pathways killed surviving GBM cells in both 2D and 3D cultures, potentially improving the therapeutic ratio of GBM.	Cannabidiol	29-32	nuclear factor kappa B subunit 1	Homo sapiens	91-100
32060308-10	2020	In contrast, co-treatment of CBD-targeted cells with inhibitors of PI3K-AKT-NF-kappaB, IKK-NF-kappaB or JAK2-STAT3 pathways killed surviving GBM cells in both 2D and 3D cultures, potentially improving the therapeutic ratio of GBM.	Cannabidiol	29-32	Janus kinase 2	Homo sapiens	104-108
32060308-10	2020	In contrast, co-treatment of CBD-targeted cells with inhibitors of PI3K-AKT-NF-kappaB, IKK-NF-kappaB or JAK2-STAT3 pathways killed surviving GBM cells in both 2D and 3D cultures, potentially improving the therapeutic ratio of GBM.	Cannabidiol	29-32	signal transducer and activator of transcription 3	Homo sapiens	109-114
32049991-3	2020	This necessitates the development of new complementary drugs, e.g., cannabinoid receptors (CB1 and CB2) agonists including tetrahydrocannabinol (THC) and cannabidiol (CBD).	Cannabidiol	154-165	cannabinoid receptor 1	Homo sapiens	91-94
32049991-3	2020	This necessitates the development of new complementary drugs, e.g., cannabinoid receptors (CB1 and CB2) agonists including tetrahydrocannabinol (THC) and cannabidiol (CBD).	Cannabidiol	154-165	cannabinoid receptor 2	Homo sapiens	99-102
32049991-14	2020	THC and CBD alone or in combination restored the epithelial phenotype, as evidenced by increased expression of CDH1 and reduced expression of CDH2 and VIM, as well as by fluorescence analysis of cellular cytoskeleton.	Cannabidiol	8-11	cadherin 1	Homo sapiens	111-115
32049991-14	2020	THC and CBD alone or in combination restored the epithelial phenotype, as evidenced by increased expression of CDH1 and reduced expression of CDH2 and VIM, as well as by fluorescence analysis of cellular cytoskeleton.	Cannabidiol	8-11	cadherin 2	Homo sapiens	142-146
32049991-14	2020	THC and CBD alone or in combination restored the epithelial phenotype, as evidenced by increased expression of CDH1 and reduced expression of CDH2 and VIM, as well as by fluorescence analysis of cellular cytoskeleton.	Cannabidiol	8-11	vimentin	Homo sapiens	151-154
32049991-17	2020	THC and CBD inhibited the proliferation and expression of EGFR in the lung cancer cells studied.	Cannabidiol	8-11	epidermal growth factor receptor	Homo sapiens	58-62
32103958-2	2020	CBD is a multi-target drug whose anti-convulsant properties are supposed to be independent of endocannabinoid receptor CB1 and might be related to several underlying mechanisms, such as antagonism on the orphan GPR55 receptor, regulation of adenosine tone, activation of 5HT1A receptors and modulation of calcium intracellular levels.	Cannabidiol	0-3	G protein-coupled receptor 55	Homo sapiens	211-216
32103958-2	2020	CBD is a multi-target drug whose anti-convulsant properties are supposed to be independent of endocannabinoid receptor CB1 and might be related to several underlying mechanisms, such as antagonism on the orphan GPR55 receptor, regulation of adenosine tone, activation of 5HT1A receptors and modulation of calcium intracellular levels.	Cannabidiol	0-3	5-hydroxytryptamine receptor 1A	Homo sapiens	271-276
32103958-10	2020	The interaction between CBD and clobazam, likely due to CYP2C19 inhibition, might contribute to some AEs, especially somnolence, but also to CBD clinical effectiveness.	Cannabidiol	24-27	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	56-63
32103958-10	2020	The interaction between CBD and clobazam, likely due to CYP2C19 inhibition, might contribute to some AEs, especially somnolence, but also to CBD clinical effectiveness.	Cannabidiol	141-144	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	56-63
32033040-2	2020	In cultures of primary mesencephalic neurons and neuroblastoma cells, we determined the capability of cannabidiol (CBD) and tetrahydrocannabinol (THC) to counteract effects elicited by complex I-inhibitor rotenone by analyzing neuron viability, morphology, gene expression of IL6, CHOP, XBP1, HO-1 (stress response), and HO-2, and in vitro HO activity.	Cannabidiol	102-113	interleukin 6	Mus musculus	276-279
32033040-2	2020	In cultures of primary mesencephalic neurons and neuroblastoma cells, we determined the capability of cannabidiol (CBD) and tetrahydrocannabinol (THC) to counteract effects elicited by complex I-inhibitor rotenone by analyzing neuron viability, morphology, gene expression of IL6, CHOP, XBP1, HO-1 (stress response), and HO-2, and in vitro HO activity.	Cannabidiol	102-113	DNA-damage inducible transcript 3	Mus musculus	281-285
32033040-2	2020	In cultures of primary mesencephalic neurons and neuroblastoma cells, we determined the capability of cannabidiol (CBD) and tetrahydrocannabinol (THC) to counteract effects elicited by complex I-inhibitor rotenone by analyzing neuron viability, morphology, gene expression of IL6, CHOP, XBP1, HO-1 (stress response), and HO-2, and in vitro HO activity.	Cannabidiol	102-113	X-box binding protein 1	Mus musculus	287-291
32033040-2	2020	In cultures of primary mesencephalic neurons and neuroblastoma cells, we determined the capability of cannabidiol (CBD) and tetrahydrocannabinol (THC) to counteract effects elicited by complex I-inhibitor rotenone by analyzing neuron viability, morphology, gene expression of IL6, CHOP, XBP1, HO-1 (stress response), and HO-2, and in vitro HO activity.	Cannabidiol	102-113	heme oxygenase 1	Mus musculus	293-297
32033040-2	2020	In cultures of primary mesencephalic neurons and neuroblastoma cells, we determined the capability of cannabidiol (CBD) and tetrahydrocannabinol (THC) to counteract effects elicited by complex I-inhibitor rotenone by analyzing neuron viability, morphology, gene expression of IL6, CHOP, XBP1, HO-1 (stress response), and HO-2, and in vitro HO activity.	Cannabidiol	102-113	heme oxygenase 2	Mus musculus	321-325
32033040-9	2020	CBD triggered the expression of HO-1 and other cell stress markers.	Cannabidiol	0-3	heme oxygenase 1	Mus musculus	32-36
32033040-12	2020	Our findings indicate that CBD induces HO-1 and increases the cellular capacity to convert heme when stressful conditions are met.	Cannabidiol	27-30	heme oxygenase 1	Mus musculus	39-43
31706993-6	2020	Further, we investigated the pathway involved in the analgesic effect of the CBD through the co-administration with a fatty acid amide hydrolase (FAAH) inhibitor, increasing the endogenous anandamide levels, and possible targets from anandamide, i.e., the cannabinoid receptors subtype 1 and 2 (CB1 and CB2) and the transient receptor potential vanilloid type 1 (TRPV1).	Cannabidiol	77-80	fatty acid amide hydrolase	Homo sapiens	118-144
31926846-0	2020	Response to cannabidiol in epilepsy of infancy with migrating focal seizures associated with KCNT1 mutations: An open-label, prospective, interventional study.	Cannabidiol	12-23	potassium sodium-activated channel subfamily T member 1	Homo sapiens	93-98
31926846-5	2020	Here we evaluate the response of three patients, all diagnosed with EIMFS secondary to KCNT1 mutations, to pharmaceutical grade CBD.	Cannabidiol	128-131	potassium sodium-activated channel subfamily T member 1	Homo sapiens	87-92
31648363-0	2020	A time-dependent contribution of hippocampal CB1, CB2, and PPARgamma receptors to cannabidiol-induced disruption of fear memory consolidation.	Cannabidiol	82-93	cannabinoid receptor 1	Rattus norvegicus	45-48
31648363-0	2020	A time-dependent contribution of hippocampal CB1, CB2, and PPARgamma receptors to cannabidiol-induced disruption of fear memory consolidation.	Cannabidiol	82-93	cannabinoid receptor 2	Rattus norvegicus	50-53
31648363-0	2020	A time-dependent contribution of hippocampal CB1, CB2, and PPARgamma receptors to cannabidiol-induced disruption of fear memory consolidation.	Cannabidiol	82-93	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	59-68
31648363-8	2020	Immediately after fear conditioning, the CBD effect was abolished by CB1 or CB2 receptor blockade, partly reduced by 5-HT1A or A2A antagonism, and remained unchanged after antagonism of PPARgamma receptors.	Cannabidiol	41-44	cannabinoid receptor 1	Rattus norvegicus	69-72
31648363-8	2020	Immediately after fear conditioning, the CBD effect was abolished by CB1 or CB2 receptor blockade, partly reduced by 5-HT1A or A2A antagonism, and remained unchanged after antagonism of PPARgamma receptors.	Cannabidiol	41-44	cannabinoid receptor 2	Rattus norvegicus	76-79
31648363-8	2020	Immediately after fear conditioning, the CBD effect was abolished by CB1 or CB2 receptor blockade, partly reduced by 5-HT1A or A2A antagonism, and remained unchanged after antagonism of PPARgamma receptors.	Cannabidiol	41-44	5-hydroxytryptamine receptor 1A	Rattus norvegicus	117-123
31648363-8	2020	Immediately after fear conditioning, the CBD effect was abolished by CB1 or CB2 receptor blockade, partly reduced by 5-HT1A or A2A antagonism, and remained unchanged after antagonism of PPARgamma receptors.	Cannabidiol	41-44	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	186-195
31648363-9	2020	1 h after fear conditioning, the CBD effect was only prevented by PPARgamma receptor antagonism.	Cannabidiol	33-36	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	66-75
31693171-5	2020	Key Results CBD activity is partially dependent upon the mitochondrial glycine cleavage system component, GcvH1 in Dictyostelium, orthologous to the human GCSH protein, which is functionally linked to folate one-carbon metabolism (FOCM).	Cannabidiol	12-15	glycine cleavage system protein H	Homo sapiens	155-159
31706993-6	2020	Further, we investigated the pathway involved in the analgesic effect of the CBD through the co-administration with a fatty acid amide hydrolase (FAAH) inhibitor, increasing the endogenous anandamide levels, and possible targets from anandamide, i.e., the cannabinoid receptors subtype 1 and 2 (CB1 and CB2) and the transient receptor potential vanilloid type 1 (TRPV1).	Cannabidiol	77-80	fatty acid amide hydrolase	Homo sapiens	146-150
31706993-6	2020	Further, we investigated the pathway involved in the analgesic effect of the CBD through the co-administration with a fatty acid amide hydrolase (FAAH) inhibitor, increasing the endogenous anandamide levels, and possible targets from anandamide, i.e., the cannabinoid receptors subtype 1 and 2 (CB1 and CB2) and the transient receptor potential vanilloid type 1 (TRPV1).	Cannabidiol	77-80	cannabinoid receptor 1	Homo sapiens	295-298
31706993-6	2020	Further, we investigated the pathway involved in the analgesic effect of the CBD through the co-administration with a fatty acid amide hydrolase (FAAH) inhibitor, increasing the endogenous anandamide levels, and possible targets from anandamide, i.e., the cannabinoid receptors subtype 1 and 2 (CB1 and CB2) and the transient receptor potential vanilloid type 1 (TRPV1).	Cannabidiol	77-80	cannabinoid receptor 2	Homo sapiens	303-306
31706993-6	2020	Further, we investigated the pathway involved in the analgesic effect of the CBD through the co-administration with a fatty acid amide hydrolase (FAAH) inhibitor, increasing the endogenous anandamide levels, and possible targets from anandamide, i.e., the cannabinoid receptors subtype 1 and 2 (CB1 and CB2) and the transient receptor potential vanilloid type 1 (TRPV1).	Cannabidiol	77-80	transient receptor potential cation channel subfamily V member 1	Homo sapiens	316-361
31706993-6	2020	Further, we investigated the pathway involved in the analgesic effect of the CBD through the co-administration with a fatty acid amide hydrolase (FAAH) inhibitor, increasing the endogenous anandamide levels, and possible targets from anandamide, i.e., the cannabinoid receptors subtype 1 and 2 (CB1 and CB2) and the transient receptor potential vanilloid type 1 (TRPV1).	Cannabidiol	77-80	transient receptor potential cation channel subfamily V member 1	Homo sapiens	363-368
31706993-8	2020	Moreover, ineffective doses of either FAAH inhibitor or TRPV1 receptor antagonist potentialized the CBD-evoked antinociception while an inverse agonist of the CB1 and CB2 receptor prevented the antinociceptive effect of the CBD.	Cannabidiol	224-227	cannabinoid receptor 1	Homo sapiens	159-162
31706993-8	2020	Moreover, ineffective doses of either FAAH inhibitor or TRPV1 receptor antagonist potentialized the CBD-evoked antinociception while an inverse agonist of the CB1 and CB2 receptor prevented the antinociceptive effect of the CBD.	Cannabidiol	224-227	cannabinoid receptor 2	Homo sapiens	167-170
31706993-10	2020	They also suggest that CB1 and TRPV1 receptors are important for CBD-induced analgesia and that CBD could produce these analgesic effects increasing endogenous anandamide levels.	Cannabidiol	65-68	cannabinoid receptor 1	Homo sapiens	23-26
31706993-10	2020	They also suggest that CB1 and TRPV1 receptors are important for CBD-induced analgesia and that CBD could produce these analgesic effects increasing endogenous anandamide levels.	Cannabidiol	65-68	transient receptor potential cation channel subfamily V member 1	Homo sapiens	31-36
32019055-5	2020	Interestingly, only an unadulterated CBD oil had strong and statistically significant suppressive effects on the pI3K/Akt/mTOR signaling pathway with an EC50 value of 143 microM and a slow-acting timescale requiring hours.	Cannabidiol	37-40	AKT serine/threonine kinase 1	Homo sapiens	118-121
31653969-3	2020	Overexpression of TRPV2 is observed in high-grade urothelial cancers and treatment with the TRPV2 agonist cannabidiol induces apoptosis.	Cannabidiol	106-117	transient receptor potential cation channel subfamily V member 2	Homo sapiens	18-23
31653969-3	2020	Overexpression of TRPV2 is observed in high-grade urothelial cancers and treatment with the TRPV2 agonist cannabidiol induces apoptosis.	Cannabidiol	106-117	transient receptor potential cation channel subfamily V member 2	Homo sapiens	92-97
31837295-10	2020	CBD inhibited heroin and 6-MAM hydrolysis in a reversible manner, with IC50s of 14.7 and 12.1 muM, respectively.	Cannabidiol	0-3	sarcoglycan gamma	Homo sapiens	27-30
31837295-13	2020	CBD exhibited potent in vitro inhibition toward both heroin and 6-MAM hydrolysis, which may be of potential clinical relevance.	Cannabidiol	0-3	sarcoglycan gamma	Homo sapiens	66-69
31941059-7	2020	RESULTS: Both CBD and CBG inhibited NPY and POMC gene expression and decreased the 3-HK/KA ratio in the hypothalamus.	Cannabidiol	14-17	neuropeptide Y	Rattus norvegicus	36-39
31941059-7	2020	RESULTS: Both CBD and CBG inhibited NPY and POMC gene expression and decreased the 3-HK/KA ratio in the hypothalamus.	Cannabidiol	14-17	proopiomelanocortin	Rattus norvegicus	44-48
32019055-5	2020	Interestingly, only an unadulterated CBD oil had strong and statistically significant suppressive effects on the pI3K/Akt/mTOR signaling pathway with an EC50 value of 143 microM and a slow-acting timescale requiring hours.	Cannabidiol	37-40	mechanistic target of rapamycin kinase	Homo sapiens	122-126
31492610-6	2020	A fusion protein consisting of fibroblast growth factor 2 (FGF-2) fused to CBD bound the chitin gel, and was released time-dependently rather than as an initial burst during lysozyme degradation, suggesting that this system could provide a means for controlled drug release in biological systems.	Cannabidiol	75-78	fibroblast growth factor 2	Homo sapiens	31-57
31492610-6	2020	A fusion protein consisting of fibroblast growth factor 2 (FGF-2) fused to CBD bound the chitin gel, and was released time-dependently rather than as an initial burst during lysozyme degradation, suggesting that this system could provide a means for controlled drug release in biological systems.	Cannabidiol	75-78	fibroblast growth factor 2	Homo sapiens	59-64
31848037-4	2020	Given the increasing interest in medicinal cannabis (or cannabidiol or CBD) as an anti-epileptic drug, CBD may help with seizure control in glioma patients with treatment-refractory seizures.	Cannabidiol	56-67	opsin 1, medium wave sensitive	Homo sapiens	103-106
31518892-0	2020	Cannabidiol induces antioxidant pathways in keratinocytes by targeting BACH1.	Cannabidiol	0-11	BTB domain and CNC homolog 1	Homo sapiens	71-76
31518892-5	2020	In addition, CBD induced the expression of several NRF2 target genes, with heme oxygenase 1 (HMOX1) being the gene and the protein most upregulated by CBD.	Cannabidiol	13-16	NFE2 like bZIP transcription factor 2	Homo sapiens	51-55
31518892-5	2020	In addition, CBD induced the expression of several NRF2 target genes, with heme oxygenase 1 (HMOX1) being the gene and the protein most upregulated by CBD.	Cannabidiol	13-16	heme oxygenase 1	Homo sapiens	75-91
31518892-5	2020	In addition, CBD induced the expression of several NRF2 target genes, with heme oxygenase 1 (HMOX1) being the gene and the protein most upregulated by CBD.	Cannabidiol	13-16	heme oxygenase 1	Homo sapiens	93-98
31518892-5	2020	In addition, CBD induced the expression of several NRF2 target genes, with heme oxygenase 1 (HMOX1) being the gene and the protein most upregulated by CBD.	Cannabidiol	151-154	NFE2 like bZIP transcription factor 2	Homo sapiens	51-55
31518892-5	2020	In addition, CBD induced the expression of several NRF2 target genes, with heme oxygenase 1 (HMOX1) being the gene and the protein most upregulated by CBD.	Cannabidiol	151-154	heme oxygenase 1	Homo sapiens	75-91
31518892-5	2020	In addition, CBD induced the expression of several NRF2 target genes, with heme oxygenase 1 (HMOX1) being the gene and the protein most upregulated by CBD.	Cannabidiol	151-154	heme oxygenase 1	Homo sapiens	93-98
31518892-8	2020	In vivo studies showed that topical CBD increased the levels of HMOX1 and of the proliferation and wound-repair associated keratins 16 and 17 in the skin of mice.	Cannabidiol	36-39	heme oxygenase 1	Mus musculus	64-69
31518892-9	2020	Altogether, our study identifies BACH1 as a molecular target for CBD in keratinocytes and sets the basis for the use of topical CBD for the treatment of different skin diseases including atopic dermatitis and keratin disorders.	Cannabidiol	65-68	BTB domain and CNC homolog 1	Homo sapiens	33-38
31518892-9	2020	Altogether, our study identifies BACH1 as a molecular target for CBD in keratinocytes and sets the basis for the use of topical CBD for the treatment of different skin diseases including atopic dermatitis and keratin disorders.	Cannabidiol	128-131	BTB domain and CNC homolog 1	Homo sapiens	33-38
32715862-2	2020	Cannabidiol (CBD), a non-psychoactive component of cannabis is marketed as a treatment for many conditions and sales rose to more than 820 million in 2017.	Cannabidiol	0-11	opsin 1, medium wave sensitive	Homo sapiens	13-16
32009043-6	2020	However, CBD has very low affinity (in the micromolar range) for the CB1 receptor, as well as for the CB2 receptor, and its underlying mechanism remains obscure.	Cannabidiol	9-12	cannabinoid receptor 2	Homo sapiens	102-105
31857855-0	2019	Correction: Inhibition of ATM kinase upregulates levels of cell death induced by cannabidiol and gamma-irradiation in human glioblastoma cells.	Cannabidiol	81-92	ATM serine/threonine kinase	Homo sapiens	26-29
31938604-8	2019	In this report, we present the use of cannabidiol (CBD) for the management of chronic pain and concomitant mood disorder in an NF1 patient.	Cannabidiol	38-49	neurofibromin 1	Homo sapiens	127-130
31938604-8	2019	In this report, we present the use of cannabidiol (CBD) for the management of chronic pain and concomitant mood disorder in an NF1 patient.	Cannabidiol	51-54	neurofibromin 1	Homo sapiens	127-130
31437494-7	2019	CBD significantly attenuated LPS-induced NF-kappaB activity, IL-8, and MCP-1 release from macrophages.	Cannabidiol	0-3	nuclear factor kappa B subunit 1	Homo sapiens	41-50
31446830-11	2019	Molecular docking studies suggest a non-covalent interaction site for Myrcene in TRPV1 and identifies key residues that form partially overlapping Myrcene and Cannabidiol binding sites.	Cannabidiol	159-170	transient receptor potential cation channel subfamily V member 1	Homo sapiens	81-86
31446830-10	2019	Myrcene pre-application and residency at TRPV1 appears to negatively impact subsequent responses to TRPV1 ligands such as Cannabidiol, indicating allosteric modulation and possible competition by Myrcene.	Cannabidiol	122-133	transient receptor potential cation channel subfamily V member 1	Homo sapiens	100-105
31378964-16	2019	By looking for mediators of the apoptotic CBD effect downstream of the CB1 receptor, enhanced Erk1/2 phosphorylation could be detected after CBD treatment.	Cannabidiol	42-45	cannabinoid receptor 1	Homo sapiens	71-74
31378964-16	2019	By looking for mediators of the apoptotic CBD effect downstream of the CB1 receptor, enhanced Erk1/2 phosphorylation could be detected after CBD treatment.	Cannabidiol	42-45	mitogen-activated protein kinase 3	Homo sapiens	94-100
31378964-18	2019	The present study demonstrates that CBD promotes apoptosis and [Ca2+ ]i elevation in human articular chondrocytes via a CB1-receptor-mediated mechanism.	Cannabidiol	36-39	cannabinoid receptor 1	Homo sapiens	120-123
31801206-6	2019	The treatment with CBD downregulates the pro-inflammatory pathway mediated by the IL-1 family, including its receptor while MOR is less efficient.	Cannabidiol	19-22	interleukin 1 alpha	Homo sapiens	82-86
31752240-6	2019	In particular, the pre-treatment with CBD at a 5 microM dose decreased TNF-alpha levels and increased IL10 and IL-37 expression.	Cannabidiol	38-41	tumor necrosis factor	Homo sapiens	71-80
31752240-6	2019	In particular, the pre-treatment with CBD at a 5 microM dose decreased TNF-alpha levels and increased IL10 and IL-37 expression.	Cannabidiol	38-41	interleukin 10	Homo sapiens	102-106
31752240-6	2019	In particular, the pre-treatment with CBD at a 5 microM dose decreased TNF-alpha levels and increased IL10 and IL-37 expression.	Cannabidiol	38-41	interleukin 37	Homo sapiens	111-116
31752240-8	2019	CBG and CBD co-administered at a 5 microM dose decreased iNOS expression and increased Nrf2 levels.	Cannabidiol	8-11	nitric oxide synthase 2	Homo sapiens	57-61
31752240-8	2019	CBG and CBD co-administered at a 5 microM dose decreased iNOS expression and increased Nrf2 levels.	Cannabidiol	8-11	NFE2 like bZIP transcription factor 2	Homo sapiens	87-91
31718076-1	2019	The protective effect of cannabidiol (CBD), the non-psychoactive component of Cannabis sativa, against neuronal toxicity induced by cadmium chloride (CdCl2 10 muM) was investigated in a retinoic acid (RA)-differentiated SH-SY5Y neuroblastoma cell line.	Cannabidiol	25-36	latexin	Homo sapiens	159-162
31718076-2	2019	CBD (1 muM) was applied 24 h before and removed during cadmium (Cd) treatment.	Cannabidiol	0-3	latexin	Homo sapiens	7-10
31718076-4	2019	CBD significantly prevented the endoplasmic reticulum (ER) stress (GRP78 increase) and the subcellular distribution of the cytochrome C, as well as the overexpression of the pro-apoptotic protein BAX.	Cannabidiol	0-3	heat shock protein family A (Hsp70) member 5	Homo sapiens	67-72
31718076-4	2019	CBD significantly prevented the endoplasmic reticulum (ER) stress (GRP78 increase) and the subcellular distribution of the cytochrome C, as well as the overexpression of the pro-apoptotic protein BAX.	Cannabidiol	0-3	cytochrome c, somatic	Homo sapiens	123-135
31718076-4	2019	CBD significantly prevented the endoplasmic reticulum (ER) stress (GRP78 increase) and the subcellular distribution of the cytochrome C, as well as the overexpression of the pro-apoptotic protein BAX.	Cannabidiol	0-3	BCL2 associated X, apoptosis regulator	Homo sapiens	196-199
31718076-5	2019	Immunocytochemical analysis as well as quantitative protein evaluation by western blotting revealed that CBD partially counteracted the depletion of the growth associated protein 43 (GAP43) and of the neuronal specific class III beta-tubulin (beta3 tubulin) induced by Cd treatment.	Cannabidiol	105-108	growth associated protein 43	Homo sapiens	153-181
31718076-5	2019	Immunocytochemical analysis as well as quantitative protein evaluation by western blotting revealed that CBD partially counteracted the depletion of the growth associated protein 43 (GAP43) and of the neuronal specific class III beta-tubulin (beta3 tubulin) induced by Cd treatment.	Cannabidiol	105-108	growth associated protein 43	Homo sapiens	183-188
31699976-0	2019	Cannabidiol promotes apoptosis via regulation of XIAP/Smac in gastric cancer.	Cannabidiol	0-11	X-linked inhibitor of apoptosis	Homo sapiens	49-53
31699976-0	2019	Cannabidiol promotes apoptosis via regulation of XIAP/Smac in gastric cancer.	Cannabidiol	0-11	diablo IAP-binding mitochondrial protein	Homo sapiens	54-58
31699976-4	2019	We suggest that CBD induced apoptosis by suppressing X-linked inhibitor apoptosis (XIAP), a member of the IAP protein family.	Cannabidiol	16-19	X-linked inhibitor of apoptosis	Homo sapiens	53-81
31699976-4	2019	We suggest that CBD induced apoptosis by suppressing X-linked inhibitor apoptosis (XIAP), a member of the IAP protein family.	Cannabidiol	16-19	X-linked inhibitor of apoptosis	Homo sapiens	83-87
31699976-5	2019	CBD reduced XIAP protein levels while increasing ubiquitination of XIAP.	Cannabidiol	0-3	X-linked inhibitor of apoptosis	Homo sapiens	12-16
31699976-5	2019	CBD reduced XIAP protein levels while increasing ubiquitination of XIAP.	Cannabidiol	0-3	X-linked inhibitor of apoptosis	Homo sapiens	67-71
31699976-6	2019	The expression of Smac, a known inhibitor of XIAP, was found to be elevated during CBD treatment.	Cannabidiol	83-86	diablo IAP-binding mitochondrial protein	Homo sapiens	18-22
31699976-6	2019	The expression of Smac, a known inhibitor of XIAP, was found to be elevated during CBD treatment.	Cannabidiol	83-86	X-linked inhibitor of apoptosis	Homo sapiens	45-49
31699976-7	2019	Moreover, CBD treatment increased the interaction between XIAP and Smac by increasing Smac release from mitochondria to the cytosol.	Cannabidiol	10-13	X-linked inhibitor of apoptosis	Homo sapiens	58-62
31699976-7	2019	Moreover, CBD treatment increased the interaction between XIAP and Smac by increasing Smac release from mitochondria to the cytosol.	Cannabidiol	10-13	diablo IAP-binding mitochondrial protein	Homo sapiens	67-71
31699976-7	2019	Moreover, CBD treatment increased the interaction between XIAP and Smac by increasing Smac release from mitochondria to the cytosol.	Cannabidiol	10-13	diablo IAP-binding mitochondrial protein	Homo sapiens	86-90
31690747-2	2019	The CBs, Delta9-THC, cannabidiol, HU-210, and CP 55,940 caused alcohol-like effects on craniofacial and brain development, phenocopying Shh mutations.	Cannabidiol	21-32	sonic hedgehog	Mus musculus	136-139
31529613-1	2019	(-)-Cannabidiol ((-)-CBD), a non-psychoactive phytocannabinoid from Cannabis, and its structural analogs have received growing attention in recent years because of their potential therapeutic benefits, including neuroprotective, anti-epileptic, anti-inflammatory, anxiolytic, anti-cancer properties.	Cannabidiol	0-15	opsin 1, medium wave sensitive	Homo sapiens	21-24
31356922-4	2019	THC + CBD treatment attenuated EAE and caused significant decrease in inflammatory cytokines such as IL-17 and IFN-gamma while promoting the induction of anti-inflammatory cytokines such as IL-10 and TGF-beta.	Cannabidiol	6-9	interleukin 17A	Mus musculus	101-106
31356922-4	2019	THC + CBD treatment attenuated EAE and caused significant decrease in inflammatory cytokines such as IL-17 and IFN-gamma while promoting the induction of anti-inflammatory cytokines such as IL-10 and TGF-beta.	Cannabidiol	6-9	interferon gamma	Mus musculus	111-120
31356922-4	2019	THC + CBD treatment attenuated EAE and caused significant decrease in inflammatory cytokines such as IL-17 and IFN-gamma while promoting the induction of anti-inflammatory cytokines such as IL-10 and TGF-beta.	Cannabidiol	6-9	interleukin 10	Mus musculus	190-195
31356922-4	2019	THC + CBD treatment attenuated EAE and caused significant decrease in inflammatory cytokines such as IL-17 and IFN-gamma while promoting the induction of anti-inflammatory cytokines such as IL-10 and TGF-beta.	Cannabidiol	6-9	transforming growth factor alpha	Mus musculus	200-208
31625159-5	2019	METHODS: We examined whether CBD inhibits human CYP3A4 and CYP2C19 mediated metabolism of clobazam and N-desmethylclobazam (N-CLB), respectively, and performed studies assessing the effects of CBD on brain and plasma pharmacokinetics of clobazam in mice.	Cannabidiol	29-32	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	48-54
31625159-5	2019	METHODS: We examined whether CBD inhibits human CYP3A4 and CYP2C19 mediated metabolism of clobazam and N-desmethylclobazam (N-CLB), respectively, and performed studies assessing the effects of CBD on brain and plasma pharmacokinetics of clobazam in mice.	Cannabidiol	29-32	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	59-66
31625159-9	2019	RESULTS: CBD potently inhibited CYP3A4 mediated metabolism of clobazam and CYP2C19 mediated metabolism of N-CLB.	Cannabidiol	9-12	cytochrome P450 family 3 subfamily A member 4, gene 2 L homeolog	Xenopus laevis	32-38
31625159-10	2019	Combination CBD-clobazam treatment resulted in greater anticonvulsant efficacy in Scn1a+/- mice, but only when an anticonvulsant dose of CBD was used.	Cannabidiol	12-15	sodium channel, voltage-gated, type I, alpha	Mus musculus	82-87
31437494-7	2019	CBD significantly attenuated LPS-induced NF-kappaB activity, IL-8, and MCP-1 release from macrophages.	Cannabidiol	0-3	C-X-C motif chemokine ligand 8	Homo sapiens	61-65
31437494-7	2019	CBD significantly attenuated LPS-induced NF-kappaB activity, IL-8, and MCP-1 release from macrophages.	Cannabidiol	0-3	C-C motif chemokine ligand 2	Homo sapiens	71-76
31437494-10	2019	CBD and dexamethasone treatments reduced the IL-8 level induced by LPS when the cells were treated individually, but showed antagonistic effects when used in combination via MCPIP (monocytic chemotactic protein-induced protein).	Cannabidiol	0-3	C-X-C motif chemokine ligand 8	Homo sapiens	45-49
31437494-10	2019	CBD and dexamethasone treatments reduced the IL-8 level induced by LPS when the cells were treated individually, but showed antagonistic effects when used in combination via MCPIP (monocytic chemotactic protein-induced protein).	Cannabidiol	0-3	zinc finger CCCH-type containing 12A	Homo sapiens	174-179
31437494-10	2019	CBD and dexamethasone treatments reduced the IL-8 level induced by LPS when the cells were treated individually, but showed antagonistic effects when used in combination via MCPIP (monocytic chemotactic protein-induced protein).	Cannabidiol	0-3	zinc finger CCCH-type containing 12A	Homo sapiens	181-226
31673072-5	2019	Further analysis showed that these histone methylation signals were differentially enriched in the binding sites of certain transcription factors, such as ZNF143 and FoxA1, suggesting that these transcription factors may play important roles in CBD mediated immune modulation.	Cannabidiol	245-248	forkhead box A1	Mus musculus	166-171
31570536-0	2019	Cannabidiol Counteracts the Psychotropic Side-Effects of Delta-9-Tetrahydrocannabinol in the Ventral Hippocampus through Bidirectional Control of ERK1-2 Phosphorylation.	Cannabidiol	0-11	mitogen activated protein kinase 3	Rattus norvegicus	146-152
31680972-0	2019	2-APB and CBD-Mediated Targeting of Charged Cytotoxic Compounds Into Tumor Cells Suggests the Involvement of TRPV2 Channels.	Cannabidiol	10-13	transient receptor potential cation channel subfamily V member 2	Homo sapiens	109-114
31680972-7	2019	We show that co-application of either cannabidiol (CBD) or 2-APB, the activators of TRPV2 channels, together with doxorubicin leads to significantly higher accumulation of doxorubicin in BNL1 ME cells than in BNL1 ME cells that were exposed to doxorubicin alone.	Cannabidiol	38-49	transient receptor potential cation channel subfamily V member 2	Homo sapiens	84-89
31680972-7	2019	We show that co-application of either cannabidiol (CBD) or 2-APB, the activators of TRPV2 channels, together with doxorubicin leads to significantly higher accumulation of doxorubicin in BNL1 ME cells than in BNL1 ME cells that were exposed to doxorubicin alone.	Cannabidiol	51-54	transient receptor potential cation channel subfamily V member 2	Homo sapiens	84-89
31680972-10	2019	We suggest that CBD may have a dual effect in promoting doxorubicin-mediated cell death by facilitating the entry of doxorubicin via TRPV2 channels and preventing its clearance from the cells by inhibiting P-glycoprotein ATPase transporter.	Cannabidiol	16-19	transient receptor potential cation channel subfamily V member 2	Homo sapiens	133-138
31012522-2	2019	CBD is metabolized by cytochrome P450 (CYP)3A4 and CYP2C19 with a growing body of evidence suggesting it is also a potent inhibitor of these pathways.	Cannabidiol	0-3	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	22-46
31012522-2	2019	CBD is metabolized by cytochrome P450 (CYP)3A4 and CYP2C19 with a growing body of evidence suggesting it is also a potent inhibitor of these pathways.	Cannabidiol	0-3	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	51-58
31499052-13	2019	AST and ALT concentration were reduced in CBD treated groups.	Cannabidiol	42-45	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	0-3
31433338-6	2019	FINDINGS: After comparing the in vitro inhibition parameters to physiologically achievable cannabinoid concentrations, it was concluded that CYP2C9, CYP1A1/2, and CYP1B1 are likely to be inhibited by all 3 major cannabinoids Delta-tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabinol (CBN).	Cannabidiol	259-270	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
31032942-0	2019	Cannabidiol protects livers against nonalcoholic steatohepatitis induced by high-fat high cholesterol diet via regulating NF-kappaB and NLRP3 inflammasome pathway.	Cannabidiol	0-11	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	122-131
31032942-0	2019	Cannabidiol protects livers against nonalcoholic steatohepatitis induced by high-fat high cholesterol diet via regulating NF-kappaB and NLRP3 inflammasome pathway.	Cannabidiol	0-11	NLR family, pyrin domain containing 3	Mus musculus	136-141
31566564-0	2019	Molecular mechanism of TRPV2 channel modulation by cannabidiol.	Cannabidiol	51-62	transient receptor potential cation channel, subfamily V, member 2	Rattus norvegicus	23-28
31566564-2	2019	Cannabidiol (CBD), the non-psychotropic therapeutically active ingredient of Cannabis sativa, is an activator of TRPV2 and also modulates other transient receptor potential (TRP) channels.	Cannabidiol	0-11	transient receptor potential cation channel, subfamily V, member 2	Rattus norvegicus	113-118
31566564-2	2019	Cannabidiol (CBD), the non-psychotropic therapeutically active ingredient of Cannabis sativa, is an activator of TRPV2 and also modulates other transient receptor potential (TRP) channels.	Cannabidiol	13-16	transient receptor potential cation channel, subfamily V, member 2	Rattus norvegicus	113-118
31566564-3	2019	Here, we determined structures of the full-length rat TRPV2 channel in apo and CBD-bound states in nanodiscs by cryo-electron microscopy.	Cannabidiol	79-82	transient receptor potential cation channel, subfamily V, member 2	Rattus norvegicus	54-59
31566564-4	2019	We show that CBD interacts with TRPV2 through a hydrophobic pocket located between S5 and S6 helices of adjacent subunits, which differs from known ligand and lipid binding sites in other TRP channels.	Cannabidiol	13-16	transient receptor potential cation channel, subfamily V, member 2	Rattus norvegicus	32-37
31566564-5	2019	CBD-bound TRPV2 structures revealed that the S4-S5 linker plays a critical role in channel gating upon CBD binding.	Cannabidiol	0-3	transient receptor potential cation channel, subfamily V, member 2	Rattus norvegicus	10-15
31566564-5	2019	CBD-bound TRPV2 structures revealed that the S4-S5 linker plays a critical role in channel gating upon CBD binding.	Cannabidiol	103-106	transient receptor potential cation channel, subfamily V, member 2	Rattus norvegicus	10-15
31611800-2	2019	Contrary to most cannabinoids present in the Cannabis plant, some, such as O-1602 and abnormal cannabidiol, have no or only little affinity to the CB1 or CB2 cannabinoid receptors and instead exert their effects through other receptors.	Cannabidiol	95-106	cannabinoid receptor 1	Homo sapiens	147-150
31611800-2	2019	Contrary to most cannabinoids present in the Cannabis plant, some, such as O-1602 and abnormal cannabidiol, have no or only little affinity to the CB1 or CB2 cannabinoid receptors and instead exert their effects through other receptors.	Cannabidiol	95-106	cannabinoid receptor 2	Homo sapiens	154-157
31611800-6	2019	The effects of O-1602 and abnormal cannabidiol on cell viability were completely blocked by the combination of GPR55 and GPR18-specific siRNAs.	Cannabidiol	35-46	G protein-coupled receptor 55	Homo sapiens	111-116
31611800-6	2019	The effects of O-1602 and abnormal cannabidiol on cell viability were completely blocked by the combination of GPR55 and GPR18-specific siRNAs.	Cannabidiol	35-46	G protein-coupled receptor 18	Homo sapiens	121-126
31611802-11	2019	CBD administration resulted in normal function associated with normal mOL and MBP, as well as normal axon density and myelin thickness in all areas.	Cannabidiol	0-3	myelin basic protein	Rattus norvegicus	78-81
31433338-6	2019	FINDINGS: After comparing the in vitro inhibition parameters to physiologically achievable cannabinoid concentrations, it was concluded that CYP2C9, CYP1A1/2, and CYP1B1 are likely to be inhibited by all 3 major cannabinoids Delta-tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabinol (CBN).	Cannabidiol	259-270	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	149-155
31433338-6	2019	FINDINGS: After comparing the in vitro inhibition parameters to physiologically achievable cannabinoid concentrations, it was concluded that CYP2C9, CYP1A1/2, and CYP1B1 are likely to be inhibited by all 3 major cannabinoids Delta-tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabinol (CBN).	Cannabidiol	259-270	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	163-169
31433338-6	2019	FINDINGS: After comparing the in vitro inhibition parameters to physiologically achievable cannabinoid concentrations, it was concluded that CYP2C9, CYP1A1/2, and CYP1B1 are likely to be inhibited by all 3 major cannabinoids Delta-tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabinol (CBN).	Cannabidiol	272-275	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
31433338-6	2019	FINDINGS: After comparing the in vitro inhibition parameters to physiologically achievable cannabinoid concentrations, it was concluded that CYP2C9, CYP1A1/2, and CYP1B1 are likely to be inhibited by all 3 major cannabinoids Delta-tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabinol (CBN).	Cannabidiol	272-275	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	149-155
31433338-6	2019	FINDINGS: After comparing the in vitro inhibition parameters to physiologically achievable cannabinoid concentrations, it was concluded that CYP2C9, CYP1A1/2, and CYP1B1 are likely to be inhibited by all 3 major cannabinoids Delta-tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabinol (CBN).	Cannabidiol	272-275	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	163-169
31433338-7	2019	The isoforms CYP2D6, CYP2C19, CYP2B6, and CYP2J2 are inhibited by THC and CBD.	Cannabidiol	74-77	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	13-19
31433338-7	2019	The isoforms CYP2D6, CYP2C19, CYP2B6, and CYP2J2 are inhibited by THC and CBD.	Cannabidiol	74-77	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-28
31433338-7	2019	The isoforms CYP2D6, CYP2C19, CYP2B6, and CYP2J2 are inhibited by THC and CBD.	Cannabidiol	74-77	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	30-36
31433338-7	2019	The isoforms CYP2D6, CYP2C19, CYP2B6, and CYP2J2 are inhibited by THC and CBD.	Cannabidiol	74-77	cytochrome P450 family 2 subfamily J member 2	Homo sapiens	42-48
31433338-8	2019	CYP3A4/5/7 is potentially inhibited by CBD.	Cannabidiol	39-42	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
31433338-10	2019	For non-CYP drug-metabolizing enzymes, UGT1A9 is inhibited by CBD and CBN, whereas UGT2B7 is inhibited by CBD but activated by CBN.	Cannabidiol	62-65	peptidylprolyl isomerase G	Homo sapiens	8-11
31433338-10	2019	For non-CYP drug-metabolizing enzymes, UGT1A9 is inhibited by CBD and CBN, whereas UGT2B7 is inhibited by CBD but activated by CBN.	Cannabidiol	62-65	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	39-45
31433338-10	2019	For non-CYP drug-metabolizing enzymes, UGT1A9 is inhibited by CBD and CBN, whereas UGT2B7 is inhibited by CBD but activated by CBN.	Cannabidiol	106-109	peptidylprolyl isomerase G	Homo sapiens	8-11
31433338-10	2019	For non-CYP drug-metabolizing enzymes, UGT1A9 is inhibited by CBD and CBN, whereas UGT2B7 is inhibited by CBD but activated by CBN.	Cannabidiol	106-109	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	83-89
31433338-11	2019	Carboxylesterase 1 (CES1) is potentially inhibited by THC and CBD.	Cannabidiol	62-65	carboxylesterase 1	Homo sapiens	0-18
31433338-11	2019	Carboxylesterase 1 (CES1) is potentially inhibited by THC and CBD.	Cannabidiol	62-65	carboxylesterase 1	Homo sapiens	20-24
31433338-12	2019	Clinical studies suggest inhibition of CYP2C19 by CBD, inhibition of CYP2C9 by various cannabis products, and induction of CYP1A2 through cannabis smoking.	Cannabidiol	50-53	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	39-46
31054943-0	2019	Cannabidiol attenuates aggressive behavior induced by social isolation in mice: Involvement of 5-HT1A and CB1 receptors.	Cannabidiol	0-11	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	95-101
31054943-0	2019	Cannabidiol attenuates aggressive behavior induced by social isolation in mice: Involvement of 5-HT1A and CB1 receptors.	Cannabidiol	0-11	cannabinoid receptor 1 (brain)	Mus musculus	106-119
31054943-12	2019	CBD anti-aggressive effects were attenuated by the 5-HT1A receptor antagonist WAY100635 (0.3 mg/kg) and the CB1 antagonist AM251 (1 mg/kg), suggesting that CBD decreases social isolation-induced aggressive behaviors through a mechanism associated with the activation of 5-HT1A and CB1 receptors.	Cannabidiol	0-3	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	51-66
31054943-12	2019	CBD anti-aggressive effects were attenuated by the 5-HT1A receptor antagonist WAY100635 (0.3 mg/kg) and the CB1 antagonist AM251 (1 mg/kg), suggesting that CBD decreases social isolation-induced aggressive behaviors through a mechanism associated with the activation of 5-HT1A and CB1 receptors.	Cannabidiol	0-3	cannabinoid receptor 1 (brain)	Mus musculus	108-111
31054943-12	2019	CBD anti-aggressive effects were attenuated by the 5-HT1A receptor antagonist WAY100635 (0.3 mg/kg) and the CB1 antagonist AM251 (1 mg/kg), suggesting that CBD decreases social isolation-induced aggressive behaviors through a mechanism associated with the activation of 5-HT1A and CB1 receptors.	Cannabidiol	0-3	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	51-57
31054943-12	2019	CBD anti-aggressive effects were attenuated by the 5-HT1A receptor antagonist WAY100635 (0.3 mg/kg) and the CB1 antagonist AM251 (1 mg/kg), suggesting that CBD decreases social isolation-induced aggressive behaviors through a mechanism associated with the activation of 5-HT1A and CB1 receptors.	Cannabidiol	0-3	cannabinoid receptor 1 (brain)	Mus musculus	281-284
31054943-12	2019	CBD anti-aggressive effects were attenuated by the 5-HT1A receptor antagonist WAY100635 (0.3 mg/kg) and the CB1 antagonist AM251 (1 mg/kg), suggesting that CBD decreases social isolation-induced aggressive behaviors through a mechanism associated with the activation of 5-HT1A and CB1 receptors.	Cannabidiol	156-159	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	51-66
31054943-12	2019	CBD anti-aggressive effects were attenuated by the 5-HT1A receptor antagonist WAY100635 (0.3 mg/kg) and the CB1 antagonist AM251 (1 mg/kg), suggesting that CBD decreases social isolation-induced aggressive behaviors through a mechanism associated with the activation of 5-HT1A and CB1 receptors.	Cannabidiol	156-159	cannabinoid receptor 1 (brain)	Mus musculus	108-111
31054943-12	2019	CBD anti-aggressive effects were attenuated by the 5-HT1A receptor antagonist WAY100635 (0.3 mg/kg) and the CB1 antagonist AM251 (1 mg/kg), suggesting that CBD decreases social isolation-induced aggressive behaviors through a mechanism associated with the activation of 5-HT1A and CB1 receptors.	Cannabidiol	156-159	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	51-57
31054943-12	2019	CBD anti-aggressive effects were attenuated by the 5-HT1A receptor antagonist WAY100635 (0.3 mg/kg) and the CB1 antagonist AM251 (1 mg/kg), suggesting that CBD decreases social isolation-induced aggressive behaviors through a mechanism associated with the activation of 5-HT1A and CB1 receptors.	Cannabidiol	156-159	cannabinoid receptor 1 (brain)	Mus musculus	281-284
31497013-6	2019	THC+CBD treatment also caused a decrease in the levels of brain infiltrating CD4+ T cells and pro-inflammatory molecules (IL-17, INF-gamma, TNF-alpha, IL-1beta, IL-6, and TBX21), while increasing anti-inflammatory phenotype such as FoxP3, STAT5b, IL-4, IL-10, and TGF-beta.	Cannabidiol	4-7	interleukin 17A	Mus musculus	122-127
31497013-6	2019	THC+CBD treatment also caused a decrease in the levels of brain infiltrating CD4+ T cells and pro-inflammatory molecules (IL-17, INF-gamma, TNF-alpha, IL-1beta, IL-6, and TBX21), while increasing anti-inflammatory phenotype such as FoxP3, STAT5b, IL-4, IL-10, and TGF-beta.	Cannabidiol	4-7	tumor necrosis factor	Mus musculus	140-149
31497013-6	2019	THC+CBD treatment also caused a decrease in the levels of brain infiltrating CD4+ T cells and pro-inflammatory molecules (IL-17, INF-gamma, TNF-alpha, IL-1beta, IL-6, and TBX21), while increasing anti-inflammatory phenotype such as FoxP3, STAT5b, IL-4, IL-10, and TGF-beta.	Cannabidiol	4-7	interleukin 1 beta	Mus musculus	151-159
31497013-6	2019	THC+CBD treatment also caused a decrease in the levels of brain infiltrating CD4+ T cells and pro-inflammatory molecules (IL-17, INF-gamma, TNF-alpha, IL-1beta, IL-6, and TBX21), while increasing anti-inflammatory phenotype such as FoxP3, STAT5b, IL-4, IL-10, and TGF-beta.	Cannabidiol	4-7	interleukin 6	Mus musculus	161-165
31497013-6	2019	THC+CBD treatment also caused a decrease in the levels of brain infiltrating CD4+ T cells and pro-inflammatory molecules (IL-17, INF-gamma, TNF-alpha, IL-1beta, IL-6, and TBX21), while increasing anti-inflammatory phenotype such as FoxP3, STAT5b, IL-4, IL-10, and TGF-beta.	Cannabidiol	4-7	T-box 21	Mus musculus	171-176
31497013-6	2019	THC+CBD treatment also caused a decrease in the levels of brain infiltrating CD4+ T cells and pro-inflammatory molecules (IL-17, INF-gamma, TNF-alpha, IL-1beta, IL-6, and TBX21), while increasing anti-inflammatory phenotype such as FoxP3, STAT5b, IL-4, IL-10, and TGF-beta.	Cannabidiol	4-7	forkhead box P3	Mus musculus	232-237
31497013-6	2019	THC+CBD treatment also caused a decrease in the levels of brain infiltrating CD4+ T cells and pro-inflammatory molecules (IL-17, INF-gamma, TNF-alpha, IL-1beta, IL-6, and TBX21), while increasing anti-inflammatory phenotype such as FoxP3, STAT5b, IL-4, IL-10, and TGF-beta.	Cannabidiol	4-7	signal transducer and activator of transcription 5B	Mus musculus	239-245
31497013-6	2019	THC+CBD treatment also caused a decrease in the levels of brain infiltrating CD4+ T cells and pro-inflammatory molecules (IL-17, INF-gamma, TNF-alpha, IL-1beta, IL-6, and TBX21), while increasing anti-inflammatory phenotype such as FoxP3, STAT5b, IL-4, IL-10, and TGF-beta.	Cannabidiol	4-7	interleukin 4	Mus musculus	247-251
31497013-6	2019	THC+CBD treatment also caused a decrease in the levels of brain infiltrating CD4+ T cells and pro-inflammatory molecules (IL-17, INF-gamma, TNF-alpha, IL-1beta, IL-6, and TBX21), while increasing anti-inflammatory phenotype such as FoxP3, STAT5b, IL-4, IL-10, and TGF-beta.	Cannabidiol	4-7	interleukin 10	Mus musculus	253-258
31497013-6	2019	THC+CBD treatment also caused a decrease in the levels of brain infiltrating CD4+ T cells and pro-inflammatory molecules (IL-17, INF-gamma, TNF-alpha, IL-1beta, IL-6, and TBX21), while increasing anti-inflammatory phenotype such as FoxP3, STAT5b, IL-4, IL-10, and TGF-beta.	Cannabidiol	4-7	transforming growth factor, beta 1	Mus musculus	264-272
31382646-4	2019	Spectrophotometric results show that CBD significantly enhances the activity of antioxidant enzymes such as superoxide dismutase and thioredoxin reductase in UV irradiated keratinocytes.	Cannabidiol	37-40	peroxiredoxin 5	Homo sapiens	133-154
31158702-5	2019	RESULTS: In behavioral experiments, CBD (5 mg/ml) or CBN (1 mg/ml) decreased NGF-induced mechanical sensitization.	Cannabidiol	36-39	nerve growth factor	Rattus norvegicus	77-80
31417379-1	2019	Background: Delta9-Tetrahydrocannabinol (THC, a CB1 receptor agonist) and Cannabidiol (CBD, a non-competitive antagonist of endogenous CB1 and CB2 ligands) are two primary components of Cannabis species, and may modulate fear learning in mammals.	Cannabidiol	74-85	cannabinoid receptor 1	Rattus norvegicus	135-138
31417379-1	2019	Background: Delta9-Tetrahydrocannabinol (THC, a CB1 receptor agonist) and Cannabidiol (CBD, a non-competitive antagonist of endogenous CB1 and CB2 ligands) are two primary components of Cannabis species, and may modulate fear learning in mammals.	Cannabidiol	74-85	cannabinoid receptor 2	Rattus norvegicus	143-146
31417379-1	2019	Background: Delta9-Tetrahydrocannabinol (THC, a CB1 receptor agonist) and Cannabidiol (CBD, a non-competitive antagonist of endogenous CB1 and CB2 ligands) are two primary components of Cannabis species, and may modulate fear learning in mammals.	Cannabidiol	87-90	cannabinoid receptor 1	Rattus norvegicus	135-138
31417379-1	2019	Background: Delta9-Tetrahydrocannabinol (THC, a CB1 receptor agonist) and Cannabidiol (CBD, a non-competitive antagonist of endogenous CB1 and CB2 ligands) are two primary components of Cannabis species, and may modulate fear learning in mammals.	Cannabidiol	87-90	cannabinoid receptor 2	Rattus norvegicus	143-146
31077084-6	2019	The protective action of cannabidiol and KLS-13019 against paclitaxel-induced toxicity during a 5-h test period was significantly attenuated after a 4-day knockdown of mNCX-1 that was not attributable to toxicity.	Cannabidiol	25-36	solute carrier family 8 (sodium/calcium exchanger), member 1	Mus musculus	168-174
30610611-0	2019	Adenosine A2A-Cannabinoid CB1 Receptor Heteromers in the Hippocampus: Cannabidiol Blunts Delta9-Tetrahydrocannabinol-Induced Cognitive Impairment.	Cannabidiol	70-81	cannabinoid receptor 1	Homo sapiens	26-29
31349651-0	2019	Cannabidiol Induces Cell Cycle Arrest and Cell Apoptosis in Human Gastric Cancer SGC-7901 Cells.	Cannabidiol	0-11	sarcoglycan beta	Homo sapiens	81-84
31349651-2	2019	The present study examined the in vitro effects of CBD on human gastric cancer SGC-7901 cells.	Cannabidiol	51-54	sarcoglycan beta	Homo sapiens	79-82
30898678-0	2019	Cannabidiol attenuates mechanical allodynia in streptozotocin-induced diabetic rats via serotonergic system activation through 5-HT1A receptors.	Cannabidiol	0-11	5-hydroxytryptamine receptor 1A	Rattus norvegicus	127-133
31149342-1	2019	The phospholipid l-alpha-lysophosphatidylinositol (LPI), an endogenous ligand for GPR55, is elevated in patients with acute coronary syndrome, and a GPR55 antagonist cannabidiol (CBD) reduces experimental ischemia/reperfusion (I/R) injury.	Cannabidiol	166-177	G protein-coupled receptor 55	Homo sapiens	149-154
31211851-2	2019	CBD is metabolized via UDP-glucuronosyltransferase (UGT) and cytochrome 450 (CYP) enzymes, but information on interactions with common anticonvulsive drugs is incomplete.	Cannabidiol	0-3	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	23-50
31211851-2	2019	CBD is metabolized via UDP-glucuronosyltransferase (UGT) and cytochrome 450 (CYP) enzymes, but information on interactions with common anticonvulsive drugs is incomplete.	Cannabidiol	0-3	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	52-55
31211851-5	2019	One possible mechanism contributing at least partially to increasing BRV level is the inhibition of CYP2C19 by cannabidiol.	Cannabidiol	111-122	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	100-107
31212965-0	2019	Paradoxical Patterns of Sinusoidal Obstruction Syndrome-Like Liver Injury in Aged Female CD-1 Mice Triggered by Cannabidiol-Rich Cannabis Extract and Acetaminophen Co-Administration.	Cannabidiol	112-123	CD1 antigen complex	Mus musculus	89-93
31212965-1	2019	The goal of this study was to investigate the potential for a cannabidiol-rich cannabis extract (CRCE) to interact with the most common over-the-counter drug and the major known cause of drug-induced liver injury-acetaminophen (APAP)-in aged female CD-1 mice.	Cannabidiol	62-73	CD1 antigen complex	Mus musculus	249-253
31195721-0	2019	Cannabidiol Overcomes Oxaliplatin Resistance by Enhancing NOS3- and SOD2-Induced Autophagy in Human Colorectal Cancer Cells.	Cannabidiol	0-11	nitric oxide synthase 3	Homo sapiens	58-62
31195721-0	2019	Cannabidiol Overcomes Oxaliplatin Resistance by Enhancing NOS3- and SOD2-Induced Autophagy in Human Colorectal Cancer Cells.	Cannabidiol	0-11	superoxide dismutase 2	Homo sapiens	68-72
31195721-7	2019	Combined treatment with oxaliplatin and CBD reduced phospho-NOS3 levels and nitric oxide (NO) production and resulted in the production of reactive oxygen species (ROS) by reducing the levels of superoxide dismutase 2, an antioxidant present in the mitochondria, causing mitochondrial dysfunction.	Cannabidiol	40-43	nitric oxide synthase 3	Homo sapiens	60-64
31195721-9	2019	The combination of oxaliplatin and CBD decreased NOS3 phosphorylation, which resulted in autophagy, by inducing the overproduction of ROS through mitochondrial dysfunction, thus overcoming oxaliplatin resistance.	Cannabidiol	35-38	nitric oxide synthase 3	Homo sapiens	49-53
31063743-0	2019	Cannabidiol (CBD) reduces anxiety-related behavior in mice via an FMRP-independent mechanism.	Cannabidiol	0-11	fragile X messenger ribonucleoprotein 1	Mus musculus	66-70
31063743-0	2019	Cannabidiol (CBD) reduces anxiety-related behavior in mice via an FMRP-independent mechanism.	Cannabidiol	13-16	fragile X messenger ribonucleoprotein 1	Mus musculus	66-70
31063743-10	2019	Brain concentrations of CBD were equivalent between genotypes, but in animals sacrificed 90 min post-administration, decreased plasma CBD in Fmr1 KO mice compared to WT suggested more rapid clearance of CBD by transgenic animals.	Cannabidiol	24-27	fragile X messenger ribonucleoprotein 1	Mus musculus	141-145
31063743-10	2019	Brain concentrations of CBD were equivalent between genotypes, but in animals sacrificed 90 min post-administration, decreased plasma CBD in Fmr1 KO mice compared to WT suggested more rapid clearance of CBD by transgenic animals.	Cannabidiol	134-137	fragile X messenger ribonucleoprotein 1	Mus musculus	141-145
31178718-0	2019	Cannabidiol Affects the Bezold-Jarisch Reflex via TRPV1 and 5-HT3 Receptors and Has Peripheral Sympathomimetic Effects in Spontaneously Hypertensive and Normotensive Rats.	Cannabidiol	0-11	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	50-55
31178718-10	2019	The CBD-induced fall in HR but not in BP was diminished by the TRPV1 receptor antagonist capsazepine and almost completely abolished if CBD was re-injected after previous administration.	Cannabidiol	4-7	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	63-68
31178718-14	2019	Conclusions: Cannabidiol (1) induces the Bezold-Jarisch reflex likely via TRPV1 receptors (which undergo tachyphylaxis) more markedly in SHR than in WKY; (2) inhibits the Bezold-Jarisch reflex induced by activation of 5-HT3 but not TRPV1 receptors; (3) has peripheral sympathomimetic, (4) vasodilatory, and (5) negative inotropic effects.	Cannabidiol	13-24	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	74-79
31178718-14	2019	Conclusions: Cannabidiol (1) induces the Bezold-Jarisch reflex likely via TRPV1 receptors (which undergo tachyphylaxis) more markedly in SHR than in WKY; (2) inhibits the Bezold-Jarisch reflex induced by activation of 5-HT3 but not TRPV1 receptors; (3) has peripheral sympathomimetic, (4) vasodilatory, and (5) negative inotropic effects.	Cannabidiol	13-24	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	232-237
31054246-12	2019	Palmitoylethanolamide and cannabidiol prevented an inflammation-induced fall in TRPV1 and increase in PPARalpha transcription (P &lt; 0.0001).	Cannabidiol	26-37	transient receptor potential cation channel subfamily V member 1	Homo sapiens	80-85
31054246-12	2019	Palmitoylethanolamide and cannabidiol prevented an inflammation-induced fall in TRPV1 and increase in PPARalpha transcription (P &lt; 0.0001).	Cannabidiol	26-37	peroxisome proliferator activated receptor alpha	Homo sapiens	102-111
30684511-0	2019	Cannabidiol modulates phosphorylated rpS6 signalling in a zebrafish model of Tuberous Sclerosis Complex.	Cannabidiol	0-11	ribosomal protein S6	Danio rerio	37-41
30684511-5	2019	CBD treatment did, however, reduce the number of phosphorylated rpS6 positive cells, and their cross-sectional cell size.	Cannabidiol	0-3	ribosomal protein S6	Danio rerio	64-68
30684511-7	2019	Taken together, these data suggest that CBD selectively modulates levels of phosphorylated rpS6 in the brain and additionally provides an anxiolytic effect.	Cannabidiol	40-43	ribosomal protein S6	Danio rerio	91-95
30684511-9	2019	Additional work is necessary to identify upstream signal modulation and to further justify the use of CBD as a possible therapeutic strategy to manage TSC.	Cannabidiol	102-105	TSC complex subunit 2	Danio rerio	151-154
29338068-2	2019	We determined whether CBD ameliorates cognitive deficits and withdrawal signs induced by cannabinoid CB1 /CB2 receptor agonists or produces these pharmacological effects on its own.	Cannabidiol	22-25	cannabinoid receptor 1 (brain)	Mus musculus	101-104
29338068-2	2019	We determined whether CBD ameliorates cognitive deficits and withdrawal signs induced by cannabinoid CB1 /CB2 receptor agonists or produces these pharmacological effects on its own.	Cannabidiol	22-25	cannabinoid receptor 2 (macrophage)	Mus musculus	106-109
29981240-4	2019	CBD and CBD-DMH binding was simulated with models of human CB1 or CB2 receptors, based on the recently published crystal structures of agonist-bound (5XRA) or antagonist-bound (5TGZ) human CB1 receptors.	Cannabidiol	0-3	cannabinoid receptor 1	Homo sapiens	59-62
29981240-4	2019	CBD and CBD-DMH binding was simulated with models of human CB1 or CB2 receptors, based on the recently published crystal structures of agonist-bound (5XRA) or antagonist-bound (5TGZ) human CB1 receptors.	Cannabidiol	0-3	cannabinoid receptor 2	Homo sapiens	66-69
29981240-4	2019	CBD and CBD-DMH binding was simulated with models of human CB1 or CB2 receptors, based on the recently published crystal structures of agonist-bound (5XRA) or antagonist-bound (5TGZ) human CB1 receptors.	Cannabidiol	0-3	cannabinoid receptor 1	Homo sapiens	189-192
29981240-9	2019	CBD, CP55,940 and SR144528 shared a binding site in the CB2 receptor models that was separate from CBD-DMH.	Cannabidiol	0-3	cannabinoid receptor 2	Homo sapiens	56-59
29981240-10	2019	CONCLUSION AND IMPLICATIONS: The pharmacological activity of CBD and CBD-DMH in HEK293A cells and their modelled binding sites at CB1 and CB2 receptors may explain their in vivo effects and illuminates the difficulties associated with the development of allosteric modulators for CB1 and CB2 receptors.	Cannabidiol	61-64	cannabinoid receptor 1	Homo sapiens	130-133
29981240-10	2019	CONCLUSION AND IMPLICATIONS: The pharmacological activity of CBD and CBD-DMH in HEK293A cells and their modelled binding sites at CB1 and CB2 receptors may explain their in vivo effects and illuminates the difficulties associated with the development of allosteric modulators for CB1 and CB2 receptors.	Cannabidiol	61-64	cannabinoid receptor 2	Homo sapiens	138-141
29981240-10	2019	CONCLUSION AND IMPLICATIONS: The pharmacological activity of CBD and CBD-DMH in HEK293A cells and their modelled binding sites at CB1 and CB2 receptors may explain their in vivo effects and illuminates the difficulties associated with the development of allosteric modulators for CB1 and CB2 receptors.	Cannabidiol	61-64	cannabinoid receptor 1	Homo sapiens	280-283
29981240-10	2019	CONCLUSION AND IMPLICATIONS: The pharmacological activity of CBD and CBD-DMH in HEK293A cells and their modelled binding sites at CB1 and CB2 receptors may explain their in vivo effects and illuminates the difficulties associated with the development of allosteric modulators for CB1 and CB2 receptors.	Cannabidiol	61-64	cannabinoid receptor 2	Homo sapiens	288-291
30074247-8	2019	KEY RESULTS: CBD and CBDV promoted the differentiation of murine C2C12 myoblast cells into myotubes by increasing [Ca2+ ]i mostly via TRPV1 activation, an effect that undergoes rapid desensitization.	Cannabidiol	13-16	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	134-139
30833288-6	2019	The inhibition of CES1 by THC, CBD, and CBN was reversible and appears to proceed through a mixed competitive-noncompetitive mechanism.	Cannabidiol	31-34	carboxylesterase 1	Homo sapiens	18-22
30833288-9	2019	Compared with the potential unbound plasma concentrations attainable clinically, the K i values suggest a potential for clinically significant inhibition of CES1 by THC and CBD.	Cannabidiol	173-176	carboxylesterase 1	Homo sapiens	157-161
30879928-10	2019	In vitro exposure of monocytes to CBD led to significant increase in PPFIA2 expression.	Cannabidiol	34-37	PTPRF interacting protein alpha 2	Homo sapiens	69-75
31039613-14	2019	The development of a structure-function relationship for cCBD-LL37 and fCBD-LL37 demonstrates promise for using QCM-D predictions to inform the rational design of novel, antimicrobial, and noncytotoxic CBD-LL37 for clinical applications.	Cannabidiol	58-61	cathelicidin antimicrobial peptide	Homo sapiens	62-66
31039613-14	2019	The development of a structure-function relationship for cCBD-LL37 and fCBD-LL37 demonstrates promise for using QCM-D predictions to inform the rational design of novel, antimicrobial, and noncytotoxic CBD-LL37 for clinical applications.	Cannabidiol	58-61	cathelicidin antimicrobial peptide	Homo sapiens	76-80
30660647-0	2019	Cannabidiol-induced apoptosis is mediated by activation of Noxa in human colorectal cancer cells.	Cannabidiol	0-11	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	59-63
30660647-4	2019	CBD induced apoptosis by regulating many pro- and anti-apoptotic proteins, of which Noxa showed significantly higher expression.	Cannabidiol	0-3	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	84-88
30660647-5	2019	To understand the relationship between Noxa and CBD-induced apoptosis, Noxa levels were downregulated using siRNA, and the expression of apoptosis markers decreased.	Cannabidiol	48-51	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	39-43
30660647-5	2019	To understand the relationship between Noxa and CBD-induced apoptosis, Noxa levels were downregulated using siRNA, and the expression of apoptosis markers decreased.	Cannabidiol	48-51	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	71-75
30660647-7	2019	As a result, CBD induced apoptosis in a Noxa-and-ROS-dependent manner.	Cannabidiol	13-16	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	40-44
30971453-4	2019	CBD conjugation or fusion decreases the systemic toxicity of both alphaCTLA4 + alphaPD-L1 combination therapy and IL-2, for example, eliminating hepatotoxicity with the CPI molecules and ameliorating pulmonary edema with IL-2.	Cannabidiol	0-3	interleukin 2	Mus musculus	114-118
30971453-4	2019	CBD conjugation or fusion decreases the systemic toxicity of both alphaCTLA4 + alphaPD-L1 combination therapy and IL-2, for example, eliminating hepatotoxicity with the CPI molecules and ameliorating pulmonary edema with IL-2.	Cannabidiol	0-3	interleukin 2	Mus musculus	221-225
30971453-6	2019	In an orthotopic breast cancer model, combination treatment with CPI and IL-2 eradicated tumors in 9 of 13 animals with the CBD-modified drugs, whereas it did so in only 1 of 13 animals with the unmodified drugs.	Cannabidiol	124-127	interleukin 2	Mus musculus	73-77
30879928-13	2019	The findings warrant further exploration of the role of PPFIA2 in cannabis induced changes of neuropsychological function, particularly in relation to CBD.	Cannabidiol	151-154	PTPRF interacting protein alpha 2	Homo sapiens	56-62
30796934-0	2019	DMH-CBD, a cannabidiol analog with reduced cytotoxicity, inhibits TNF production by targeting NF-kB activity dependent on A2A receptor.	Cannabidiol	11-22	tumor necrosis factor	Homo sapiens	66-69
30796934-4	2019	CBD and DMH-CBD suppressed LPS-induced TNF production and NF-kB activity in a concentration-dependent manner.	Cannabidiol	0-3	tumor necrosis factor	Homo sapiens	39-42
30984001-0	2019	Attenuation of Novelty-Induced Hyperactivity of Gria1-/- Mice by Cannabidiol and Hippocampal Inhibitory Chemogenetics.	Cannabidiol	65-76	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	48-53
30984001-3	2019	Now we found that systemic cannabidiol strongly blunted the hyperactivity and the hippocampal c-Fos expression of the Gria1-/- mice, while not affecting the wild-type littermate controls.	Cannabidiol	27-38	FBJ osteosarcoma oncogene	Mus musculus	94-99
30984001-3	2019	Now we found that systemic cannabidiol strongly blunted the hyperactivity and the hippocampal c-Fos expression of the Gria1-/- mice, while not affecting the wild-type littermate controls.	Cannabidiol	27-38	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	118-123
30984001-4	2019	Acute bilateral intra-dorsal hippocampal infusion of cannabidiol partially blocked the hyperactivity of the Gria1-/- mice, but had no effect on wild-types.	Cannabidiol	53-64	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	108-113
30721081-0	2019	Cannabidiol Increases Proliferation, Migration, Tubulogenesis, and Integrity of Human Brain Endothelial Cells through TRPV2 Activation.	Cannabidiol	0-11	transient receptor potential cation channel subfamily V member 2	Homo sapiens	118-123
30721081-1	2019	The effect of cannabidiol (CBD), a high-affinity agonist of the transient receptor potential vanilloid-2 (TRPV2) channel, has been poorly investigated in human brain microvessel endothelial cells (BMEC) forming the blood-brain barrier (BBB).	Cannabidiol	14-25	transient receptor potential cation channel subfamily V member 2	Homo sapiens	64-104
30721081-1	2019	The effect of cannabidiol (CBD), a high-affinity agonist of the transient receptor potential vanilloid-2 (TRPV2) channel, has been poorly investigated in human brain microvessel endothelial cells (BMEC) forming the blood-brain barrier (BBB).	Cannabidiol	14-25	transient receptor potential cation channel subfamily V member 2	Homo sapiens	106-111
30721081-1	2019	The effect of cannabidiol (CBD), a high-affinity agonist of the transient receptor potential vanilloid-2 (TRPV2) channel, has been poorly investigated in human brain microvessel endothelial cells (BMEC) forming the blood-brain barrier (BBB).	Cannabidiol	27-30	transient receptor potential cation channel subfamily V member 2	Homo sapiens	64-104
30721081-1	2019	The effect of cannabidiol (CBD), a high-affinity agonist of the transient receptor potential vanilloid-2 (TRPV2) channel, has been poorly investigated in human brain microvessel endothelial cells (BMEC) forming the blood-brain barrier (BBB).	Cannabidiol	27-30	transient receptor potential cation channel subfamily V member 2	Homo sapiens	106-111
30721081-5	2019	CBD dose-dependently induced the hCMEC/D3 cell number (EC50 0.3 +- 0.1 muM), and this effect was fully abolished by TNL or TRPV2 siRNA.	Cannabidiol	0-3	latexin	Homo sapiens	71-74
30721081-5	2019	CBD dose-dependently induced the hCMEC/D3 cell number (EC50 0.3 +- 0.1 muM), and this effect was fully abolished by TNL or TRPV2 siRNA.	Cannabidiol	0-3	transient receptor potential cation channel subfamily V member 2	Homo sapiens	123-128
29941868-0	2019	GPR3, GPR6, and GPR12 as novel molecular targets: their biological functions and interaction with cannabidiol.	Cannabidiol	98-109	G protein-coupled receptor 3	Homo sapiens	0-4
29941868-0	2019	GPR3, GPR6, and GPR12 as novel molecular targets: their biological functions and interaction with cannabidiol.	Cannabidiol	98-109	G protein-coupled receptor 6	Homo sapiens	6-10
29941868-0	2019	GPR3, GPR6, and GPR12 as novel molecular targets: their biological functions and interaction with cannabidiol.	Cannabidiol	98-109	G protein-coupled receptor 12	Homo sapiens	16-21
29941868-5	2019	Using beta-arrestin2 recruitment and cAMP accumulation assays, we recently found that the nonpsychoactive phytocannabinoid cannabidiol (CBD) is an inverse agonist for GPR3, GPR6, and GPR12.	Cannabidiol	123-134	arrestin beta 2	Homo sapiens	6-20
29941868-5	2019	Using beta-arrestin2 recruitment and cAMP accumulation assays, we recently found that the nonpsychoactive phytocannabinoid cannabidiol (CBD) is an inverse agonist for GPR3, GPR6, and GPR12.	Cannabidiol	123-134	G protein-coupled receptor 3	Homo sapiens	167-171
29941868-5	2019	Using beta-arrestin2 recruitment and cAMP accumulation assays, we recently found that the nonpsychoactive phytocannabinoid cannabidiol (CBD) is an inverse agonist for GPR3, GPR6, and GPR12.	Cannabidiol	123-134	G protein-coupled receptor 6	Homo sapiens	173-177
29941868-5	2019	Using beta-arrestin2 recruitment and cAMP accumulation assays, we recently found that the nonpsychoactive phytocannabinoid cannabidiol (CBD) is an inverse agonist for GPR3, GPR6, and GPR12.	Cannabidiol	123-134	G protein-coupled receptor 12	Homo sapiens	183-188
29941868-5	2019	Using beta-arrestin2 recruitment and cAMP accumulation assays, we recently found that the nonpsychoactive phytocannabinoid cannabidiol (CBD) is an inverse agonist for GPR3, GPR6, and GPR12.	Cannabidiol	136-139	arrestin beta 2	Homo sapiens	6-20
29941868-5	2019	Using beta-arrestin2 recruitment and cAMP accumulation assays, we recently found that the nonpsychoactive phytocannabinoid cannabidiol (CBD) is an inverse agonist for GPR3, GPR6, and GPR12.	Cannabidiol	136-139	G protein-coupled receptor 3	Homo sapiens	167-171
29941868-5	2019	Using beta-arrestin2 recruitment and cAMP accumulation assays, we recently found that the nonpsychoactive phytocannabinoid cannabidiol (CBD) is an inverse agonist for GPR3, GPR6, and GPR12.	Cannabidiol	136-139	G protein-coupled receptor 6	Homo sapiens	173-177
29941868-5	2019	Using beta-arrestin2 recruitment and cAMP accumulation assays, we recently found that the nonpsychoactive phytocannabinoid cannabidiol (CBD) is an inverse agonist for GPR3, GPR6, and GPR12.	Cannabidiol	136-139	G protein-coupled receptor 12	Homo sapiens	183-188
29941868-7	2019	Furthermore, identification of CBD as a new inverse agonist for GPR3, GPR6, and GPR12 provides the initial chemical scaffolds upon which potent and efficacious agents acting on these receptors can be developed, with the goal of developing chemical tools for studying these orphan receptors and ultimately new therapeutic agents.	Cannabidiol	31-34	G protein-coupled receptor 3	Homo sapiens	64-68
29941868-7	2019	Furthermore, identification of CBD as a new inverse agonist for GPR3, GPR6, and GPR12 provides the initial chemical scaffolds upon which potent and efficacious agents acting on these receptors can be developed, with the goal of developing chemical tools for studying these orphan receptors and ultimately new therapeutic agents.	Cannabidiol	31-34	G protein-coupled receptor 6	Homo sapiens	70-74
29941868-7	2019	Furthermore, identification of CBD as a new inverse agonist for GPR3, GPR6, and GPR12 provides the initial chemical scaffolds upon which potent and efficacious agents acting on these receptors can be developed, with the goal of developing chemical tools for studying these orphan receptors and ultimately new therapeutic agents.	Cannabidiol	31-34	G protein-coupled receptor 12	Homo sapiens	80-85
30202014-7	2019	Finally, the neurophysiological effects of CBD were illustrated at the molecular level, and dopamine receptor 3 (DRD3) was further predicted to be an active target for CBD.	Cannabidiol	168-171	dopamine receptor D3	Homo sapiens	113-117
30538288-9	2019	Interestingly, the effects of PFC THC vs. CBD were found to be mediated through dissociable CB1 vs. 5-HT1A-dependent receptor signaling mechanisms, directly in the PFC.	Cannabidiol	42-45	cannabinoid receptor 1	Rattus norvegicus	92-95
30841431-0	2019	Novel protective effect of O-1602 and abnormal cannabidiol, GPR55 agonists, on ER stress-induced apoptosis in pancreatic beta-cells.	Cannabidiol	47-58	G protein-coupled receptor 55	Mus musculus	60-65
30955420-20	2019	OBJECTIVE: Since 2014, cannabidiol (CBD) has been administered to patients with treatment-resistant epilepsies (TREs) in an ongoing expanded access program (EAP).	Cannabidiol	23-34	glutamyl aminopeptidase	Homo sapiens	157-160
30597288-0	2019	Cannabidiol Affects Extracellular Vesicle Release, miR21 and miR126, and Reduces Prohibitin Protein in Glioblastoma Multiforme Cells.	Cannabidiol	0-11	microRNA 21	Homo sapiens	51-56
30597288-0	2019	Cannabidiol Affects Extracellular Vesicle Release, miR21 and miR126, and Reduces Prohibitin Protein in Glioblastoma Multiforme Cells.	Cannabidiol	0-11	microRNA 126	Homo sapiens	61-67
30597288-0	2019	Cannabidiol Affects Extracellular Vesicle Release, miR21 and miR126, and Reduces Prohibitin Protein in Glioblastoma Multiforme Cells.	Cannabidiol	0-11	prohibitin 1	Homo sapiens	81-91
30597288-5	2019	Compared to controls, CBD-treated cells released EVs containing lower levels of pro-oncogenic miR21 and increased levels of anti-oncogenic miR126; these effects were greater than with TMZ alone.	Cannabidiol	22-25	microRNA 21	Homo sapiens	94-99
30597288-5	2019	Compared to controls, CBD-treated cells released EVs containing lower levels of pro-oncogenic miR21 and increased levels of anti-oncogenic miR126; these effects were greater than with TMZ alone.	Cannabidiol	22-25	microRNA 126	Homo sapiens	139-145
30742662-14	2019	Accordingly, we found that Nrf2-mediated expression of redox-dependent genes defines a Mox-like phenotype in CBD treated BV-2 cells.	Cannabidiol	109-112	nuclear factor, erythroid derived 2, like 2	Mus musculus	27-31
30702341-10	2019	CB-1 antagonist AM251 has been shown to inhibit osteoclast differentiation and activity, while GPR55 antagonist cannabidiol increases osteoblast activity and decreases osteoclast function.	Cannabidiol	112-123	G protein-coupled receptor 55	Homo sapiens	95-100
30496751-3	2019	Both the schizophrenia-like phenotype and altered transcriptional regulation of CB1 receptors were reversed by peripubertal treatment (from PND 19 to PND 39) with the non-psychotropic phytocannabinoid cannabidiol (30 mg/kg/day), or, in part, by treatment with the cannabinoid CB1 receptor antagonist/inverse agonist AM251 (0.5 mg/kg/day), but not with haloperidol (0.6 mg/kg/day).	Cannabidiol	201-212	cannabinoid receptor 1	Rattus norvegicus	80-83
30496751-3	2019	Both the schizophrenia-like phenotype and altered transcriptional regulation of CB1 receptors were reversed by peripubertal treatment (from PND 19 to PND 39) with the non-psychotropic phytocannabinoid cannabidiol (30 mg/kg/day), or, in part, by treatment with the cannabinoid CB1 receptor antagonist/inverse agonist AM251 (0.5 mg/kg/day), but not with haloperidol (0.6 mg/kg/day).	Cannabidiol	201-212	cannabinoid receptor 1	Rattus norvegicus	276-279
30496751-4	2019	These results suggest that early treatment with cannabidiol may prevent both the appearance of schizophrenia-like deficits as well as CB1 alterations in the PFC at adulthood, supporting that peripubertal cannabidiol treatment might be protective against MAM insult.	Cannabidiol	48-59	cannabinoid receptor 1	Rattus norvegicus	134-137
29869197-0	2019	Cannabidiol Induces Rapid and Sustained Antidepressant-Like Effects Through Increased BDNF Signaling and Synaptogenesis in the Prefrontal Cortex.	Cannabidiol	0-11	brain-derived neurotrophic factor	Rattus norvegicus	86-90
29869197-10	2019	Intracerebroventricular injection of the TrkB antagonist, K252a (0.05 nmol/muL), or the mTOR inhibitor, rapamycin (1 nmol/muL), abolished the behavioral effects of CBD.	Cannabidiol	164-167	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	41-45
29869197-10	2019	Intracerebroventricular injection of the TrkB antagonist, K252a (0.05 nmol/muL), or the mTOR inhibitor, rapamycin (1 nmol/muL), abolished the behavioral effects of CBD.	Cannabidiol	164-167	mechanistic target of rapamycin kinase	Rattus norvegicus	88-92
30430393-10	2019	Cannabidiol improved memory performance and reduced hippocampal levels of inflammation markers (inducible nitric oxide synthase, ionized calcium-binding adapter molecule 1, glial fibrillary acidic protein, and arginase 1).	Cannabidiol	0-11	allograft inflammatory factor 1	Rattus norvegicus	129-171
30430393-10	2019	Cannabidiol improved memory performance and reduced hippocampal levels of inflammation markers (inducible nitric oxide synthase, ionized calcium-binding adapter molecule 1, glial fibrillary acidic protein, and arginase 1).	Cannabidiol	0-11	glial fibrillary acidic protein	Rattus norvegicus	173-220
30430393-11	2019	Cannabidiol attenuated the decrease in hippocampal levels of brain-derived neurotrophic factor induced by CCH in diabetic animals, but it did not affect the levels of neuroplasticity markers (growth-associated protein-43 and synaptophysin) in middle-aged diabetic rats.	Cannabidiol	0-11	brain-derived neurotrophic factor	Rattus norvegicus	61-94
30783513-0	2019	Inhibition of ATM kinase upregulates levels of cell death induced by cannabidiol and gamma-irradiation in human glioblastoma cells.	Cannabidiol	69-80	ATM serine/threonine kinase	Homo sapiens	14-17
30481497-3	2019	Cannabidiol (CBD) is known to exert immunomodulatory effects through the activation of cannabinoid-1 and - 2 (CB1 and CB2) receptors located in the central nervous system and immune cells, respectively.	Cannabidiol	0-11	cannabinoid receptor 1	Homo sapiens	110-113
30481497-3	2019	Cannabidiol (CBD) is known to exert immunomodulatory effects through the activation of cannabinoid-1 and - 2 (CB1 and CB2) receptors located in the central nervous system and immune cells, respectively.	Cannabidiol	0-11	cannabinoid receptor 2	Homo sapiens	118-121
30481497-3	2019	Cannabidiol (CBD) is known to exert immunomodulatory effects through the activation of cannabinoid-1 and - 2 (CB1 and CB2) receptors located in the central nervous system and immune cells, respectively.	Cannabidiol	13-16	cannabinoid receptor 1	Homo sapiens	110-113
30481497-3	2019	Cannabidiol (CBD) is known to exert immunomodulatory effects through the activation of cannabinoid-1 and - 2 (CB1 and CB2) receptors located in the central nervous system and immune cells, respectively.	Cannabidiol	13-16	cannabinoid receptor 2	Homo sapiens	118-121
30644434-6	2019	Network activity profiles evoked by conolidine and cannabidiol closely matched that of omega-conotoxin CVIE, a potent and selective Cav2.2 calcium channel blocker with proposed antinociceptive action suggesting that they too would block this channel.	Cannabidiol	51-62	calcium voltage-gated channel subunit alpha1 B	Homo sapiens	132-138
30644434-8	2019	Remarkably, conolidine and cannabidiol both inhibited Cav2.2, providing a glimpse into the MOA that could underlie their antinociceptive action.	Cannabidiol	27-38	calcium voltage-gated channel subunit alpha1 B	Homo sapiens	54-60
30997003-8	2019	Subsequently, the [F-Al(ORF)3]- anion abstracted the [Me3Si]+ moiety from [Me4C4-SiMe3]+, probably releasing CBD.	Cannabidiol	109-112	ankyrin repeat, SAM and basic leucine zipper domain containing 1	Homo sapiens	24-29
30391635-10	2019	Treatment with the non-psychoactive cannabinoid cannabidiol abolished memory impairment of nicotine withdrawal and microglia reactivity, reduced the expression of IL1beta and IFNgamma in the hippocampus and the prefrontal cortex, respectively, and normalized Ki67 levels.	Cannabidiol	48-59	interleukin 1 alpha	Mus musculus	163-170
30391635-10	2019	Treatment with the non-psychoactive cannabinoid cannabidiol abolished memory impairment of nicotine withdrawal and microglia reactivity, reduced the expression of IL1beta and IFNgamma in the hippocampus and the prefrontal cortex, respectively, and normalized Ki67 levels.	Cannabidiol	48-59	interferon gamma	Mus musculus	175-183
30391635-10	2019	Treatment with the non-psychoactive cannabinoid cannabidiol abolished memory impairment of nicotine withdrawal and microglia reactivity, reduced the expression of IL1beta and IFNgamma in the hippocampus and the prefrontal cortex, respectively, and normalized Ki67 levels.	Cannabidiol	48-59	antigen identified by monoclonal antibody Ki 67	Mus musculus	259-263
30636988-7	2019	The inhibitory constant (Ki) values of  9-THC and CBD were 6.62 and 2010 nM, respectively, showing a high affinity of  9-THC and a low affinity of CBD for the CB1 receptor, respectively.	Cannabidiol	50-53	cannabinoid receptor 1 (brain)	Mus musculus	159-162
30460546-18	2019	Four (15.4%) had changes in antiepileptic drug concentrations and three had elevated aspartate aminotransferase and alanine aminotransferase levels when cannabidiol was administered together with valproate.	Cannabidiol	153-164	glutamic--pyruvic transaminase	Homo sapiens	116-140
30636988-7	2019	The inhibitory constant (Ki) values of  9-THC and CBD were 6.62 and 2010 nM, respectively, showing a high affinity of  9-THC and a low affinity of CBD for the CB1 receptor, respectively.	Cannabidiol	147-150	cannabinoid receptor 1 (brain)	Mus musculus	159-162
30157131-1	2019	Clinical studies indicate that cannabidiol (CBD), the primary nonaddictive component of cannabis that interacts with the serotonin (5-HT)1A receptor, may possess analgesic and anxiolytic effects.	Cannabidiol	31-42	5-hydroxytryptamine receptor 1A	Rattus norvegicus	121-148
30157131-1	2019	Clinical studies indicate that cannabidiol (CBD), the primary nonaddictive component of cannabis that interacts with the serotonin (5-HT)1A receptor, may possess analgesic and anxiolytic effects.	Cannabidiol	44-47	5-hydroxytryptamine receptor 1A	Rattus norvegicus	121-148
30157131-7	2019	Repeated treatment with CBD (5 mg/kg/day, subcutaneously [s.c.], for 7 days) increased 5-HT firing through desensitization of 5-HT1A receptors.	Cannabidiol	24-27	5-hydroxytryptamine receptor 1A	Rattus norvegicus	126-132
30157131-11	2019	Overall, repeated treatment with low-dose CBD induces analgesia predominantly through TRPV1 activation, reduces anxiety through 5-HT1A receptor activation, and rescues impaired 5-HT neurotransmission under neuropathic pain conditions.	Cannabidiol	42-45	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	86-91
30157131-11	2019	Overall, repeated treatment with low-dose CBD induces analgesia predominantly through TRPV1 activation, reduces anxiety through 5-HT1A receptor activation, and rescues impaired 5-HT neurotransmission under neuropathic pain conditions.	Cannabidiol	42-45	5-hydroxytryptamine receptor 1A	Rattus norvegicus	128-134