PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
19909294-1	2010	BACKGROUND: Palmitoylethanolamide (PEA) is an anti-inflammatory mediator that enhances the activation by anandamide (AEA) of cannabinoid receptors and transient receptor potential vanilloid type-1 (TRPV1) channels, and directly activates peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	12-33	transient receptor potential cation channel subfamily V member 1	Homo sapiens	151-196
19833407-6	2010	The endogenous acylethanolamines, oleoylethanolamide and palmitoylethanolamide regulate feeding and body weight, stimulate fat utilization and have neuroprotective effects mediated through PPARalpha.	palmidrol	57-78	peroxisome proliferator activated receptor alpha	Homo sapiens	189-198
22125609-2	2011	These include the cannabinoid ligand anandamide (AEA) and the peroxisome proliferator-activated receptor-alpha ligand palmitoylethanolamide (PEA).	palmidrol	118-139	peroxisome proliferator activated receptor alpha	Homo sapiens	62-110
20353771-5	2010	PEA and OEA can activate several different receptors and inhibit some ion channels, e.g., PPARalpha, vanilloid receptor, K(+) channels (Kv4.3, Kv1.5), and OEA can activate GPR119 and inhibit ceramidases.	palmidrol	0-3	peroxisome proliferator activated receptor alpha	Rattus norvegicus	90-99
20353771-5	2010	PEA and OEA can activate several different receptors and inhibit some ion channels, e.g., PPARalpha, vanilloid receptor, K(+) channels (Kv4.3, Kv1.5), and OEA can activate GPR119 and inhibit ceramidases.	palmidrol	0-3	potassium voltage-gated channel subfamily D member 3	Rattus norvegicus	136-141
20353771-5	2010	PEA and OEA can activate several different receptors and inhibit some ion channels, e.g., PPARalpha, vanilloid receptor, K(+) channels (Kv4.3, Kv1.5), and OEA can activate GPR119 and inhibit ceramidases.	palmidrol	0-3	potassium voltage-gated channel subfamily A member 5	Rattus norvegicus	143-148
20353771-5	2010	PEA and OEA can activate several different receptors and inhibit some ion channels, e.g., PPARalpha, vanilloid receptor, K(+) channels (Kv4.3, Kv1.5), and OEA can activate GPR119 and inhibit ceramidases.	palmidrol	0-3	G protein-coupled receptor 119	Rattus norvegicus	172-178
20462810-1	2010	Endogenous ethanolamides (fatty acid amides), including arachidonyl ethanolamide (anandamide, AEA), oleoyl ethanolamide (OEA), and palmitoyl ethanolamide (PEA), are substrates of fatty acid amide hydrolase (FAAH).	palmidrol	131-153	fatty acid amide hydrolase	Homo sapiens	207-211
20462810-1	2010	Endogenous ethanolamides (fatty acid amides), including arachidonyl ethanolamide (anandamide, AEA), oleoyl ethanolamide (OEA), and palmitoyl ethanolamide (PEA), are substrates of fatty acid amide hydrolase (FAAH).	palmidrol	155-158	fatty acid amide hydrolase	Homo sapiens	207-211
19909294-1	2010	BACKGROUND: Palmitoylethanolamide (PEA) is an anti-inflammatory mediator that enhances the activation by anandamide (AEA) of cannabinoid receptors and transient receptor potential vanilloid type-1 (TRPV1) channels, and directly activates peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	12-33	transient receptor potential cation channel subfamily V member 1	Homo sapiens	198-203
19909294-1	2010	BACKGROUND: Palmitoylethanolamide (PEA) is an anti-inflammatory mediator that enhances the activation by anandamide (AEA) of cannabinoid receptors and transient receptor potential vanilloid type-1 (TRPV1) channels, and directly activates peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	12-33	peroxisome proliferator activated receptor alpha	Homo sapiens	238-286
19909294-1	2010	BACKGROUND: Palmitoylethanolamide (PEA) is an anti-inflammatory mediator that enhances the activation by anandamide (AEA) of cannabinoid receptors and transient receptor potential vanilloid type-1 (TRPV1) channels, and directly activates peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	12-33	peroxisome proliferator activated receptor alpha	Homo sapiens	288-298
19909294-1	2010	BACKGROUND: Palmitoylethanolamide (PEA) is an anti-inflammatory mediator that enhances the activation by anandamide (AEA) of cannabinoid receptors and transient receptor potential vanilloid type-1 (TRPV1) channels, and directly activates peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	35-38	transient receptor potential cation channel subfamily V member 1	Homo sapiens	151-196
19909294-1	2010	BACKGROUND: Palmitoylethanolamide (PEA) is an anti-inflammatory mediator that enhances the activation by anandamide (AEA) of cannabinoid receptors and transient receptor potential vanilloid type-1 (TRPV1) channels, and directly activates peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	35-38	transient receptor potential cation channel subfamily V member 1	Homo sapiens	198-203
19909294-1	2010	BACKGROUND: Palmitoylethanolamide (PEA) is an anti-inflammatory mediator that enhances the activation by anandamide (AEA) of cannabinoid receptors and transient receptor potential vanilloid type-1 (TRPV1) channels, and directly activates peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	35-38	peroxisome proliferator activated receptor alpha	Homo sapiens	238-286
19909294-1	2010	BACKGROUND: Palmitoylethanolamide (PEA) is an anti-inflammatory mediator that enhances the activation by anandamide (AEA) of cannabinoid receptors and transient receptor potential vanilloid type-1 (TRPV1) channels, and directly activates peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	35-38	peroxisome proliferator activated receptor alpha	Homo sapiens	288-298
19909294-9	2010	PEA (5-10 mg/kg, intraperitoneal) also inhibited DNFB-induced ear inflammation in mice in vivo, in a way attenuated by TRPV1 antagonism.	palmidrol	0-3	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	119-124
19403796-1	2009	Inhibitors of fatty acid amide hydrolase (FAAH) increase endogenous levels of anandamide (a cannabinoid CB(1)-receptor ligand) and oleoylethanolamide and palmitoylethanolamide (OEA and PEA, ligands for alpha-type peroxisome proliferator-activated nuclear receptors, PPAR-alpha) when and where they are naturally released in the brain.	palmidrol	154-175	fatty-acid amide hydrolase-like	Rattus norvegicus	14-40
20022504-1	2010	N-Acylethanolamines, including N-palmitoyl-ethanolamine (PEA), are hydrolyzed to the corresponding fatty acids and ethanolamine by fatty acid amide hydrolase (FAAH).	palmidrol	31-55	fatty acid amide hydrolase	Homo sapiens	159-163
20022504-1	2010	N-Acylethanolamines, including N-palmitoyl-ethanolamine (PEA), are hydrolyzed to the corresponding fatty acids and ethanolamine by fatty acid amide hydrolase (FAAH).	palmidrol	57-60	fatty acid amide hydrolase	Homo sapiens	159-163
19926788-4	2010	In homogenate activity assays, FAAH-2 hydrolyzed AEA and palmitoylethanolamide (PEA) with activities approximately 6 and approximately 20% those of FAAH, respectively.	palmidrol	57-78	fatty acid amide hydrolase 2	Homo sapiens	31-37
19926788-4	2010	In homogenate activity assays, FAAH-2 hydrolyzed AEA and palmitoylethanolamide (PEA) with activities approximately 6 and approximately 20% those of FAAH, respectively.	palmidrol	57-78	fatty acid amide hydrolase	Homo sapiens	31-35
19926788-4	2010	In homogenate activity assays, FAAH-2 hydrolyzed AEA and palmitoylethanolamide (PEA) with activities approximately 6 and approximately 20% those of FAAH, respectively.	palmidrol	80-83	fatty acid amide hydrolase 2	Homo sapiens	31-37
19926788-4	2010	In homogenate activity assays, FAAH-2 hydrolyzed AEA and palmitoylethanolamide (PEA) with activities approximately 6 and approximately 20% those of FAAH, respectively.	palmidrol	80-83	fatty acid amide hydrolase	Homo sapiens	31-35
19625089-0	2010	Effects of palmitoylethanolamide on immunologically induced histamine, PGD2 and TNFalpha release from canine skin mast cells.	palmidrol	11-32	tumor necrosis factor	Canis lupus familiaris	80-88
19625089-8	2010	Finally, PEA inhibited TNFalpha release to 29.2+/-2.0% and 22.1+/-7.2%, at concentrations of 10(-5)M and 3x10(-6)M, respectively.	palmidrol	9-12	tumor necrosis factor	Canis lupus familiaris	23-31
19926854-0	2009	Selective N-acylethanolamine-hydrolyzing acid amidase inhibition reveals a key role for endogenous palmitoylethanolamide in inflammation.	palmidrol	99-120	N-acylethanolamine acid amidase	Mus musculus	10-53
19926854-2	2009	Palmitoylethanolamide (PEA) is a naturally occurring lipid amide that, when administered as a drug, inhibits inflammatory responses by engaging peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Mus musculus	144-192
19926854-2	2009	Palmitoylethanolamide (PEA) is a naturally occurring lipid amide that, when administered as a drug, inhibits inflammatory responses by engaging peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Mus musculus	194-204
19926854-2	2009	Palmitoylethanolamide (PEA) is a naturally occurring lipid amide that, when administered as a drug, inhibits inflammatory responses by engaging peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	23-26	peroxisome proliferator activated receptor alpha	Mus musculus	144-192
19926854-2	2009	Palmitoylethanolamide (PEA) is a naturally occurring lipid amide that, when administered as a drug, inhibits inflammatory responses by engaging peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	23-26	peroxisome proliferator activated receptor alpha	Mus musculus	194-204
19716430-1	2009	Fatty acid amide hydrolase (FAAH) is responsible for the hydrolysis of several important endogenous fatty acid amides (FAAs), including anandamide, oleoylethanolamide and palmitoylethanolamide.	palmidrol	171-192	fatty acid amide hydrolase	Homo sapiens	28-32
19386271-0	2009	Central administration of palmitoylethanolamide reduces hyperalgesia in mice via inhibition of NF-kappaB nuclear signalling in dorsal root ganglia.	palmidrol	26-47	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	95-104
19386271-2	2009	Palmitoylethanolamide (PEA), a member of the fatty-acid ethanolamide family, acts peripherally as an endogenous PPAR-alpha agonist, exerting analgesic and anti-inflammatory effects.	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Mus musculus	112-122
19386271-2	2009	Palmitoylethanolamide (PEA), a member of the fatty-acid ethanolamide family, acts peripherally as an endogenous PPAR-alpha agonist, exerting analgesic and anti-inflammatory effects.	palmidrol	23-26	peroxisome proliferator activated receptor alpha	Mus musculus	112-122
19931394-9	2010	Pharmacological elevation of endocannabinoids and palmitoylethanolamide, obtained separately by arachidonoylserotonin and exogenous palmitoylethanolamide treatment, dose-dependently reduced inflammatory hallmarks including tumor necrosis factor-alpha as well as granuloma-dependent angiogenesis.	palmidrol	50-71	tumor necrosis factor	Rattus norvegicus	223-250
19521349-1	2010	N-oleoylethanolamine (OEA) and N-palmitoylethanolamine (PEA) are endogenous lipids that activate peroxisome proliferator-activated receptor-alpha with high and intermediate potency, and exert anorectic and anti-inflammatory actions in rats, respectively.	palmidrol	31-54	peroxisome proliferator activated receptor alpha	Rattus norvegicus	97-145
19521349-1	2010	N-oleoylethanolamine (OEA) and N-palmitoylethanolamine (PEA) are endogenous lipids that activate peroxisome proliferator-activated receptor-alpha with high and intermediate potency, and exert anorectic and anti-inflammatory actions in rats, respectively.	palmidrol	56-59	peroxisome proliferator activated receptor alpha	Rattus norvegicus	97-145
19289116-12	2009	The facilitative action of palmitoylethanolamide affects the vanilloid TRPV1 as well as the cannabinoid CB(1) receptor-mediated effects of endocannabinoids on the blood pressure control.	palmidrol	27-48	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	71-76
19403796-1	2009	Inhibitors of fatty acid amide hydrolase (FAAH) increase endogenous levels of anandamide (a cannabinoid CB(1)-receptor ligand) and oleoylethanolamide and palmitoylethanolamide (OEA and PEA, ligands for alpha-type peroxisome proliferator-activated nuclear receptors, PPAR-alpha) when and where they are naturally released in the brain.	palmidrol	154-175	fatty-acid amide hydrolase-like	Rattus norvegicus	42-46
18289091-5	2008	FAAH inhibitors can be divided in two major groups, the first one includes the inhibitors inspired by the chemical structures of FAAH substrates, which carry an arachidonoyl-, oleoyl- or palmitoyl-carbon chain that mimic the fatty acid chains of anandamide, oleamide and palmitoylethanolamide.	palmidrol	271-292	fatty acid amide hydrolase	Homo sapiens	0-4
18695637-0	2008	"Entourage" effects of N-palmitoylethanolamide and N-oleoylethanolamide on vasorelaxation to anandamide occur through TRPV1 receptors.	palmidrol	23-46	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	118-123
18695637-5	2008	The potentiation by PEA and OEA was endothelium-independent and abolished by treatment with capsaicin (10 microM), which desensitizes the transient receptor potential vanilloid type 1 (TRPV1) receptor system, or by the TRPV1 receptor antagonist, N-(3-methoxyphenyl)-4-chlorocinnamide (SB366791) (2 microM).	palmidrol	20-23	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	138-183
18695637-5	2008	The potentiation by PEA and OEA was endothelium-independent and abolished by treatment with capsaicin (10 microM), which desensitizes the transient receptor potential vanilloid type 1 (TRPV1) receptor system, or by the TRPV1 receptor antagonist, N-(3-methoxyphenyl)-4-chlorocinnamide (SB366791) (2 microM).	palmidrol	20-23	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	185-190
18695637-5	2008	The potentiation by PEA and OEA was endothelium-independent and abolished by treatment with capsaicin (10 microM), which desensitizes the transient receptor potential vanilloid type 1 (TRPV1) receptor system, or by the TRPV1 receptor antagonist, N-(3-methoxyphenyl)-4-chlorocinnamide (SB366791) (2 microM).	palmidrol	20-23	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	219-224
18695637-10	2008	CONCLUSION AND IMPLICATIONS: This study shows that PEA and OEA potentiate relaxant responses to anandamide through TRPV1 receptors in rat small mesenteric arteries.	palmidrol	51-54	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	115-120
18545985-6	2008	The FAAH inhibitor URB597 inhibited FAAH activity (IC50 = 12.8 nM) and elevated levels of fatty-acid amides (N-palmitoyl ethanolamine and N-oleoyl ethanolamine) in hamster brain.	palmidrol	109-133	fatty-acid amide hydrolase 1	Mesocricetus auratus	4-8
18524639-8	2008	The amnesic effect of WIN-55,212-2 and VDM-11 was not due to state-dependency and was completely reversed by co-infusion of the CB1 receptor antagonist AM-251 and mimicked by the CB1 receptor agonist ACEA but not by the CB2 receptor agonists JWH-015 and palmitoylethanolamide.	palmidrol	254-275	cannabinoid receptor 1	Rattus norvegicus	128-131
18367664-2	2008	Palmitoylethanolamide (PEA), the naturally occurring amide of palmitic acid and ethanolamine, reduces pain and inflammation through a mechanism dependent on PPAR-alpha activation.	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Mus musculus	157-167
18367664-2	2008	Palmitoylethanolamide (PEA), the naturally occurring amide of palmitic acid and ethanolamine, reduces pain and inflammation through a mechanism dependent on PPAR-alpha activation.	palmidrol	23-26	peroxisome proliferator activated receptor alpha	Mus musculus	157-167
19131941-11	2009	In view of its virtual lack of toxicity, PEA might become a potentially interesting candidate molecule in the prevention of obesity-associated insulin resistance.	palmidrol	41-44	insulin	Homo sapiens	143-150
18793752-1	2008	N-Acylethanolamine-hydrolyzing acid amidase (NAAA) is a lysosomal enzyme which hydrolyzes bioactive N-acylethanolamines, including anandamide and N-palmitoylethanolamine.	palmidrol	146-169	N-acylethanolamine acid amidase	Homo sapiens	0-43
18793752-1	2008	N-Acylethanolamine-hydrolyzing acid amidase (NAAA) is a lysosomal enzyme which hydrolyzes bioactive N-acylethanolamines, including anandamide and N-palmitoylethanolamine.	palmidrol	146-169	N-acylethanolamine acid amidase	Homo sapiens	45-49
18602217-0	2008	The endogenous fatty acid amide, palmitoylethanolamide, has anti-allodynic and anti-hyperalgesic effects in a murine model of neuropathic pain: involvement of CB(1), TRPV1 and PPARgamma receptors and neurotrophic factors.	palmidrol	33-54	cannabinoid receptor 1 (brain)	Mus musculus	159-164
18602217-0	2008	The endogenous fatty acid amide, palmitoylethanolamide, has anti-allodynic and anti-hyperalgesic effects in a murine model of neuropathic pain: involvement of CB(1), TRPV1 and PPARgamma receptors and neurotrophic factors.	palmidrol	33-54	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	166-171
18602217-0	2008	The endogenous fatty acid amide, palmitoylethanolamide, has anti-allodynic and anti-hyperalgesic effects in a murine model of neuropathic pain: involvement of CB(1), TRPV1 and PPARgamma receptors and neurotrophic factors.	palmidrol	33-54	peroxisome proliferator activated receptor gamma	Mus musculus	176-185
18289091-5	2008	FAAH inhibitors can be divided in two major groups, the first one includes the inhibitors inspired by the chemical structures of FAAH substrates, which carry an arachidonoyl-, oleoyl- or palmitoyl-carbon chain that mimic the fatty acid chains of anandamide, oleamide and palmitoylethanolamide.	palmidrol	271-292	fatty acid amide hydrolase	Homo sapiens	129-133
17675189-2	2008	On the other hand, genetic deletion of fatty acid amide hydrolase (FAAH), the enzyme responsible for degradation of fatty acid amides, including endogenous cannabinoid N-arachidonoyl ethanolamine (anandamide; AEA), N-palmitoyl ethanolamine (PEA), N-oleoyl ethanolamine (OEA), and oleamide, also elicits anti-edema, but does not produce any apparent cannabinoid effects.	palmidrol	215-239	fatty acid amide hydrolase	Mus musculus	50-65
17675189-2	2008	On the other hand, genetic deletion of fatty acid amide hydrolase (FAAH), the enzyme responsible for degradation of fatty acid amides, including endogenous cannabinoid N-arachidonoyl ethanolamine (anandamide; AEA), N-palmitoyl ethanolamine (PEA), N-oleoyl ethanolamine (OEA), and oleamide, also elicits anti-edema, but does not produce any apparent cannabinoid effects.	palmidrol	215-239	fatty acid amide hydrolase	Mus musculus	67-71
17675189-2	2008	On the other hand, genetic deletion of fatty acid amide hydrolase (FAAH), the enzyme responsible for degradation of fatty acid amides, including endogenous cannabinoid N-arachidonoyl ethanolamine (anandamide; AEA), N-palmitoyl ethanolamine (PEA), N-oleoyl ethanolamine (OEA), and oleamide, also elicits anti-edema, but does not produce any apparent cannabinoid effects.	palmidrol	241-244	fatty acid amide hydrolase	Mus musculus	50-65
17675189-2	2008	On the other hand, genetic deletion of fatty acid amide hydrolase (FAAH), the enzyme responsible for degradation of fatty acid amides, including endogenous cannabinoid N-arachidonoyl ethanolamine (anandamide; AEA), N-palmitoyl ethanolamine (PEA), N-oleoyl ethanolamine (OEA), and oleamide, also elicits anti-edema, but does not produce any apparent cannabinoid effects.	palmidrol	241-244	fatty acid amide hydrolase	Mus musculus	67-71
17565008-0	2007	Acute intracerebroventricular administration of palmitoylethanolamide, an endogenous peroxisome proliferator-activated receptor-alpha agonist, modulates carrageenan-induced paw edema in mice.	palmidrol	48-69	peroxisome proliferator activated receptor alpha	Mus musculus	85-133
17980170-1	2007	N-acylethanolamine-hydrolyzing acid amidase (NAAA) is a lysosomal enzyme hydrolyzing bioactive N-acylethanolamines, including anandamide and N-palmitoylethanolamine.	palmidrol	141-164	N-acylethanolamine acid amidase	Homo sapiens	0-43
17980170-1	2007	N-acylethanolamine-hydrolyzing acid amidase (NAAA) is a lysosomal enzyme hydrolyzing bioactive N-acylethanolamines, including anandamide and N-palmitoylethanolamine.	palmidrol	141-164	N-acylethanolamine acid amidase	Homo sapiens	45-49
17876300-6	2007	They also compared the distribution of GPR55 and CB1 mRNA in mouse and report that GPR55 couples to Galpha13, that it is activated by virodhamine, palmitoylethanolamide and oleoylethanolamide, and that virodhamine displays relatively high efficacy as a GPR55 agonist.	palmidrol	147-168	cannabinoid receptor 1 (brain)	Mus musculus	49-52
17876300-6	2007	They also compared the distribution of GPR55 and CB1 mRNA in mouse and report that GPR55 couples to Galpha13, that it is activated by virodhamine, palmitoylethanolamide and oleoylethanolamide, and that virodhamine displays relatively high efficacy as a GPR55 agonist.	palmidrol	147-168	G protein-coupled receptor 55	Mus musculus	83-88
17876300-6	2007	They also compared the distribution of GPR55 and CB1 mRNA in mouse and report that GPR55 couples to Galpha13, that it is activated by virodhamine, palmitoylethanolamide and oleoylethanolamide, and that virodhamine displays relatively high efficacy as a GPR55 agonist.	palmidrol	147-168	G protein-coupled receptor 55	Mus musculus	83-88
17704824-5	2007	Similarly, palmitoylethanolamide regulates feeding and lipid metabolism and has anti-inflammatory properties mediated by PPAR alpha.	palmidrol	11-32	peroxisome proliferator activated receptor alpha	Homo sapiens	121-131
17565008-3	2007	Palmitoylethanolamide (PEA), a member of the fatty-acid ethanolamide family, acts peripherally as an endogenous PPAR-alpha ligand, exerting analgesic and anti-inflammatory effects.	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Mus musculus	112-122
17565008-3	2007	Palmitoylethanolamide (PEA), a member of the fatty-acid ethanolamide family, acts peripherally as an endogenous PPAR-alpha ligand, exerting analgesic and anti-inflammatory effects.	palmidrol	23-26	peroxisome proliferator activated receptor alpha	Mus musculus	112-122
17558434-0	2007	The effect of the palmitoylethanolamide analogue, palmitoylallylamide (L-29) on pain behaviour in rodent models of neuropathy.	palmidrol	18-39	ribosomal protein L29	Homo sapiens	71-75
17558434-3	2007	Here, we investigate the analgesic effect of the palmitoylethanolamide (PEA) analogue, palmitoylallylamide (L-29), which via inhibition of fatty acid amide hydrolase (FAAH) may potentiate endocannabinoids thereby avoiding psychotropic side effects.	palmidrol	49-70	ribosomal protein L29	Homo sapiens	108-112
17558434-3	2007	Here, we investigate the analgesic effect of the palmitoylethanolamide (PEA) analogue, palmitoylallylamide (L-29), which via inhibition of fatty acid amide hydrolase (FAAH) may potentiate endocannabinoids thereby avoiding psychotropic side effects.	palmidrol	49-70	fatty acid amide hydrolase	Homo sapiens	167-171
17558434-3	2007	Here, we investigate the analgesic effect of the palmitoylethanolamide (PEA) analogue, palmitoylallylamide (L-29), which via inhibition of fatty acid amide hydrolase (FAAH) may potentiate endocannabinoids thereby avoiding psychotropic side effects.	palmidrol	72-75	ribosomal protein L29	Homo sapiens	108-112
17558434-3	2007	Here, we investigate the analgesic effect of the palmitoylethanolamide (PEA) analogue, palmitoylallylamide (L-29), which via inhibition of fatty acid amide hydrolase (FAAH) may potentiate endocannabinoids thereby avoiding psychotropic side effects.	palmidrol	72-75	fatty acid amide hydrolase	Homo sapiens	167-171
17068202-1	2007	The endolipid N-palmitoylethanolamine (PEA) shows a pleiotropic pattern of bioactivities, whose mechanistic characterization is still unclear and whose pharmacological potential is substantially limited by rapid metabolization by the amido hydrolyzing enzymes fatty acid amide hydrolases and N-acylethanolamine-hydrolyzing acid amidase.	palmidrol	14-37	N-acylethanolamine acid amidase	Homo sapiens	292-335
17712833-1	2007	Bioactive N-acylethanolamines, including the endocannabinoid anandamide and anti-inflammatory N-palmitoylethanolamine, are hydrolyzed to fatty acids and ethanolamine in animal tissues by the catalysis of fatty acid amide hydrolase (FAAH).	palmidrol	94-117	fatty-acid amide hydrolase-like	Rattus norvegicus	232-236
17336288-2	2007	The hydrolysis of this lipid involves the activity of the fatty acid amide hydrolase (FAAH), which additionally catalyzes the degradation of the satiety factor oleoylethanolamide and the analgesic-inducing lipid palmitoylethanolamide.	palmidrol	212-233	fatty-acid amide hydrolase-like	Rattus norvegicus	86-90
17336288-3	2007	It has been demonstrated that the inhibition of the FAAH by URB597 increases levels of anandamide, oleoylethanolamide and palmitoylethanolamide in the brain of rats.	palmidrol	122-143	fatty-acid amide hydrolase-like	Rattus norvegicus	52-56
17336288-8	2007	We additionally found out that, compared to controls, c-Fos immunoreactivity in hypothalamus and dorsal raphe nucleus was increased in rats that received URB597, oleoylethanolamide or palmitoylethanolamide (10, 20 microg/5 microl, i.c.v.).	palmidrol	184-205	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
17336288-13	2007	Our results suggest that FAAH activity as well as two molecules that are catalyzed by this enzyme, oleoylethanolamide and palmitoylethanolamide, participate in the regulation of the waking state.	palmidrol	122-143	fatty-acid amide hydrolase-like	Rattus norvegicus	25-29
17068202-1	2007	The endolipid N-palmitoylethanolamine (PEA) shows a pleiotropic pattern of bioactivities, whose mechanistic characterization is still unclear and whose pharmacological potential is substantially limited by rapid metabolization by the amido hydrolyzing enzymes fatty acid amide hydrolases and N-acylethanolamine-hydrolyzing acid amidase.	palmidrol	39-42	N-acylethanolamine acid amidase	Homo sapiens	292-335
16143133-1	2005	BACKGROUND & AIMS: Fatty acid amide hydrolase (FAAH) catalyzes the hydrolysis both of the endocannabinoids (which are known to inhibit intestinal motility) and other bioactive amides (palmitoylethanolamide, oleamide, and oleoylethanolamide), which might affect intestinal motility.	palmidrol	188-209	fatty acid amide hydrolase	Mus musculus	23-49
16866345-2	2006	Most of the physiological substrates of FAAH characterized to date belong to the N-acyl ethanolamine (NAE) class of fatty acid amides, including the endocannabinoid anandamide, the anti-inflammatory lipid N-palmitoyl ethanolamine, and the satiating factor N-oleoyl ethanolamine.	palmidrol	205-229	fatty acid amide hydrolase	Mus musculus	40-44
16760367-1	2006	Fatty acid amide hydrolase (FAAH) is a membrane-associated enzyme that catalyzes the hydrolysis of several endogenous bioactive lipids, including anandamide (AEA), N-palmitoylethanolamine (PEA), oleamide, and N-oleoylethanolamine (OEA).	palmidrol	164-187	fatty acid amide hydrolase	Homo sapiens	0-26
16760367-1	2006	Fatty acid amide hydrolase (FAAH) is a membrane-associated enzyme that catalyzes the hydrolysis of several endogenous bioactive lipids, including anandamide (AEA), N-palmitoylethanolamine (PEA), oleamide, and N-oleoylethanolamine (OEA).	palmidrol	164-187	fatty acid amide hydrolase	Homo sapiens	28-32
16760367-1	2006	Fatty acid amide hydrolase (FAAH) is a membrane-associated enzyme that catalyzes the hydrolysis of several endogenous bioactive lipids, including anandamide (AEA), N-palmitoylethanolamine (PEA), oleamide, and N-oleoylethanolamine (OEA).	palmidrol	189-192	fatty acid amide hydrolase	Homo sapiens	0-26
16760367-1	2006	Fatty acid amide hydrolase (FAAH) is a membrane-associated enzyme that catalyzes the hydrolysis of several endogenous bioactive lipids, including anandamide (AEA), N-palmitoylethanolamine (PEA), oleamide, and N-oleoylethanolamine (OEA).	palmidrol	189-192	fatty acid amide hydrolase	Homo sapiens	28-32
16143133-1	2005	BACKGROUND & AIMS: Fatty acid amide hydrolase (FAAH) catalyzes the hydrolysis both of the endocannabinoids (which are known to inhibit intestinal motility) and other bioactive amides (palmitoylethanolamide, oleamide, and oleoylethanolamide), which might affect intestinal motility.	palmidrol	188-209	fatty acid amide hydrolase	Mus musculus	51-55
16143133-5	2005	RESULTS: Motility was inhibited by N-arachidonoylserotonin (AA-5-HT) and palmitoylisopropylamide, 2 selective FAAH inhibitors, as well as by the FAAH substrates palmitoylethanolamide, oleamide, and oleoylethanolamide.	palmidrol	161-182	fatty acid amide hydrolase	Mus musculus	145-149
14998370-0	2004	Biosynthesis of anandamide and N-palmitoylethanolamine by sequential actions of phospholipase A2 and lysophospholipase D.	palmidrol	31-54	phospholipase A2 group IB	Rattus norvegicus	80-96
15655246-8	2005	The recombinant human NAAA overexpressed in HEK293 cells hydrolyzed various N-acylethanolamines with N-palmitoylethanolamine as the most reactive substrate.	palmidrol	101-124	N-acylethanolamine acid amidase	Homo sapiens	22-26
14998370-7	2004	In addition, we found wide distribution of lysoPLD activity generating N-palmitoylethanolamine from N-palmitoyl-lysoPE in rat tissues, with higher activities in the brain and testis.	palmidrol	71-94	ectonucleotide pyrophosphatase/phosphodiesterase 2	Rattus norvegicus	43-50
14998370-0	2004	Biosynthesis of anandamide and N-palmitoylethanolamine by sequential actions of phospholipase A2 and lysophospholipase D.	palmidrol	31-54	ectonucleotide pyrophosphatase/phosphodiesterase 2	Rattus norvegicus	101-120
14998370-9	2004	sPLA2-IB dose dependently enhanced the production of N-palmitoylethanolamine from N-palmitoyl-PE in the brain homogenate showing the lysoPLD activity.	palmidrol	53-76	phospholipase A2 group IIA	Rattus norvegicus	0-5
14998370-9	2004	sPLA2-IB dose dependently enhanced the production of N-palmitoylethanolamine from N-palmitoyl-PE in the brain homogenate showing the lysoPLD activity.	palmidrol	53-76	ectonucleotide pyrophosphatase/phosphodiesterase 2	Rattus norvegicus	133-140
14652680-8	2003	The effect of cigarette smoke solution from IR5F cigarettes upon the beta-hexosaminidase release elicited by compound 48/80 (in quercetin-treated cells) and by concanavalin A (in cells cultured on fibronectin-coated wells) could be prevented by N-acetyl-L-cysteine, but not with either hemoglobin, alpha-tocopherol, catalase or palmitoylethanolamide.	palmidrol	328-349	O-GlcNAcase	Rattus norvegicus	69-88
14561475-3	2003	In this study, a binary phase diagram of hydrated mixtures of N-palmitoylethanolamine (NP-E)--an endogenous ligand for the peripheral cannabinoid receptor (CB-2)--with dipalmitoylphosphatidylcholine (DPPC) is established by high-sensitivity differential scanning calorimetry (DSC).	palmidrol	62-85	cannabinoid receptor 2	Homo sapiens	156-160
12941436-2	2003	In the present study we examined the effects of AEA and the naturally occurring cannabinoid 2 (CB(2)) receptor agonist palmitylethanolamide (PEA) on basal and resiniferatoxin (RTX)-induced release of calcitonin gene-related peptide (CGRP) and somatostatin in vivo.	palmidrol	119-139	calcitonin-related polypeptide alpha	Rattus norvegicus	200-231
12031775-7	2002	Furthermore, anandamide (25 mg/kg) and PEA (2.5 mg/kg) reduced intra-vesical NGF-evoked spinal cord Fos expression at the appropriate level (L6) by 35 and 43%, respectively.	palmidrol	39-42	nerve growth factor	Homo sapiens	77-80
12672243-3	2003	In the present study, we have investigated whether substitution of the headgroup of the endogenous alternative FAAH substrate palmitoylethanolamide (PEA) can result in the identification of novel compounds preventing AEA metabolism.	palmidrol	126-147	fatty-acid amide hydrolase 1	Cricetulus griseus	111-115
12672243-3	2003	In the present study, we have investigated whether substitution of the headgroup of the endogenous alternative FAAH substrate palmitoylethanolamide (PEA) can result in the identification of novel compounds preventing AEA metabolism.	palmidrol	149-152	fatty-acid amide hydrolase 1	Cricetulus griseus	111-115
12023948-19	2002	It is concluded that although palmitoylethanolamide has entourage-like effects at VR1 receptors expressed on hVR1-HEK293 cells, other N-acyl ethanolamines have even more dramatic potentiating effects.	palmidrol	30-51	transient receptor potential cation channel subfamily V member 1	Homo sapiens	82-85
12023948-19	2002	It is concluded that although palmitoylethanolamide has entourage-like effects at VR1 receptors expressed on hVR1-HEK293 cells, other N-acyl ethanolamines have even more dramatic potentiating effects.	palmidrol	30-51	transient receptor potential cation channel subfamily V member 1	Homo sapiens	109-113
12773040-1	2003	Fatty acid amide hydrolase (FAAH), an intracellular serine hydrolase enzyme, participates in the deactivation of fatty acid ethanolamides such as the endogenous cannabinoid anandamide, the intestinal satiety factor oleoylethanolamide, and the peripheral analgesic and anti-inflammatory factor palmitoylethanolamide.	palmidrol	293-314	fatty-acid amide hydrolase-like	Rattus norvegicus	28-32
12031775-7	2002	Furthermore, anandamide (25 mg/kg) and PEA (2.5 mg/kg) reduced intra-vesical NGF-evoked spinal cord Fos expression at the appropriate level (L6) by 35 and 43%, respectively.	palmidrol	39-42	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	100-103
11602256-0	2001	Palmitoylethanolamide enhances anandamide stimulation of human vanilloid VR1 receptors.	palmidrol	0-21	transient receptor potential cation channel subfamily V member 1	Homo sapiens	73-76
11602256-1	2001	In human embryonic kidney cells over-expressing the human vanilloid receptor type 1 (VR1), palmitoylethanolamide (PEA, 0.5-10 microM) enhanced the effect of arachidonoylethanolamide (AEA, 50 nM) on the VR1-mediated increase of the intracellular Ca2+ concentration.	palmidrol	91-112	transient receptor potential cation channel subfamily V member 1	Homo sapiens	58-88
11602256-1	2001	In human embryonic kidney cells over-expressing the human vanilloid receptor type 1 (VR1), palmitoylethanolamide (PEA, 0.5-10 microM) enhanced the effect of arachidonoylethanolamide (AEA, 50 nM) on the VR1-mediated increase of the intracellular Ca2+ concentration.	palmidrol	91-112	transient receptor potential cation channel subfamily V member 1	Homo sapiens	85-88
11602256-1	2001	In human embryonic kidney cells over-expressing the human vanilloid receptor type 1 (VR1), palmitoylethanolamide (PEA, 0.5-10 microM) enhanced the effect of arachidonoylethanolamide (AEA, 50 nM) on the VR1-mediated increase of the intracellular Ca2+ concentration.	palmidrol	114-117	transient receptor potential cation channel subfamily V member 1	Homo sapiens	58-88
11602256-1	2001	In human embryonic kidney cells over-expressing the human vanilloid receptor type 1 (VR1), palmitoylethanolamide (PEA, 0.5-10 microM) enhanced the effect of arachidonoylethanolamide (AEA, 50 nM) on the VR1-mediated increase of the intracellular Ca2+ concentration.	palmidrol	114-117	transient receptor potential cation channel subfamily V member 1	Homo sapiens	85-88
11585048-1	2001	Fatty acid amide hydrolase (FAAH) is responsible for the hydrolysis of a number of important endogenous fatty acid amides, including the endogenous cannabimimetic agent anandamide (AEA), the sleep-inducing compound oleamide, and the putative anti-inflammatory agent palmitoylethanolamide (PEA).	palmidrol	266-287	fatty acid amide hydrolase	Homo sapiens	28-32
11606334-7	2001	Palmitoylethanolamide, a selective CB(2) receptor agonist, did not relax precontracted coronary arteries.	palmidrol	0-21	cannabinoid receptor 2	Rattus norvegicus	35-49
11309246-1	2001	The endogenous cannabinoid receptor agonist anandamide (AEA) and the related compound palmitoylethanolamide (PEA) are inactivated by transport into cells followed by metabolism by fatty acid amide hydrolase (FAAH).	palmidrol	86-107	fatty-acid amide hydrolase-like	Rattus norvegicus	208-212
11485574-0	2001	Palmitoylethanolamide inhibits the expression of fatty acid amide hydrolase and enhances the anti-proliferative effect of anandamide in human breast cancer cells.	palmidrol	0-21	fatty acid amide hydrolase	Homo sapiens	49-75
11485574-1	2001	Palmitoylethanolamide (PEA) has been shown to act in synergy with anandamide (arachidonoylethanolamide; AEA), an endogenous agonist of cannabinoid receptor type 1 (CB(1)).	palmidrol	0-21	cannabinoid receptor 1	Homo sapiens	135-169
11485574-1	2001	Palmitoylethanolamide (PEA) has been shown to act in synergy with anandamide (arachidonoylethanolamide; AEA), an endogenous agonist of cannabinoid receptor type 1 (CB(1)).	palmidrol	23-26	cannabinoid receptor 1	Homo sapiens	135-169
11485041-2	2001	In the present study, we have reinvestigated the effects of palmitoylethanolamide upon antigen-induced release of [3H]serotonin and beta-hexosaminidase from rat basophilic leukemia RBL-2H3 cells and compared these effects with those of 2-arachidonoylglycerol, anandamide and R1-methanandamide.	palmidrol	60-81	O-GlcNAcase	Rattus norvegicus	132-151
11485041-2	2001	In the present study, we have reinvestigated the effects of palmitoylethanolamide upon antigen-induced release of [3H]serotonin and beta-hexosaminidase from rat basophilic leukemia RBL-2H3 cells and compared these effects with those of 2-arachidonoylglycerol, anandamide and R1-methanandamide.	palmidrol	60-81	RB transcriptional corepressor like 2	Rattus norvegicus	181-186
11498512-2	2001	The ability of a series of homologues and analogues of palmitoylethanolamide to inhibit the uptake and fatty acid amidohydrolase (FAAH)-catalysed hydrolysis of [(3)H]-anandamide ([(3)H]-AEA) has been investigated.	palmidrol	55-76	fatty acid amide hydrolase	Homo sapiens	103-128
11498512-2	2001	The ability of a series of homologues and analogues of palmitoylethanolamide to inhibit the uptake and fatty acid amidohydrolase (FAAH)-catalysed hydrolysis of [(3)H]-anandamide ([(3)H]-AEA) has been investigated.	palmidrol	55-76	fatty acid amide hydrolase	Homo sapiens	130-134
11309246-1	2001	The endogenous cannabinoid receptor agonist anandamide (AEA) and the related compound palmitoylethanolamide (PEA) are inactivated by transport into cells followed by metabolism by fatty acid amide hydrolase (FAAH).	palmidrol	109-112	fatty-acid amide hydrolase-like	Rattus norvegicus	208-212
10614630-3	2000	Beta-NGF-induced HBCC proliferation was potently inhibited (IC50 = 50-600 nM) by the synthetic cannabinoid HU-210, 2-AG, anandamide, and its metabolically stable analogs, but not by the anandamide congener, palmitoylethanolamide, or the selective agonist of CB2 cannabinoid receptors, BML-190.	palmidrol	207-228	nerve growth factor	Homo sapiens	0-8
11374613-12	2001	CONCLUSIONS: Anandamide (via CB1 receptors) and palmitoylethanolamide (putatively via CB2 receptors) attenuated a referred hyperalgesia in a dose-dependent fashion.	palmidrol	48-69	cannabinoid receptor 2	Rattus norvegicus	86-89
10677581-1	2000	In the present study, the pharmacological properties of fatty acid amide hydrolase (FAAH) in subcellular fractions of rat brain were investigated using palmitoylethanolamide (PEA) and arachidonyl ethanolamide (anandamide, AEA) as substrates.	palmidrol	152-173	fatty-acid amide hydrolase-like	Rattus norvegicus	56-82
10677581-1	2000	In the present study, the pharmacological properties of fatty acid amide hydrolase (FAAH) in subcellular fractions of rat brain were investigated using palmitoylethanolamide (PEA) and arachidonyl ethanolamide (anandamide, AEA) as substrates.	palmidrol	152-173	fatty-acid amide hydrolase-like	Rattus norvegicus	84-88
10677581-1	2000	In the present study, the pharmacological properties of fatty acid amide hydrolase (FAAH) in subcellular fractions of rat brain were investigated using palmitoylethanolamide (PEA) and arachidonyl ethanolamide (anandamide, AEA) as substrates.	palmidrol	175-178	fatty-acid amide hydrolase-like	Rattus norvegicus	56-82
10677581-1	2000	In the present study, the pharmacological properties of fatty acid amide hydrolase (FAAH) in subcellular fractions of rat brain were investigated using palmitoylethanolamide (PEA) and arachidonyl ethanolamide (anandamide, AEA) as substrates.	palmidrol	175-178	fatty-acid amide hydrolase-like	Rattus norvegicus	84-88
10692582-3	2000	FAAH (K(m)=5.0+/-0.5 microM, V(max)=160+/-15 pmol min(-1) mg protein(-1)) was competitively inhibited by palmitoylethanolamide.	palmidrol	105-126	fatty acid amide hydrolase	Homo sapiens	0-4
9774165-1	1998	Anandamide, an endogenous ligand at the CB1 cannabinoid receptor and palmitoylethanolamide (a putative endogenous ligand at the CB2 receptor) have both been shown to possess anti-hyperalgesic properties in models of somatic and visceral inflammation.	palmidrol	69-90	cannabinoid receptor 2	Rattus norvegicus	128-131
10431820-8	1999	Furthermore, the enzyme of CMK cells was much less sensitive to phenylmethylsulfonyl fluoride and methyl arachidonoyl fluorophosphonate potently inhibiting anandamide amidohydrolase, and effectively hydrolyzed palmitoylethanolamide, which was a poor substrate for anandamide amidohydrolase.	palmidrol	210-231	C-X-C motif chemokine ligand 9	Homo sapiens	27-30
10469888-4	1999	The capability of palmitoylethanolamide, an anti-inflammatory metabolite, to activate CB2-like receptors is still being debated.	palmidrol	18-39	cannabinoid receptor 2	Homo sapiens	86-89
9563506-3	1998	Comparison with other fatty acid cannabinoid ligands such as (R)-methanandamide, a ligand with improved selectivity for the CB1 receptor, or palmitylethanolamide, an endogenous ligand for the CB2 receptor, showed a very similar effect, suggesting that cell growth enhancement by anandamide or its analogs could be mediated through either receptor subtype.	palmidrol	141-161	cannabinoid receptor 2 (macrophage)	Mus musculus	192-195
9685157-3	1998	Palmitylethanolamide (PEA), which is released together with anandamide from a common phospholipid precursor, exerts a similar effect by activating peripheral CB2-like receptors.	palmidrol	0-20	cannabinoid receptor 2	Homo sapiens	158-161
9685157-3	1998	Palmitylethanolamide (PEA), which is released together with anandamide from a common phospholipid precursor, exerts a similar effect by activating peripheral CB2-like receptors.	palmidrol	22-25	cannabinoid receptor 2	Homo sapiens	158-161
9696473-2	1998	(1) The therapeutic effects of the cannabinoid anandamide and the putative CB2 agonist palmitoylethanolamide were tested in a model of persistent visceral pain (turpentine inflammation of the urinary bladder).	palmidrol	87-108	cannabinoid receptor 2	Rattus norvegicus	75-78
9696473-8	1998	The anti-nociceptive effect of the putative CB2 receptor agonist, palmitoylethanolamide, is particularly interesting since it is believed to be a peripherally mediated effect.	palmidrol	66-87	cannabinoid receptor 2	Rattus norvegicus	44-47
9696473-0	1998	The anti-hyperalgesic actions of the cannabinoid anandamide and the putative CB2 receptor agonist palmitoylethanolamide in visceral and somatic inflammatory pain.	palmidrol	98-119	cannabinoid receptor 2	Rattus norvegicus	77-80
8670178-8	1996	Finally, as previously shown in central neurons, on stimulation with ionomycin, J774 macrophages also produced a mixture of AEs including AnNH and palmitoylethanolamide, which has been proposed as the preferential endogenous ligand at the peripheral cannabinoid receptor CB2 and, consequently, as a possible down-modulator of mast cells.	palmidrol	147-168	cannabinoid receptor 2 (macrophage)	Mus musculus	271-274
9718090-4	1998	Palmitoylethanolamide (750 nmol x kg(-1)) diminished the level of TNF-alpha in BALF by 31.5% but had no effect on neutrophil recruitment.	palmidrol	0-21	tumor necrosis factor	Mus musculus	66-75
9253958-3	1997	Palmitoylethanolamide inhibited interleukin-4, interleukin-6, interleukin-8 synthesis and the production of p75 TNF-alpha soluble receptors at concentrations similar to those of anandamide but failed to influence TNF-alpha and interferon-gamma production.	palmidrol	0-21	interleukin 4	Homo sapiens	32-45
9253958-3	1997	Palmitoylethanolamide inhibited interleukin-4, interleukin-6, interleukin-8 synthesis and the production of p75 TNF-alpha soluble receptors at concentrations similar to those of anandamide but failed to influence TNF-alpha and interferon-gamma production.	palmidrol	0-21	interleukin 6	Homo sapiens	47-60
9253958-3	1997	Palmitoylethanolamide inhibited interleukin-4, interleukin-6, interleukin-8 synthesis and the production of p75 TNF-alpha soluble receptors at concentrations similar to those of anandamide but failed to influence TNF-alpha and interferon-gamma production.	palmidrol	0-21	C-X-C motif chemokine ligand 8	Homo sapiens	62-75
9253958-3	1997	Palmitoylethanolamide inhibited interleukin-4, interleukin-6, interleukin-8 synthesis and the production of p75 TNF-alpha soluble receptors at concentrations similar to those of anandamide but failed to influence TNF-alpha and interferon-gamma production.	palmidrol	0-21	TNF receptor superfamily member 1B	Homo sapiens	108-111
9253958-3	1997	Palmitoylethanolamide inhibited interleukin-4, interleukin-6, interleukin-8 synthesis and the production of p75 TNF-alpha soluble receptors at concentrations similar to those of anandamide but failed to influence TNF-alpha and interferon-gamma production.	palmidrol	0-21	tumor necrosis factor	Homo sapiens	112-121
9253958-3	1997	Palmitoylethanolamide inhibited interleukin-4, interleukin-6, interleukin-8 synthesis and the production of p75 TNF-alpha soluble receptors at concentrations similar to those of anandamide but failed to influence TNF-alpha and interferon-gamma production.	palmidrol	0-21	interferon gamma	Homo sapiens	227-243
8739213-4	1996	Recently, N-(2-hydroxyethyl)hexadecanamide (LG 2110/1) has been reported to down-modulate mast cell activation in vitro by behaving as an agonist at the peripheral cannabinoid CB2 receptor.	palmidrol	10-42	cannabinoid receptor 2	Rattus norvegicus	176-179
8633002-8	1996	Cannabinoids, which like palmitoylethanolamide are functionally active at the peripheral cannabinoid receptor CB2 on mast cells, also prevented neuron loss in this delayed postglutamate model.	palmidrol	25-46	cannabinoid receptor 2 (macrophage)	Mus musculus	110-113
8633002-9	1996	Furthermore, the neuroprotective effects of palmitoylethanolamide, as well as that of the active cannabinoids, were efficiently antagonized by the candidate central cannabinoid receptor (CB1) agonist anandamide.	palmidrol	44-65	cannabinoid receptor 1 (brain)	Mus musculus	187-190
8633002-12	1996	The results suggest that (i) non-CB1 cannabinoid receptors control, upon agonist binding, the downstream consequences of an excitotoxic stimulus; (ii) palmitoylethanolamide, unlike anandamide, behaves as an endogenous agonist for CB2-like receptors on granule cells; and (iii) activation of such receptors may serve to downmodulate deleterious cellular processes following pathological events or noxious stimuli in both the nervous and immune systems.	palmidrol	151-172	cannabinoid receptor 2 (macrophage)	Mus musculus	230-233
7724569-7	1995	Although both palmitoylethanolamide and anandamide bind to the CB2 receptor, only the former downmodulates mast cell activation in vitro.	palmidrol	14-35	cannabinoid receptor 2	Homo sapiens	63-66
33808491-8	2021	Interestingly, the incubation with 25D3 or 1,25D3 or palmitoylethanolamide, an endogenous ligand of peroxisome proliferator-activated-receptor-alpha (PPAR-alpha), reduced most of these effects.	palmidrol	53-74	peroxisome proliferator activated receptor alpha	Mus musculus	100-148
33808491-8	2021	Interestingly, the incubation with 25D3 or 1,25D3 or palmitoylethanolamide, an endogenous ligand of peroxisome proliferator-activated-receptor-alpha (PPAR-alpha), reduced most of these effects.	palmidrol	53-74	peroxisome proliferator activated receptor alpha	Mus musculus	150-160
34799468-1	2021	OBJECTIVE: To observe the inhibitory effects of the peroxisome proliferator-activated receptor alpha (PPARalpha) agonist palmitoylethanolamide (PEA) on inflammatory responses and oxidative stress injury in rats with spinal cord injury (SCI).	palmidrol	121-142	peroxisome proliferator activated receptor alpha	Rattus norvegicus	52-100
33799405-1	2021	Palmitoylethanolamide (PEA) is an N-acylethanolamide produced on-demand by the enzyme N-acylphosphatidylethanolamine-preferring phospholipase D (NAPE-PLD).	palmidrol	0-21	N-acyl phosphatidylethanolamine phospholipase D	Mus musculus	86-143
33799405-1	2021	Palmitoylethanolamide (PEA) is an N-acylethanolamide produced on-demand by the enzyme N-acylphosphatidylethanolamine-preferring phospholipase D (NAPE-PLD).	palmidrol	0-21	N-acyl phosphatidylethanolamine phospholipase D	Mus musculus	145-153
33799405-1	2021	Palmitoylethanolamide (PEA) is an N-acylethanolamide produced on-demand by the enzyme N-acylphosphatidylethanolamine-preferring phospholipase D (NAPE-PLD).	palmidrol	23-26	N-acyl phosphatidylethanolamine phospholipase D	Mus musculus	86-143
33799405-1	2021	Palmitoylethanolamide (PEA) is an N-acylethanolamide produced on-demand by the enzyme N-acylphosphatidylethanolamine-preferring phospholipase D (NAPE-PLD).	palmidrol	23-26	N-acyl phosphatidylethanolamine phospholipase D	Mus musculus	145-153
34655598-3	2021	N-acylethanolamine acid amidase (NAAA)-regulated palmitoylethanolamide (PEA) signaling play an important role in the control of inflammation.	palmidrol	49-70	N-acylethanolamine acid amidase	Homo sapiens	33-37
34256657-1	2021	N-acylethanolamine acid amidase (NAAA) is an N-terminal nucleophile (Ntn) hydrolase that catalyses the intracellular deactivation of the endogenous analgesic and anti-inflammatory agent palmitoylethanolamide (PEA).	palmidrol	186-207	N-acylethanolamine acid amidase	Homo sapiens	0-31
34256657-1	2021	N-acylethanolamine acid amidase (NAAA) is an N-terminal nucleophile (Ntn) hydrolase that catalyses the intracellular deactivation of the endogenous analgesic and anti-inflammatory agent palmitoylethanolamide (PEA).	palmidrol	186-207	N-acylethanolamine acid amidase	Homo sapiens	33-37
34256657-1	2021	N-acylethanolamine acid amidase (NAAA) is an N-terminal nucleophile (Ntn) hydrolase that catalyses the intracellular deactivation of the endogenous analgesic and anti-inflammatory agent palmitoylethanolamide (PEA).	palmidrol	209-212	N-acylethanolamine acid amidase	Homo sapiens	0-31
34256657-1	2021	N-acylethanolamine acid amidase (NAAA) is an N-terminal nucleophile (Ntn) hydrolase that catalyses the intracellular deactivation of the endogenous analgesic and anti-inflammatory agent palmitoylethanolamide (PEA).	palmidrol	209-212	N-acylethanolamine acid amidase	Homo sapiens	33-37
34799468-1	2021	OBJECTIVE: To observe the inhibitory effects of the peroxisome proliferator-activated receptor alpha (PPARalpha) agonist palmitoylethanolamide (PEA) on inflammatory responses and oxidative stress injury in rats with spinal cord injury (SCI).	palmidrol	121-142	peroxisome proliferator activated receptor alpha	Rattus norvegicus	102-111
34799468-1	2021	OBJECTIVE: To observe the inhibitory effects of the peroxisome proliferator-activated receptor alpha (PPARalpha) agonist palmitoylethanolamide (PEA) on inflammatory responses and oxidative stress injury in rats with spinal cord injury (SCI).	palmidrol	144-147	peroxisome proliferator activated receptor alpha	Rattus norvegicus	52-100
34799468-1	2021	OBJECTIVE: To observe the inhibitory effects of the peroxisome proliferator-activated receptor alpha (PPARalpha) agonist palmitoylethanolamide (PEA) on inflammatory responses and oxidative stress injury in rats with spinal cord injury (SCI).	palmidrol	144-147	peroxisome proliferator activated receptor alpha	Rattus norvegicus	102-111
34712137-9	2021	Moreover, PEA exerted a clear anti-inflammatory effect though ameliorating the expression of inflammatory mediators and suppressing the NLRP3 inflammasome pathway activation.	palmidrol	10-13	NLR family, pyrin domain containing 3	Mus musculus	136-141
34777770-5	2021	We designed a probe to release palmitoylethanolamide (PEA), a GPR55 agonist known to stimulate glucose-stimulated insulin secretion (GSIS).	palmidrol	31-52	G protein-coupled receptor 55	Homo sapiens	62-67
34658885-10	2021	In EGCs, treatment with PEA counteracted the increment of S100-beta, TLR-4, NF-kappaB p65 and IL-1beta release induced by LPS and Abeta.	palmidrol	24-27	S100 calcium binding protein A1	Mus musculus	58-67
34658885-10	2021	In EGCs, treatment with PEA counteracted the increment of S100-beta, TLR-4, NF-kappaB p65 and IL-1beta release induced by LPS and Abeta.	palmidrol	24-27	toll-like receptor 4	Mus musculus	69-74
34658885-10	2021	In EGCs, treatment with PEA counteracted the increment of S100-beta, TLR-4, NF-kappaB p65 and IL-1beta release induced by LPS and Abeta.	palmidrol	24-27	interleukin 1 alpha	Mus musculus	94-102
34658885-10	2021	In EGCs, treatment with PEA counteracted the increment of S100-beta, TLR-4, NF-kappaB p65 and IL-1beta release induced by LPS and Abeta.	palmidrol	24-27	amyloid beta (A4) precursor protein	Mus musculus	130-135
34469137-2	2021	In fact, NAAA inhibition preserves endogenous palmitoylethanolamide (PEA) from degradation, thus increasing and prolonging its anti-inflammatory and analgesic efficacy at the inflamed site.	palmidrol	46-67	N-acylethanolamine acid amidase	Homo sapiens	9-13
34469137-2	2021	In fact, NAAA inhibition preserves endogenous palmitoylethanolamide (PEA) from degradation, thus increasing and prolonging its anti-inflammatory and analgesic efficacy at the inflamed site.	palmidrol	69-72	N-acylethanolamine acid amidase	Homo sapiens	9-13
34777770-5	2021	We designed a probe to release palmitoylethanolamide (PEA), a GPR55 agonist known to stimulate glucose-stimulated insulin secretion (GSIS).	palmidrol	31-52	insulin	Homo sapiens	114-121
34777770-5	2021	We designed a probe to release palmitoylethanolamide (PEA), a GPR55 agonist known to stimulate glucose-stimulated insulin secretion (GSIS).	palmidrol	54-57	G protein-coupled receptor 55	Homo sapiens	62-67
34777770-5	2021	We designed a probe to release palmitoylethanolamide (PEA), a GPR55 agonist known to stimulate glucose-stimulated insulin secretion (GSIS).	palmidrol	54-57	insulin	Homo sapiens	114-121
34396611-0	2021	In vivo brain levels of acetylcholine and 5-hydroxytryptamine after oleoylethanolamide or palmitoylethanolamide administrations are mediated by PPARalpha engagement.	palmidrol	90-111	peroxisome proliferator activated receptor alpha	Homo sapiens	144-153
34265624-5	2021	The present study examined the effects of intracerebral or systemic administration of the FAAH substrates N-oleoylethanolamide (OEA), N-palmitoylethanolamide (PEA) or the anandamide (AEA) analogue meth-AEA on hyperthermia and hypothalamic inflammatory gene expression following administration of the TLR3 agonist, and viral mimetic, poly I:C.	palmidrol	134-157	fatty acid amide hydrolase	Homo sapiens	90-94
34564408-0	2021	Ultramicronized Palmitoylethanolamide Inhibits NLRP3 Inflammasome Expression and Pro-Inflammatory Response Activated by SARS-CoV-2 Spike Protein in Cultured Murine Alveolar Macrophages.	palmidrol	16-37	NLR family pyrin domain containing 3	Homo sapiens	47-52
34564408-0	2021	Ultramicronized Palmitoylethanolamide Inhibits NLRP3 Inflammasome Expression and Pro-Inflammatory Response Activated by SARS-CoV-2 Spike Protein in Cultured Murine Alveolar Macrophages.	palmidrol	16-37	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	131-136
34396611-2	2021	The PPARalpha recognizes as endogenous ligands the lipids oleoylethanolamide (OEA) and palmitoylethanolamide (PEA), which in turn, if systemically injected, they exert wake-promoting effects.	palmidrol	87-108	peroxisome proliferator activated receptor alpha	Homo sapiens	4-13
34396611-2	2021	The PPARalpha recognizes as endogenous ligands the lipids oleoylethanolamide (OEA) and palmitoylethanolamide (PEA), which in turn, if systemically injected, they exert wake-promoting effects.	palmidrol	110-113	peroxisome proliferator activated receptor alpha	Homo sapiens	4-13
35176443-7	2022	PEA treatment promoted an improvement in anxiety-like behavior of obese mice and the systemic inflammation, reducing serum pro-inflammatory mediators (i.e., TNF-alpha, IL-1beta, MCP-1, LPS).	palmidrol	0-3	tumor necrosis factor	Mus musculus	157-166
34202665-0	2021	Palmitoylethanolamide/Baicalein Regulates the Androgen Receptor Signaling and NF-kappaB/Nrf2 Pathways in Benign Prostatic Hyperplasia.	palmidrol	0-21	androgen receptor	Rattus norvegicus	46-63
34202665-0	2021	Palmitoylethanolamide/Baicalein Regulates the Androgen Receptor Signaling and NF-kappaB/Nrf2 Pathways in Benign Prostatic Hyperplasia.	palmidrol	0-21	NFE2 like bZIP transcription factor 2	Rattus norvegicus	88-92
35632821-6	2022	Palmitoylethanolamide (PEA) is a lipid-derived peroxisome proliferator-activated receptor-alpha (PPAR-alpha) agonist that also counteracts SARS-CoV-2 entry and its replication.	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Homo sapiens	47-95
35632821-6	2022	Palmitoylethanolamide (PEA) is a lipid-derived peroxisome proliferator-activated receptor-alpha (PPAR-alpha) agonist that also counteracts SARS-CoV-2 entry and its replication.	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Homo sapiens	97-107
35632821-6	2022	Palmitoylethanolamide (PEA) is a lipid-derived peroxisome proliferator-activated receptor-alpha (PPAR-alpha) agonist that also counteracts SARS-CoV-2 entry and its replication.	palmidrol	23-26	peroxisome proliferator activated receptor alpha	Homo sapiens	47-95
35632821-6	2022	Palmitoylethanolamide (PEA) is a lipid-derived peroxisome proliferator-activated receptor-alpha (PPAR-alpha) agonist that also counteracts SARS-CoV-2 entry and its replication.	palmidrol	23-26	peroxisome proliferator activated receptor alpha	Homo sapiens	97-107
34276381-0	2021	Co-Ultramicronized Palmitoylethanolamide/Luteolin-Induced Oligodendrocyte Precursor Cell Differentiation is Associated With Tyro3 Receptor Upregulation.	palmidrol	19-40	TYRO3 protein tyrosine kinase	Homo sapiens	124-129
35469820-0	2022	Palmitoylethanolamide ameliorates neuroinflammation via modulating PPAR-alpha to promote the functional outcome after intracerebral hemorrhage.	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Mus musculus	67-77
35176443-7	2022	PEA treatment promoted an improvement in anxiety-like behavior of obese mice and the systemic inflammation, reducing serum pro-inflammatory mediators (i.e., TNF-alpha, IL-1beta, MCP-1, LPS).	palmidrol	0-3	interleukin 1 alpha	Mus musculus	168-176
35176443-7	2022	PEA treatment promoted an improvement in anxiety-like behavior of obese mice and the systemic inflammation, reducing serum pro-inflammatory mediators (i.e., TNF-alpha, IL-1beta, MCP-1, LPS).	palmidrol	0-3	mast cell protease 1	Mus musculus	178-183
35176443-10	2022	Moreover, PEA attenuated the immunoreactivity of Iba-1 and GFAP and reduced pro-inflammatory pathways and cytokine production in both the hypothalamus and hippocampus.	palmidrol	10-13	induction of brown adipocytes 1	Mus musculus	49-54
35176443-10	2022	Moreover, PEA attenuated the immunoreactivity of Iba-1 and GFAP and reduced pro-inflammatory pathways and cytokine production in both the hypothalamus and hippocampus.	palmidrol	10-13	glial fibrillary acidic protein	Mus musculus	59-63
35485445-0	2022	Comprehensive lipidomics of lupus-prone mice using LC-MS/MS identifies the reduction of palmitoylethanolamide that suppresses TLR9-mediated inflammation.	palmidrol	88-109	toll-like receptor 9	Mus musculus	126-130
35214069-0	2022	Palmitoylethanolamide Promotes White-to-Beige Conversion and Metabolic Reprogramming of Adipocytes: Contribution of PPAR-alpha.	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Homo sapiens	116-126
35453371-1	2022	N-Acylethanolamine acid amidase (NAAA) is an N-terminal cysteine hydrolase that preferentially catalyzes the hydrolysis of endogenous lipid mediators such as palmitoylethanolamide, which has been shown to exhibit neuroprotective and antinociceptive properties by engaging peroxisome proliferator-activated receptor-alpha.	palmidrol	158-179	N-acylethanolamine acid amidase	Homo sapiens	0-31
35453371-1	2022	N-Acylethanolamine acid amidase (NAAA) is an N-terminal cysteine hydrolase that preferentially catalyzes the hydrolysis of endogenous lipid mediators such as palmitoylethanolamide, which has been shown to exhibit neuroprotective and antinociceptive properties by engaging peroxisome proliferator-activated receptor-alpha.	palmidrol	158-179	N-acylethanolamine acid amidase	Homo sapiens	33-37
35453371-1	2022	N-Acylethanolamine acid amidase (NAAA) is an N-terminal cysteine hydrolase that preferentially catalyzes the hydrolysis of endogenous lipid mediators such as palmitoylethanolamide, which has been shown to exhibit neuroprotective and antinociceptive properties by engaging peroxisome proliferator-activated receptor-alpha.	palmidrol	158-179	peroxisome proliferator activated receptor alpha	Homo sapiens	272-320
33986036-1	2021	N-acylethanolamine acid amidase (NAAA) is an N-terminal cysteine hydrolase that stops the physiological actions of palmitoylethanolamide (PEA), an endogenous lipid messenger that activates the transcription factor, peroxisome proliferator-activated receptor-alpha.	palmidrol	115-136	N-acylethanolamine acid amidase	Mus musculus	0-31
35263737-7	2022	AEA analog palmitoylethanolamide (PEA) is also associated positively with the yearly change in eGFR.	palmidrol	11-32	epidermal growth factor receptor	Homo sapiens	95-99
35263737-7	2022	AEA analog palmitoylethanolamide (PEA) is also associated positively with the yearly change in eGFR.	palmidrol	34-37	epidermal growth factor receptor	Homo sapiens	95-99
33986036-1	2021	N-acylethanolamine acid amidase (NAAA) is an N-terminal cysteine hydrolase that stops the physiological actions of palmitoylethanolamide (PEA), an endogenous lipid messenger that activates the transcription factor, peroxisome proliferator-activated receptor-alpha.	palmidrol	115-136	N-acylethanolamine acid amidase	Mus musculus	33-37
33986036-1	2021	N-acylethanolamine acid amidase (NAAA) is an N-terminal cysteine hydrolase that stops the physiological actions of palmitoylethanolamide (PEA), an endogenous lipid messenger that activates the transcription factor, peroxisome proliferator-activated receptor-alpha.	palmidrol	115-136	peroxisome proliferator activated receptor alpha	Mus musculus	215-263
33986036-1	2021	N-acylethanolamine acid amidase (NAAA) is an N-terminal cysteine hydrolase that stops the physiological actions of palmitoylethanolamide (PEA), an endogenous lipid messenger that activates the transcription factor, peroxisome proliferator-activated receptor-alpha.	palmidrol	138-141	N-acylethanolamine acid amidase	Mus musculus	0-31
33986036-1	2021	N-acylethanolamine acid amidase (NAAA) is an N-terminal cysteine hydrolase that stops the physiological actions of palmitoylethanolamide (PEA), an endogenous lipid messenger that activates the transcription factor, peroxisome proliferator-activated receptor-alpha.	palmidrol	138-141	N-acylethanolamine acid amidase	Mus musculus	33-37
33986036-1	2021	N-acylethanolamine acid amidase (NAAA) is an N-terminal cysteine hydrolase that stops the physiological actions of palmitoylethanolamide (PEA), an endogenous lipid messenger that activates the transcription factor, peroxisome proliferator-activated receptor-alpha.	palmidrol	138-141	peroxisome proliferator activated receptor alpha	Mus musculus	215-263
33729209-8	2021	Selective CB1, CB2, non-selective cannabinoid receptor agonists (including delta-9-tetrahydrocannabinol; THC), and PPAR-alpha agonists (predominantly palmitoylethanolamide; PEA) significantly attenuated pain-associated behaviours in a broad range of inflammatory and neuropathic pain models.	palmidrol	150-171	peroxisome proliferator activated receptor alpha	Homo sapiens	115-125
33900772-2	2021	N-Acylethanolamine acid amidase (NAAA) favorably hydrolyzes lipid palmitoylethanolamide, which plays a key role in the regulation of inflammatory and pain processes.	palmidrol	66-87	N-acylethanolamine acid amidase	Homo sapiens	0-31
33900772-2	2021	N-Acylethanolamine acid amidase (NAAA) favorably hydrolyzes lipid palmitoylethanolamide, which plays a key role in the regulation of inflammatory and pain processes.	palmidrol	66-87	N-acylethanolamine acid amidase	Homo sapiens	33-37
33070154-1	2021	JNJ-42165279 is a selective inhibitor of fatty acid amide hydrolase (FAAH), the enzyme responsible for the degradation of fatty acid amides (FAA) including anandamide (AEA), palmitoylethanolamide (PEA), and N-oleoylethanolamide (OEA).	palmidrol	174-195	fatty acid amide hydrolase	Homo sapiens	41-67
33070154-1	2021	JNJ-42165279 is a selective inhibitor of fatty acid amide hydrolase (FAAH), the enzyme responsible for the degradation of fatty acid amides (FAA) including anandamide (AEA), palmitoylethanolamide (PEA), and N-oleoylethanolamide (OEA).	palmidrol	174-195	fatty acid amide hydrolase	Homo sapiens	69-73
33070154-1	2021	JNJ-42165279 is a selective inhibitor of fatty acid amide hydrolase (FAAH), the enzyme responsible for the degradation of fatty acid amides (FAA) including anandamide (AEA), palmitoylethanolamide (PEA), and N-oleoylethanolamide (OEA).	palmidrol	197-200	fatty acid amide hydrolase	Homo sapiens	41-67
33070154-1	2021	JNJ-42165279 is a selective inhibitor of fatty acid amide hydrolase (FAAH), the enzyme responsible for the degradation of fatty acid amides (FAA) including anandamide (AEA), palmitoylethanolamide (PEA), and N-oleoylethanolamide (OEA).	palmidrol	197-200	fatty acid amide hydrolase	Homo sapiens	69-73
33781184-0	2021	Micro Composite Palmitoylethanolamide/Rutin Reduces Vascular Injury through Modulation of the Nrf2/HO-1 and NF-kB Pathways.	palmidrol	16-37	NFE2 like bZIP transcription factor 2	Homo sapiens	94-98
33781184-0	2021	Micro Composite Palmitoylethanolamide/Rutin Reduces Vascular Injury through Modulation of the Nrf2/HO-1 and NF-kB Pathways.	palmidrol	16-37	heme oxygenase 1	Homo sapiens	99-103
33986673-2	2021	Palmitoylethanolamide is an endogenous lipid able to exert immunomodulatory activities and restore epithelial barrier integrity in human models of colitis, by binding the peroxisome proliferator-activated receptor-alpha (PPARalpha).	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Homo sapiens	171-219
33986673-2	2021	Palmitoylethanolamide is an endogenous lipid able to exert immunomodulatory activities and restore epithelial barrier integrity in human models of colitis, by binding the peroxisome proliferator-activated receptor-alpha (PPARalpha).	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Homo sapiens	221-230
33385371-0	2021	Palmitoylethanolamide (PEA) reduces postoperative adhesions after experimental strabismus surgery in rabbits by suppressing canonical and non-canonical TGFbeta signaling through PPARalpha.	palmidrol	0-21	peroxisome proliferator-activated receptor alpha	Oryctolagus cuniculus	178-187
33668991-4	2021	N-Palmitoylethanolamide (PEA), an emerging nutraceutical compound present in plants and animal foods, is an endogenous PPAR-alpha agonist with well-demonstrated anti-inflammatory and analgesics characteristics.	palmidrol	0-23	peroxisome proliferator activated receptor alpha	Mus musculus	119-129
33668991-4	2021	N-Palmitoylethanolamide (PEA), an emerging nutraceutical compound present in plants and animal foods, is an endogenous PPAR-alpha agonist with well-demonstrated anti-inflammatory and analgesics characteristics.	palmidrol	25-28	peroxisome proliferator activated receptor alpha	Mus musculus	119-129
32346865-0	2021	Palmitoylethanolamide counteracts brain fog improving depressive-like behaviour in obese mice: possible role of synaptic plasticity and neurogenesis.	palmidrol	0-21	zinc finger protein, multitype 1	Mus musculus	40-43
33385371-0	2021	Palmitoylethanolamide (PEA) reduces postoperative adhesions after experimental strabismus surgery in rabbits by suppressing canonical and non-canonical TGFbeta signaling through PPARalpha.	palmidrol	23-26	peroxisome proliferator-activated receptor alpha	Oryctolagus cuniculus	178-187
32346865-12	2021	At molecular level, PEA restored brain-derived neurotrophic factor signaling pathway in hippocampus and PFC, indicating an improvement of synaptic plasticity.	palmidrol	20-23	brain derived neurotrophic factor	Mus musculus	33-66
33385371-3	2021	In the present study, we found that administration of palmitoylethanolamide (PEA)attenuated postoperative inflammation and fibroproliferation through activating peroxisome proliferator-activated receptor alpha (PPARalpha), thus prevented scar formation.	palmidrol	54-75	peroxisome proliferator-activated receptor alpha	Oryctolagus cuniculus	161-209
32346865-13	2021	In particular, PEA counteracted the reduction of glutamatergic synaptic density induced by HFD in the stratum radiatum of the CA1 of the hippocampus, where it also exhibited neurogenesis promoting abilities.	palmidrol	15-18	carbonic anhydrase 1	Mus musculus	126-129
33385371-3	2021	In the present study, we found that administration of palmitoylethanolamide (PEA)attenuated postoperative inflammation and fibroproliferation through activating peroxisome proliferator-activated receptor alpha (PPARalpha), thus prevented scar formation.	palmidrol	54-75	peroxisome proliferator-activated receptor alpha	Oryctolagus cuniculus	211-220
33385371-3	2021	In the present study, we found that administration of palmitoylethanolamide (PEA)attenuated postoperative inflammation and fibroproliferation through activating peroxisome proliferator-activated receptor alpha (PPARalpha), thus prevented scar formation.	palmidrol	77-80	peroxisome proliferator-activated receptor alpha	Oryctolagus cuniculus	161-209
33385371-3	2021	In the present study, we found that administration of palmitoylethanolamide (PEA)attenuated postoperative inflammation and fibroproliferation through activating peroxisome proliferator-activated receptor alpha (PPARalpha), thus prevented scar formation.	palmidrol	77-80	peroxisome proliferator-activated receptor alpha	Oryctolagus cuniculus	211-220
33505308-4	2020	CLA is incorporated and metabolized into brain tissue where induces the biosynthesis of endogenous PPARalpha ligands palmitoylethanolamide (PEA) and oleoylethanolamide (OEA), likely through a positive feedback mechanism where PPARalpha activation sustains its own cellular effects through ligand biosynthesis.	palmidrol	117-138	peroxisome proliferator activated receptor alpha	Homo sapiens	99-108
33494185-0	2021	GPR119 and GPR55 as Receptors for Fatty Acid Ethanolamides, Oleoylethanolamide and Palmitoylethanolamide.	palmidrol	83-104	G protein-coupled receptor 119	Homo sapiens	0-6
33494185-0	2021	GPR119 and GPR55 as Receptors for Fatty Acid Ethanolamides, Oleoylethanolamide and Palmitoylethanolamide.	palmidrol	83-104	G protein-coupled receptor 55	Homo sapiens	11-16
33505308-4	2020	CLA is incorporated and metabolized into brain tissue where induces the biosynthesis of endogenous PPARalpha ligands palmitoylethanolamide (PEA) and oleoylethanolamide (OEA), likely through a positive feedback mechanism where PPARalpha activation sustains its own cellular effects through ligand biosynthesis.	palmidrol	140-143	peroxisome proliferator activated receptor alpha	Homo sapiens	99-108
33505308-4	2020	CLA is incorporated and metabolized into brain tissue where induces the biosynthesis of endogenous PPARalpha ligands palmitoylethanolamide (PEA) and oleoylethanolamide (OEA), likely through a positive feedback mechanism where PPARalpha activation sustains its own cellular effects through ligand biosynthesis.	palmidrol	140-143	peroxisome proliferator activated receptor alpha	Homo sapiens	226-235
33037452-1	2021	RATIONALE: N-acylethanolamine acid amidase (NAAA) is an intracellular cysteine hydrolase that terminates the biological actions of oleoylethanolamide (OEA) and palmitoylethanolamide (PEA), two endogenous lipid-derived agonists of the nuclear receptor, and peroxisome proliferator-activated receptor-alpha.	palmidrol	160-181	N-acylethanolamine acid amidase	Rattus norvegicus	11-42
33037452-1	2021	RATIONALE: N-acylethanolamine acid amidase (NAAA) is an intracellular cysteine hydrolase that terminates the biological actions of oleoylethanolamide (OEA) and palmitoylethanolamide (PEA), two endogenous lipid-derived agonists of the nuclear receptor, and peroxisome proliferator-activated receptor-alpha.	palmidrol	160-181	N-acylethanolamine acid amidase	Rattus norvegicus	44-48
33037452-1	2021	RATIONALE: N-acylethanolamine acid amidase (NAAA) is an intracellular cysteine hydrolase that terminates the biological actions of oleoylethanolamide (OEA) and palmitoylethanolamide (PEA), two endogenous lipid-derived agonists of the nuclear receptor, and peroxisome proliferator-activated receptor-alpha.	palmidrol	160-181	peroxisome proliferator activated receptor alpha	Rattus norvegicus	256-304
33037452-1	2021	RATIONALE: N-acylethanolamine acid amidase (NAAA) is an intracellular cysteine hydrolase that terminates the biological actions of oleoylethanolamide (OEA) and palmitoylethanolamide (PEA), two endogenous lipid-derived agonists of the nuclear receptor, and peroxisome proliferator-activated receptor-alpha.	palmidrol	183-186	N-acylethanolamine acid amidase	Rattus norvegicus	11-42
33037452-1	2021	RATIONALE: N-acylethanolamine acid amidase (NAAA) is an intracellular cysteine hydrolase that terminates the biological actions of oleoylethanolamide (OEA) and palmitoylethanolamide (PEA), two endogenous lipid-derived agonists of the nuclear receptor, and peroxisome proliferator-activated receptor-alpha.	palmidrol	183-186	N-acylethanolamine acid amidase	Rattus norvegicus	44-48
33037452-1	2021	RATIONALE: N-acylethanolamine acid amidase (NAAA) is an intracellular cysteine hydrolase that terminates the biological actions of oleoylethanolamide (OEA) and palmitoylethanolamide (PEA), two endogenous lipid-derived agonists of the nuclear receptor, and peroxisome proliferator-activated receptor-alpha.	palmidrol	183-186	peroxisome proliferator activated receptor alpha	Rattus norvegicus	256-304
32191459-2	2020	NAAA catalyzes the hydrolytic deactivation of palmitoylethanolamide (PEA), a lipid-derived peroxisome proliferator-activated receptor-alpha (PPAR-alpha) agonist that exerts profound anti-inflammatory effects in animal models.	palmidrol	46-67	N-acylethanolamine acid amidase	Homo sapiens	0-4
33117168-1	2020	N-acylethanolamine-hydrolyzing acid amidase (NAAA) is a lysosomal enzyme that inhibits the degradation of palmitoylethanolamide (PEA), an endogenous lipid that induces analgesic, anti-inflammation, and anti-multiple sclerosis through PPARalpha activation.	palmidrol	106-127	N-acylethanolamine acid amidase	Homo sapiens	0-43
33117168-1	2020	N-acylethanolamine-hydrolyzing acid amidase (NAAA) is a lysosomal enzyme that inhibits the degradation of palmitoylethanolamide (PEA), an endogenous lipid that induces analgesic, anti-inflammation, and anti-multiple sclerosis through PPARalpha activation.	palmidrol	106-127	N-acylethanolamine acid amidase	Homo sapiens	45-49
33117168-1	2020	N-acylethanolamine-hydrolyzing acid amidase (NAAA) is a lysosomal enzyme that inhibits the degradation of palmitoylethanolamide (PEA), an endogenous lipid that induces analgesic, anti-inflammation, and anti-multiple sclerosis through PPARalpha activation.	palmidrol	106-127	peroxisome proliferator activated receptor alpha	Homo sapiens	234-243
33117168-1	2020	N-acylethanolamine-hydrolyzing acid amidase (NAAA) is a lysosomal enzyme that inhibits the degradation of palmitoylethanolamide (PEA), an endogenous lipid that induces analgesic, anti-inflammation, and anti-multiple sclerosis through PPARalpha activation.	palmidrol	129-132	N-acylethanolamine acid amidase	Homo sapiens	0-43
33117168-1	2020	N-acylethanolamine-hydrolyzing acid amidase (NAAA) is a lysosomal enzyme that inhibits the degradation of palmitoylethanolamide (PEA), an endogenous lipid that induces analgesic, anti-inflammation, and anti-multiple sclerosis through PPARalpha activation.	palmidrol	129-132	N-acylethanolamine acid amidase	Homo sapiens	45-49
33117168-1	2020	N-acylethanolamine-hydrolyzing acid amidase (NAAA) is a lysosomal enzyme that inhibits the degradation of palmitoylethanolamide (PEA), an endogenous lipid that induces analgesic, anti-inflammation, and anti-multiple sclerosis through PPARalpha activation.	palmidrol	129-132	peroxisome proliferator activated receptor alpha	Homo sapiens	234-243
32634582-1	2020	N-acylethanolamine acid amidase (NAAA) deactivates the endogenous peroxisome proliferator-activated receptor-alpha (PPAR-alpha) agonist palmitoylethanolamide (PEA).	palmidrol	136-157	N-acylethanolamine acid amidase	Mus musculus	0-31
32634582-1	2020	N-acylethanolamine acid amidase (NAAA) deactivates the endogenous peroxisome proliferator-activated receptor-alpha (PPAR-alpha) agonist palmitoylethanolamide (PEA).	palmidrol	136-157	N-acylethanolamine acid amidase	Mus musculus	33-37
32634582-1	2020	N-acylethanolamine acid amidase (NAAA) deactivates the endogenous peroxisome proliferator-activated receptor-alpha (PPAR-alpha) agonist palmitoylethanolamide (PEA).	palmidrol	136-157	peroxisome proliferator activated receptor alpha	Mus musculus	66-114
32634582-1	2020	N-acylethanolamine acid amidase (NAAA) deactivates the endogenous peroxisome proliferator-activated receptor-alpha (PPAR-alpha) agonist palmitoylethanolamide (PEA).	palmidrol	136-157	peroxisome proliferator activated receptor alpha	Mus musculus	116-126
33208151-9	2020	In the striatum, non-eCB lipids were significantly increased by short-term, escalating morphine exposure, including peroxisome proliferator activator receptor alpha (PPAR-alpha) ligands N-oleoyl ethanolamide (OEA) and N-palmitoyl ethanolamide (PEA), as well as the amino acids phenylalanine and proline.	palmidrol	218-242	peroxisome proliferator activated receptor alpha	Homo sapiens	166-176
33208151-9	2020	In the striatum, non-eCB lipids were significantly increased by short-term, escalating morphine exposure, including peroxisome proliferator activator receptor alpha (PPAR-alpha) ligands N-oleoyl ethanolamide (OEA) and N-palmitoyl ethanolamide (PEA), as well as the amino acids phenylalanine and proline.	palmidrol	244-247	peroxisome proliferator activated receptor alpha	Homo sapiens	166-176
33050589-2	2020	Palmitoylethanolamide (PEA) is an endogenous potent anti-inflammatory agent, in which activity is regulated by N-acylethanolamine acid amidase (NAAA), that hydrolyzes saturated or monounsaturated fatty acid ethanolamides, such as PEA.	palmidrol	0-21	N-acylethanolamine acid amidase	Homo sapiens	111-142
33050589-2	2020	Palmitoylethanolamide (PEA) is an endogenous potent anti-inflammatory agent, in which activity is regulated by N-acylethanolamine acid amidase (NAAA), that hydrolyzes saturated or monounsaturated fatty acid ethanolamides, such as PEA.	palmidrol	0-21	N-acylethanolamine acid amidase	Homo sapiens	144-148
33050589-2	2020	Palmitoylethanolamide (PEA) is an endogenous potent anti-inflammatory agent, in which activity is regulated by N-acylethanolamine acid amidase (NAAA), that hydrolyzes saturated or monounsaturated fatty acid ethanolamides, such as PEA.	palmidrol	23-26	N-acylethanolamine acid amidase	Homo sapiens	111-142
33050589-2	2020	Palmitoylethanolamide (PEA) is an endogenous potent anti-inflammatory agent, in which activity is regulated by N-acylethanolamine acid amidase (NAAA), that hydrolyzes saturated or monounsaturated fatty acid ethanolamides, such as PEA.	palmidrol	23-26	N-acylethanolamine acid amidase	Homo sapiens	144-148
32191459-2	2020	NAAA catalyzes the hydrolytic deactivation of palmitoylethanolamide (PEA), a lipid-derived peroxisome proliferator-activated receptor-alpha (PPAR-alpha) agonist that exerts profound anti-inflammatory effects in animal models.	palmidrol	46-67	peroxisome proliferator activated receptor alpha	Homo sapiens	91-139
32191459-2	2020	NAAA catalyzes the hydrolytic deactivation of palmitoylethanolamide (PEA), a lipid-derived peroxisome proliferator-activated receptor-alpha (PPAR-alpha) agonist that exerts profound anti-inflammatory effects in animal models.	palmidrol	46-67	peroxisome proliferator activated receptor alpha	Homo sapiens	141-151
32708932-3	2020	In healthy adults, palmitoylethanolamide is an endogenous PPAR-alpha (peroxisome proliferator-activated receptor alpha) agonist through which it performs anti-inflammatory activity and provides its effects by activating the cannabinoid receptor.	palmidrol	19-40	peroxisome proliferator activated receptor alpha	Homo sapiens	58-68
32708932-3	2020	In healthy adults, palmitoylethanolamide is an endogenous PPAR-alpha (peroxisome proliferator-activated receptor alpha) agonist through which it performs anti-inflammatory activity and provides its effects by activating the cannabinoid receptor.	palmidrol	19-40	peroxisome proliferator activated receptor alpha	Homo sapiens	70-118
32077093-1	2020	BACKGROUND AND PURPOSE: Fatty acid amide hydrolase (FAAH) is an intracellular serine amidase that terminates the signaling activity of various lipid messengers involved in pain regulation, including agonists at cannabinoid receptors (e.g., anandamide) and peroxisome proliferator-activated receptor-alpha (PPAR-alpha) [e.g., palmitoylethanolamide (PEA)].	palmidrol	325-346	fatty acid amide hydrolase	Mus musculus	24-50
32077093-1	2020	BACKGROUND AND PURPOSE: Fatty acid amide hydrolase (FAAH) is an intracellular serine amidase that terminates the signaling activity of various lipid messengers involved in pain regulation, including agonists at cannabinoid receptors (e.g., anandamide) and peroxisome proliferator-activated receptor-alpha (PPAR-alpha) [e.g., palmitoylethanolamide (PEA)].	palmidrol	325-346	fatty acid amide hydrolase	Mus musculus	52-56
32326173-6	2020	This study aimed to explore the role of FXOH in the NAAA-PEA pathway and the anti-inflammatory effects based on this mechanism.	palmidrol	57-60	N-acylethanolamine acid amidase	Mus musculus	52-56
32106527-7	2020	PEA reduced (p < 0.05) myoglobin and blood lactate concentrations and increased protein kinase B phosphorylation following exercise.	palmidrol	0-3	protein tyrosine kinase 2 beta	Homo sapiens	80-96
32298438-0	2020	PPARalpha-Dependent Effects of Palmitoylethanolamide Against Retinal Neovascularization and Fibrosis.	palmidrol	31-52	peroxisome proliferator activated receptor alpha	Mus musculus	0-9
32298438-9	2020	PEA significantly alleviated inflammation and inhibited neovascularization in OIR and Vldlr-/- retinas and suppressed profibrotic changes in OIR and Vldlr-/- retinas.	palmidrol	0-3	very low density lipoprotein receptor	Mus musculus	86-91
32298438-9	2020	PEA significantly alleviated inflammation and inhibited neovascularization in OIR and Vldlr-/- retinas and suppressed profibrotic changes in OIR and Vldlr-/- retinas.	palmidrol	0-3	very low density lipoprotein receptor	Mus musculus	149-154
32047441-10	2019	The nuclear receptor peroxisome proliferator-activated receptor-alpha (PPAR-alpha) was found to mediate the PEA-associated improvements.	palmidrol	108-111	peroxisome proliferator activated receptor alpha	Mus musculus	71-81
32046269-8	2020	Lastly, topical administration of PEA-NLC ophthalmic formulation was able to significantly inhibits retinal tumor necrosis factor-alpha (TNF-alpha) levels in streptozotocin-induced diabetic rats.	palmidrol	34-37	tumor necrosis factor	Rattus norvegicus	108-135
32046269-8	2020	Lastly, topical administration of PEA-NLC ophthalmic formulation was able to significantly inhibits retinal tumor necrosis factor-alpha (TNF-alpha) levels in streptozotocin-induced diabetic rats.	palmidrol	34-37	tumor necrosis factor	Rattus norvegicus	137-146
31761726-2	2020	NAAA is a cysteine amidase which preferentially hydrolyzes the endogenous biolipids palmitoylethanolamide (PEA) and oleoylethanolamide (OEA).	palmidrol	84-105	N-acylethanolamine acid amidase	Homo sapiens	0-4
31969800-9	2019	Treatment with PEA largely restored the number of GFAP+ cells.	palmidrol	15-18	glial fibrillary acidic protein	Rattus norvegicus	50-54
31969800-11	2019	Noticeably, PEA treatment reversed the decrease in MAP-2 protein expression and largely prevented PA-induced decrease in pNF-H/M protein expression.	palmidrol	12-15	microtubule-associated protein 2	Rattus norvegicus	51-56
31761726-2	2020	NAAA is a cysteine amidase which preferentially hydrolyzes the endogenous biolipids palmitoylethanolamide (PEA) and oleoylethanolamide (OEA).	palmidrol	107-110	N-acylethanolamine acid amidase	Homo sapiens	0-4
31878942-2	2019	Several mechanisms underlie PEA actions, among which the "entourage" effect, consisting of PEA potentiation of endocannabinoid signaling at either cannabinoid receptors or transient receptor potential vanilloid type-1 (TRPV1) channels.	palmidrol	28-31	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	172-217
32248195-9	2020	These results suggest that: (i) palmitoylethanolamide inhibits the vasopressor responses to sympathetic stimulation and exogenous noradrenaline and that it induces hypotension; and (ii) all these effects are mediated by prejunctional and vascular CB1, TRPV1 and probably GPR55, but not by CB2, receptors.	palmidrol	32-53	G protein-coupled receptor 55	Rattus norvegicus	271-276
32248195-9	2020	These results suggest that: (i) palmitoylethanolamide inhibits the vasopressor responses to sympathetic stimulation and exogenous noradrenaline and that it induces hypotension; and (ii) all these effects are mediated by prejunctional and vascular CB1, TRPV1 and probably GPR55, but not by CB2, receptors.	palmidrol	32-53	cannabinoid receptor 2	Rattus norvegicus	289-292
31878942-8	2019	The effects of PEA on the activity of DAGL-alpha or -beta enzymes were assessed in COS-7 cells overexpressing the human recombinant enzyme or in RBL-2H3 cells, respectively.	palmidrol	15-18	diacylglycerol lipase, alpha	Rattus norvegicus	38-48
31878942-12	2019	PEA significantly stimulated DAGL-alpha and -beta activity and, consequently, 2-AG biosynthesis in cell-free systems.	palmidrol	0-3	diacylglycerol lipase, alpha	Rattus norvegicus	29-39
31914699-2	2020	Here, we investigate the effect of palmitoylethanolamide (PEA), an endogenous PPAR-alpha ligand, in counteracting hepatic metabolic inflexibility and mitochondrial dysfunction induced by high-fat diet (HFD) in mice.	palmidrol	35-56	peroxisome proliferator activated receptor alpha	Mus musculus	78-88
31914699-2	2020	Here, we investigate the effect of palmitoylethanolamide (PEA), an endogenous PPAR-alpha ligand, in counteracting hepatic metabolic inflexibility and mitochondrial dysfunction induced by high-fat diet (HFD) in mice.	palmidrol	58-61	peroxisome proliferator activated receptor alpha	Mus musculus	78-88
31647920-8	2020	The activity of fatty acid synthase (FAS) increased after chronic PEA treatment, suggesting an increase in the hepatic lipogenic capacity, in contrast with the mammalian model.	palmidrol	66-69	fatty acid synthase	Homo sapiens	16-35
31647920-8	2020	The activity of fatty acid synthase (FAS) increased after chronic PEA treatment, suggesting an increase in the hepatic lipogenic capacity, in contrast with the mammalian model.	palmidrol	66-69	fatty acid synthase	Homo sapiens	37-40
32248195-2	2020	Hence, this study investigated in Wistar pithed rats the role of CB1, CB2, TRPV1 and GPR55 receptors in the inhibition by palmitoylethanolamide of the vasopressor responses produced by sympathetic stimulation or exogenous noradrenaline.	palmidrol	122-143	cannabinoid receptor 1	Rattus norvegicus	65-68
32248195-2	2020	Hence, this study investigated in Wistar pithed rats the role of CB1, CB2, TRPV1 and GPR55 receptors in the inhibition by palmitoylethanolamide of the vasopressor responses produced by sympathetic stimulation or exogenous noradrenaline.	palmidrol	122-143	cannabinoid receptor 2	Rattus norvegicus	70-73
32248195-2	2020	Hence, this study investigated in Wistar pithed rats the role of CB1, CB2, TRPV1 and GPR55 receptors in the inhibition by palmitoylethanolamide of the vasopressor responses produced by sympathetic stimulation or exogenous noradrenaline.	palmidrol	122-143	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	75-80
32248195-2	2020	Hence, this study investigated in Wistar pithed rats the role of CB1, CB2, TRPV1 and GPR55 receptors in the inhibition by palmitoylethanolamide of the vasopressor responses produced by sympathetic stimulation or exogenous noradrenaline.	palmidrol	122-143	G protein-coupled receptor 55	Rattus norvegicus	85-90
32248195-9	2020	These results suggest that: (i) palmitoylethanolamide inhibits the vasopressor responses to sympathetic stimulation and exogenous noradrenaline and that it induces hypotension; and (ii) all these effects are mediated by prejunctional and vascular CB1, TRPV1 and probably GPR55, but not by CB2, receptors.	palmidrol	32-53	cannabinoid receptor 1	Rattus norvegicus	247-250
32248195-9	2020	These results suggest that: (i) palmitoylethanolamide inhibits the vasopressor responses to sympathetic stimulation and exogenous noradrenaline and that it induces hypotension; and (ii) all these effects are mediated by prejunctional and vascular CB1, TRPV1 and probably GPR55, but not by CB2, receptors.	palmidrol	32-53	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	252-257
31878942-14	2019	CONCLUSIONS: Activation of CB2 underlies the inhibitory effects on SP-induced RBL-2H3 cell degranulation by PEA alone.	palmidrol	108-111	cannabinoid receptor 2	Rattus norvegicus	27-30
31878942-2	2019	Several mechanisms underlie PEA actions, among which the "entourage" effect, consisting of PEA potentiation of endocannabinoid signaling at either cannabinoid receptors or transient receptor potential vanilloid type-1 (TRPV1) channels.	palmidrol	28-31	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	219-224
31878942-2	2019	Several mechanisms underlie PEA actions, among which the "entourage" effect, consisting of PEA potentiation of endocannabinoid signaling at either cannabinoid receptors or transient receptor potential vanilloid type-1 (TRPV1) channels.	palmidrol	91-94	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	172-217
31787870-5	2019	2-AG activated abnormal cannabidiol (abn-CBD) receptor, PEA was shown to mediate neuroprotection via peroxisome proliferator-activated receptor (PPAR)alpha.	palmidrol	56-59	peroxisome proliferator activated receptor alpha	Homo sapiens	145-155
30635472-0	2019	N-Palmitoylethanolamide Exerts Antidepressant-Like Effects in Rats: Involvement of PPARalpha Pathway in the Hippocampus.	palmidrol	0-23	peroxisome proliferator activated receptor alpha	Rattus norvegicus	83-92
30532004-6	2019	This approach led to specific FAAH overexpression at the postsynaptic site of CA1-CA3 neurons, to increased FAAH enzymatic activity, and, in consequence, to decreased hippocampal levels of AEA and palmitoylethanolamide (PEA), but the levels of the second major endocannabinoid 2-arachidonoyl glycerol (2-AG) and of oleoylethanolamide (OEA) were unchanged.	palmidrol	197-218	fatty acid amide hydrolase	Mus musculus	30-34
30532004-6	2019	This approach led to specific FAAH overexpression at the postsynaptic site of CA1-CA3 neurons, to increased FAAH enzymatic activity, and, in consequence, to decreased hippocampal levels of AEA and palmitoylethanolamide (PEA), but the levels of the second major endocannabinoid 2-arachidonoyl glycerol (2-AG) and of oleoylethanolamide (OEA) were unchanged.	palmidrol	197-218	carbonic anhydrase 1	Mus musculus	78-81
30532004-6	2019	This approach led to specific FAAH overexpression at the postsynaptic site of CA1-CA3 neurons, to increased FAAH enzymatic activity, and, in consequence, to decreased hippocampal levels of AEA and palmitoylethanolamide (PEA), but the levels of the second major endocannabinoid 2-arachidonoyl glycerol (2-AG) and of oleoylethanolamide (OEA) were unchanged.	palmidrol	197-218	carbonic anhydrase 3	Mus musculus	82-85
30532004-6	2019	This approach led to specific FAAH overexpression at the postsynaptic site of CA1-CA3 neurons, to increased FAAH enzymatic activity, and, in consequence, to decreased hippocampal levels of AEA and palmitoylethanolamide (PEA), but the levels of the second major endocannabinoid 2-arachidonoyl glycerol (2-AG) and of oleoylethanolamide (OEA) were unchanged.	palmidrol	220-223	fatty acid amide hydrolase	Mus musculus	30-34
31054246-12	2019	Palmitoylethanolamide and cannabidiol prevented an inflammation-induced fall in TRPV1 and increase in PPARalpha transcription (P &lt; 0.0001).	palmidrol	0-21	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).	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Homo sapiens	102-111
30970677-0	2019	Metabotropic Glutamate Receptor 5 and 8 Modulate the Ameliorative Effect of Ultramicronized Palmitoylethanolamide on Cognitive Decline Associated with Neuropathic Pain.	palmidrol	92-113	glutamate receptor, metabotropic 5	Mus musculus	0-33
30929760-5	2019	Circulating concentrations of anandamide and related fatty-acid amides (palmitoylethanolamide and oleoylethanolamine) that are all normally degraded by FAAH were significantly elevated in peripheral blood compared with normal control carriers of the hypomorphic single-nucleotide polymorphism.	palmidrol	72-93	fatty acid amide hydrolase	Homo sapiens	152-156
30955840-0	2019	Stimulation of Peroxisome Proliferator-Activated Receptor-alpha by N-Palmitoylethanolamine Engages Allopregnanolone Biosynthesis to Modulate Emotional Behavior.	palmidrol	67-90	peroxisome proliferator activated receptor alpha	Mus musculus	15-63
30955840-2	2019	Activation of peroxisome proliferator-activated receptor (PPAR)-alpha by the endocannabinoid congener N-palmitoylethanolamine (PEA) regulates pathophysiological systems (e.g., inflammation, oxidative stress) and induces peripheral biosynthesis of allopregnanolone, a gamma-aminobutyric acidergic neurosteroid implicated in mood disorders.	palmidrol	102-125	peroxisome proliferator activated receptor alpha	Mus musculus	14-69
30955840-2	2019	Activation of peroxisome proliferator-activated receptor (PPAR)-alpha by the endocannabinoid congener N-palmitoylethanolamine (PEA) regulates pathophysiological systems (e.g., inflammation, oxidative stress) and induces peripheral biosynthesis of allopregnanolone, a gamma-aminobutyric acidergic neurosteroid implicated in mood disorders.	palmidrol	127-130	peroxisome proliferator activated receptor alpha	Mus musculus	14-69
30439418-3	2019	An alternative indirect way to activate PPARalpha is inhibition of N-acylethanolamine acid amidase (NAAA), one of the major hydrolyzing enzyme for its endogenous agonists palmitoylethanolamide (PEA) and oleoylethanolamide (OEA).	palmidrol	171-192	peroxisome proliferator activated receptor alpha	Rattus norvegicus	40-49
30439418-3	2019	An alternative indirect way to activate PPARalpha is inhibition of N-acylethanolamine acid amidase (NAAA), one of the major hydrolyzing enzyme for its endogenous agonists palmitoylethanolamide (PEA) and oleoylethanolamide (OEA).	palmidrol	171-192	N-acylethanolamine acid amidase	Rattus norvegicus	67-98
30439418-3	2019	An alternative indirect way to activate PPARalpha is inhibition of N-acylethanolamine acid amidase (NAAA), one of the major hydrolyzing enzyme for its endogenous agonists palmitoylethanolamide (PEA) and oleoylethanolamide (OEA).	palmidrol	171-192	N-acylethanolamine acid amidase	Rattus norvegicus	100-104
30439418-3	2019	An alternative indirect way to activate PPARalpha is inhibition of N-acylethanolamine acid amidase (NAAA), one of the major hydrolyzing enzyme for its endogenous agonists palmitoylethanolamide (PEA) and oleoylethanolamide (OEA).	palmidrol	194-197	peroxisome proliferator activated receptor alpha	Rattus norvegicus	40-49
30439418-3	2019	An alternative indirect way to activate PPARalpha is inhibition of N-acylethanolamine acid amidase (NAAA), one of the major hydrolyzing enzyme for its endogenous agonists palmitoylethanolamide (PEA) and oleoylethanolamide (OEA).	palmidrol	194-197	N-acylethanolamine acid amidase	Rattus norvegicus	67-98
30439418-3	2019	An alternative indirect way to activate PPARalpha is inhibition of N-acylethanolamine acid amidase (NAAA), one of the major hydrolyzing enzyme for its endogenous agonists palmitoylethanolamide (PEA) and oleoylethanolamide (OEA).	palmidrol	194-197	N-acylethanolamine acid amidase	Rattus norvegicus	100-104
30931090-1	2019	N-Acylethanolamine acid amidase (NAAA) is one of the key enzymes involved in the degradation of fatty acid ethanolamides (FAEs), especially for palmitoylethanolamide (PEA).	palmidrol	144-165	N-acylethanolamine acid amidase	Homo sapiens	0-31
30931090-1	2019	N-Acylethanolamine acid amidase (NAAA) is one of the key enzymes involved in the degradation of fatty acid ethanolamides (FAEs), especially for palmitoylethanolamide (PEA).	palmidrol	144-165	N-acylethanolamine acid amidase	Homo sapiens	33-37
30931090-1	2019	N-Acylethanolamine acid amidase (NAAA) is one of the key enzymes involved in the degradation of fatty acid ethanolamides (FAEs), especially for palmitoylethanolamide (PEA).	palmidrol	167-170	N-acylethanolamine acid amidase	Homo sapiens	0-31
30931090-1	2019	N-Acylethanolamine acid amidase (NAAA) is one of the key enzymes involved in the degradation of fatty acid ethanolamides (FAEs), especially for palmitoylethanolamide (PEA).	palmidrol	167-170	N-acylethanolamine acid amidase	Homo sapiens	33-37
30354245-1	2018	Objective- Palmitoylethanolamide is an endogenous fatty acid mediator that is synthetized from membrane phospholipids by N-acyl phosphatidylethanolamine phospholipase D. Its biological actions are primarily mediated by PPAR-alpha (peroxisome proliferator-activated receptors alpha) and the orphan receptor GPR55.	palmidrol	11-32	peroxisome proliferator activated receptor alpha	Mus musculus	219-229
29656363-4	2018	Moreover, PEA-OXA treatment prevented dopamine depletion, increased tyrosine hydroxylase and dopamine transporter activities, and decreased alpha-synuclein aggregation in neurons.	palmidrol	10-13	synuclein, alpha	Mus musculus	140-155
30354245-1	2018	Objective- Palmitoylethanolamide is an endogenous fatty acid mediator that is synthetized from membrane phospholipids by N-acyl phosphatidylethanolamine phospholipase D. Its biological actions are primarily mediated by PPAR-alpha (peroxisome proliferator-activated receptors alpha) and the orphan receptor GPR55.	palmidrol	11-32	G protein-coupled receptor 55	Mus musculus	306-311
30354245-8	2018	Mechanistically, we found that palmitoylethanolamide, by activating GPR55, increases the expression of the phagocytosis receptor MerTK (proto-oncogene tyrosine-protein kinase MER) and enhances macrophage efferocytosis, indicative of proresolving properties.	palmidrol	31-52	G protein-coupled receptor 55	Mus musculus	68-73
30354245-8	2018	Mechanistically, we found that palmitoylethanolamide, by activating GPR55, increases the expression of the phagocytosis receptor MerTK (proto-oncogene tyrosine-protein kinase MER) and enhances macrophage efferocytosis, indicative of proresolving properties.	palmidrol	31-52	MER proto-oncogene tyrosine kinase	Mus musculus	129-134
29388323-7	2018	Upon CB1 activation, N-oleoylethanolamide and N-palmitoylethanolamide, two AEA congeners that do not interact directly with cannabinoid receptors, were enhanced in the striatum.	palmidrol	46-69	cannabinoid receptor 1 (brain)	Mus musculus	5-8
30193877-4	2018	Among endogenous lipids, palmitoylethanolamide (PEA), a PPAR-alpha agonist, has been extensively studied for its anti-inflammatory effects both at central and peripheral level.	palmidrol	25-46	peroxisome proliferator activated receptor alpha	Mus musculus	56-66
30193877-4	2018	Among endogenous lipids, palmitoylethanolamide (PEA), a PPAR-alpha agonist, has been extensively studied for its anti-inflammatory effects both at central and peripheral level.	palmidrol	48-51	peroxisome proliferator activated receptor alpha	Mus musculus	56-66
30251159-6	2018	This effect was strongly correlated with inhibition of brain FAAH activity (r2 = 1.0) and was accompanied by increased brain levels of three FAAH substrates: the endocannabinoid anandamide and the endogenous peroxisome proliferator-activated receptor-alpha (PPAR-alpha) agonists, oleoylethanolamide (OEA), and palmitoylethanolamide (PEA).	palmidrol	310-331	fatty-acid amide hydrolase-like	Rattus norvegicus	61-65
30251159-6	2018	This effect was strongly correlated with inhibition of brain FAAH activity (r2 = 1.0) and was accompanied by increased brain levels of three FAAH substrates: the endocannabinoid anandamide and the endogenous peroxisome proliferator-activated receptor-alpha (PPAR-alpha) agonists, oleoylethanolamide (OEA), and palmitoylethanolamide (PEA).	palmidrol	310-331	fatty-acid amide hydrolase-like	Rattus norvegicus	141-145
30251159-6	2018	This effect was strongly correlated with inhibition of brain FAAH activity (r2 = 1.0) and was accompanied by increased brain levels of three FAAH substrates: the endocannabinoid anandamide and the endogenous peroxisome proliferator-activated receptor-alpha (PPAR-alpha) agonists, oleoylethanolamide (OEA), and palmitoylethanolamide (PEA).	palmidrol	310-331	peroxisome proliferator activated receptor alpha	Rattus norvegicus	208-256
30251159-6	2018	This effect was strongly correlated with inhibition of brain FAAH activity (r2 = 1.0) and was accompanied by increased brain levels of three FAAH substrates: the endocannabinoid anandamide and the endogenous peroxisome proliferator-activated receptor-alpha (PPAR-alpha) agonists, oleoylethanolamide (OEA), and palmitoylethanolamide (PEA).	palmidrol	333-336	fatty-acid amide hydrolase-like	Rattus norvegicus	61-65
30251159-6	2018	This effect was strongly correlated with inhibition of brain FAAH activity (r2 = 1.0) and was accompanied by increased brain levels of three FAAH substrates: the endocannabinoid anandamide and the endogenous peroxisome proliferator-activated receptor-alpha (PPAR-alpha) agonists, oleoylethanolamide (OEA), and palmitoylethanolamide (PEA).	palmidrol	333-336	fatty-acid amide hydrolase-like	Rattus norvegicus	141-145
30251159-6	2018	This effect was strongly correlated with inhibition of brain FAAH activity (r2 = 1.0) and was accompanied by increased brain levels of three FAAH substrates: the endocannabinoid anandamide and the endogenous peroxisome proliferator-activated receptor-alpha (PPAR-alpha) agonists, oleoylethanolamide (OEA), and palmitoylethanolamide (PEA).	palmidrol	333-336	peroxisome proliferator activated receptor alpha	Rattus norvegicus	208-256
29879374-4	2018	We found that OEA, PEA, and eicosatrienoyl ethanolamide (ETEA) could directly inhibit both T-cell responses by reducing their production of TNF-alpha and IFN-gamma from CD8 T cells and TNF-alpha, IFN-gamma and IL-17 from CD4 T cells.	palmidrol	19-22	tumor necrosis factor	Homo sapiens	140-149
29879374-4	2018	We found that OEA, PEA, and eicosatrienoyl ethanolamide (ETEA) could directly inhibit both T-cell responses by reducing their production of TNF-alpha and IFN-gamma from CD8 T cells and TNF-alpha, IFN-gamma and IL-17 from CD4 T cells.	palmidrol	19-22	interferon gamma	Homo sapiens	154-163
29879374-4	2018	We found that OEA, PEA, and eicosatrienoyl ethanolamide (ETEA) could directly inhibit both T-cell responses by reducing their production of TNF-alpha and IFN-gamma from CD8 T cells and TNF-alpha, IFN-gamma and IL-17 from CD4 T cells.	palmidrol	19-22	tumor necrosis factor	Homo sapiens	185-194
29879374-4	2018	We found that OEA, PEA, and eicosatrienoyl ethanolamide (ETEA) could directly inhibit both T-cell responses by reducing their production of TNF-alpha and IFN-gamma from CD8 T cells and TNF-alpha, IFN-gamma and IL-17 from CD4 T cells.	palmidrol	19-22	interferon gamma	Homo sapiens	196-205
29879374-4	2018	We found that OEA, PEA, and eicosatrienoyl ethanolamide (ETEA) could directly inhibit both T-cell responses by reducing their production of TNF-alpha and IFN-gamma from CD8 T cells and TNF-alpha, IFN-gamma and IL-17 from CD4 T cells.	palmidrol	19-22	interleukin 17A	Homo sapiens	210-215
28802121-1	2017	N-acylethanolamine acid amidase (NAAA) is a cysteine hydrolase that participates in the deactivation of fatty acid ethanolamides, such as palmitoylethanolamide (PEA).	palmidrol	138-159	N-acylethanolamine acid amidase	Homo sapiens	0-31
29573741-0	2018	HIV-1 Tat-induced diarrhea is improved by the PPARalpha agonist, palmitoylethanolamide, by suppressing the activation of enteric glia.	palmidrol	65-86	peroxisome proliferator activated receptor alpha	Homo sapiens	46-55
29054595-1	2018	N-acylethanolamine acid amidase (NAAA), a cysteine hydrolase highly expressed in macrophages and B lymphocytes, catalyzes the degradation of palmitoylethanolamide.	palmidrol	141-162	N-acylethanolamine acid amidase	Mus musculus	0-31
29054595-1	2018	N-acylethanolamine acid amidase (NAAA), a cysteine hydrolase highly expressed in macrophages and B lymphocytes, catalyzes the degradation of palmitoylethanolamide.	palmidrol	141-162	N-acylethanolamine acid amidase	Mus musculus	33-37
29054595-2	2018	Palmitoylethanolamide is an agonist of PPAR-alpha and an important regulator of pain and innate immunity.	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Mus musculus	39-49
29403000-2	2018	Fatty acid amide hydrolase (FAAH) represents the primary degradation enzyme of the eCB anandamide (AEA), oleoylethanolamide (OEA) and palmitoylethanolamide (PEA).	palmidrol	134-155	fatty acid amide hydrolase	Mus musculus	11-26
29403000-2	2018	Fatty acid amide hydrolase (FAAH) represents the primary degradation enzyme of the eCB anandamide (AEA), oleoylethanolamide (OEA) and palmitoylethanolamide (PEA).	palmidrol	134-155	fatty acid amide hydrolase	Mus musculus	28-32
29572189-1	2018	N-Acylethanolamine acid amidase (NAAA) is a cysteine enzyme that catalyzes the hydrolysis of palmitoylethanolamide (PEA).	palmidrol	93-114	N-acylethanolamine acid amidase	Mus musculus	0-31
29572189-1	2018	N-Acylethanolamine acid amidase (NAAA) is a cysteine enzyme that catalyzes the hydrolysis of palmitoylethanolamide (PEA).	palmidrol	93-114	N-acylethanolamine acid amidase	Mus musculus	33-37
29572189-2	2018	Pharmacological blockage of NAAA elevates PEA levels and exerts powerful anti-inflammatory activities.	palmidrol	42-45	N-acylethanolamine acid amidase	Mus musculus	28-32
29311913-3	2017	Since Palmitoylethanolamide (PEA), an endogenous lipid mediator chemically related to - and co-released with- the endocannabinoid anandamide, behaves as a local autacoid down-regulator of mast cell activation and inflammation, we explored the possible contribution of PEA in allergic sensitization, by using ovalbumin (OVA) as sensitizing agent in the mouse.	palmidrol	6-27	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	308-317
29311913-3	2017	Since Palmitoylethanolamide (PEA), an endogenous lipid mediator chemically related to - and co-released with- the endocannabinoid anandamide, behaves as a local autacoid down-regulator of mast cell activation and inflammation, we explored the possible contribution of PEA in allergic sensitization, by using ovalbumin (OVA) as sensitizing agent in the mouse.	palmidrol	29-32	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	308-317
28802121-1	2017	N-acylethanolamine acid amidase (NAAA) is a cysteine hydrolase that participates in the deactivation of fatty acid ethanolamides, such as palmitoylethanolamide (PEA).	palmidrol	138-159	N-acylethanolamine acid amidase	Homo sapiens	33-37
28802121-1	2017	N-acylethanolamine acid amidase (NAAA) is a cysteine hydrolase that participates in the deactivation of fatty acid ethanolamides, such as palmitoylethanolamide (PEA).	palmidrol	161-164	N-acylethanolamine acid amidase	Homo sapiens	0-31
28802121-1	2017	N-acylethanolamine acid amidase (NAAA) is a cysteine hydrolase that participates in the deactivation of fatty acid ethanolamides, such as palmitoylethanolamide (PEA).	palmidrol	161-164	N-acylethanolamine acid amidase	Homo sapiens	33-37
28939905-8	2017	Co-ultramicronized palmitoylethanolamide/luteolin, an established anti-inflammatory/ neuroprotective agent, reduced Saa1 expression in OPCs subjected to TNF-alpha treatment.	palmidrol	19-40	tumor necrosis factor	Homo sapiens	153-162
29056914-7	2017	The gene expression levels of Pparalpha and Faah were decreased after 6 h of treatment and, after 24 h, the gene expression levels of Nape-pld and Faah, as well as the liver levels of OEA and palmitoyl ethanolamide, were increased.	palmidrol	192-214	peroxisome proliferator activated receptor alpha	Homo sapiens	30-39
29056914-7	2017	The gene expression levels of Pparalpha and Faah were decreased after 6 h of treatment and, after 24 h, the gene expression levels of Nape-pld and Faah, as well as the liver levels of OEA and palmitoyl ethanolamide, were increased.	palmidrol	192-214	fatty acid amide hydrolase	Homo sapiens	44-48
28939905-8	2017	Co-ultramicronized palmitoylethanolamide/luteolin, an established anti-inflammatory/ neuroprotective agent, reduced Saa1 expression in OPCs subjected to TNF-alpha treatment.	palmidrol	19-40	serum amyloid A1	Homo sapiens	116-120
28095731-2	2017	Recent studies showed that pharmacological modulation of NAAA could be achieved with the oxazoline of palmitoylethanolamide (PEA; PEA-OXA).	palmidrol	102-123	N-acylethanolamine acid amidase	Mus musculus	57-61
28619329-0	2017	Palmitoylethanolamide (PEA): A promising biomarker for coronary dysfunction in MOB individuals.	palmidrol	0-21	sphingomyelin synthase 1	Homo sapiens	79-82
28619329-0	2017	Palmitoylethanolamide (PEA): A promising biomarker for coronary dysfunction in MOB individuals.	palmidrol	23-26	sphingomyelin synthase 1	Homo sapiens	79-82
28336953-0	2017	Palmitoylethanolamide induces microglia changes associated with increased migration and phagocytic activity: involvement of the CB2 receptor.	palmidrol	0-21	cannabinoid receptor 2	Homo sapiens	128-131
28931663-3	2017	Cannabinoids inhibit vagal sensory nerve activation and the cough reflex, so it was hypothesised that FAAH inhibition would produce antitussive activity via elevation of endocannabinoids.Primary vagal ganglia neurons, tissue bioassay, in vivo electrophysiology and a conscious guinea pig cough model were utilised to investigate a role for fatty acid amides in modulating sensory nerve activation in vagal afferents.FAAH inhibition produced antitussive activity in guinea pigs with concomitant plasma elevation of the fatty acid amides N-arachidonoylethanolamide (anandamide), palmitoylethanolamide, N-oleoylethanolamide and linoleoylethanolamide.	palmidrol	577-598	fatty-acid amide hydrolase 1	Cavia porcellus	102-106
28237711-5	2017	Systemic administration of the FAAH inhibitor PF3845 increased levels of AEA, and related FAAH substrates N-oleoylethanolamide (OEA) and N-palmitoylethanolamide (PEA), in the frontal cortex and hippocampus of rats, an effect associated with an attenuation in the expression of pro- and anti-inflammatory cytokines and mediators measured 2hrs following systemic administration of the TLR4 agonist, lipopolysaccharide (LPS).	palmidrol	137-160	fatty-acid amide hydrolase-like	Rattus norvegicus	31-35
28237711-5	2017	Systemic administration of the FAAH inhibitor PF3845 increased levels of AEA, and related FAAH substrates N-oleoylethanolamide (OEA) and N-palmitoylethanolamide (PEA), in the frontal cortex and hippocampus of rats, an effect associated with an attenuation in the expression of pro- and anti-inflammatory cytokines and mediators measured 2hrs following systemic administration of the TLR4 agonist, lipopolysaccharide (LPS).	palmidrol	162-165	fatty-acid amide hydrolase-like	Rattus norvegicus	31-35
27916440-4	2017	Formalin injection reduced levels of the endogenous PPAR ligands N-palmitoylethanolamide (PEA) and N-oleoylethanolamide (OEA) in the lateral(l) PAG of SD rats, but not WKY rats which exhibited higher levels of these analytes compared with formalin-injected SD counterparts.	palmidrol	65-88	peroxisome proliferator activated receptor alpha	Rattus norvegicus	52-56
27989579-1	2017	BACKGROUND: Among endocannabinoid (EC)-related mediators, Oleoyl-ethanolamide (OEA) and Palmitoyl-ethanolamide (PEA), two endogenous PPARalpha agonists with lipolytic and anti-inflammatory action, respectively, are being actively investigated.	palmidrol	88-110	peroxisome proliferator activated receptor alpha	Homo sapiens	133-142
27989579-1	2017	BACKGROUND: Among endocannabinoid (EC)-related mediators, Oleoyl-ethanolamide (OEA) and Palmitoyl-ethanolamide (PEA), two endogenous PPARalpha agonists with lipolytic and anti-inflammatory action, respectively, are being actively investigated.	palmidrol	112-115	peroxisome proliferator activated receptor alpha	Homo sapiens	133-142
26642910-8	2017	AEA levels were significantly elevated in all three treatment groups as were palmitoylethanolamide and oleoylethanolamide, which are also substrates for FAAH.	palmidrol	77-98	fatty-acid amide hydrolase-like	Rattus norvegicus	153-157
27916440-4	2017	Formalin injection reduced levels of the endogenous PPAR ligands N-palmitoylethanolamide (PEA) and N-oleoylethanolamide (OEA) in the lateral(l) PAG of SD rats, but not WKY rats which exhibited higher levels of these analytes compared with formalin-injected SD counterparts.	palmidrol	90-93	peroxisome proliferator activated receptor alpha	Rattus norvegicus	52-56
28103941-7	2017	RESULTS: The acute BCCAO/R procedure is followed by increased brain tissue levels of the eCBs 2-arachidonoylglycerol and anandamide, palmitoylethanolamide, an avid ligand of PPAR-alpha, lipoperoxides, type 1 (CB1) and type 2 (CB2) cannabinoid receptors, and COX-2, and decreased brain tissue concentrations of docosahexaenoic acid (DHA), one of the major targets of lipid peroxidation.	palmidrol	133-154	peroxisome proliferator activated receptor alpha	Rattus norvegicus	174-184
27915171-1	2017	The anti-inflammatory effects resulting from raising the levels of palmitoylethanolamide (PEA), an endogenous bioactive lipid, led to envisage N-Acylethanolamine Acid Amidase (NAAA), the cysteine hydrolase mainly responsible for PEA degradation, as an attractive target for small molecule inhibitors.	palmidrol	67-88	N-acylethanolamine acid amidase	Homo sapiens	143-174
27915171-1	2017	The anti-inflammatory effects resulting from raising the levels of palmitoylethanolamide (PEA), an endogenous bioactive lipid, led to envisage N-Acylethanolamine Acid Amidase (NAAA), the cysteine hydrolase mainly responsible for PEA degradation, as an attractive target for small molecule inhibitors.	palmidrol	67-88	N-acylethanolamine acid amidase	Homo sapiens	176-180
27915171-1	2017	The anti-inflammatory effects resulting from raising the levels of palmitoylethanolamide (PEA), an endogenous bioactive lipid, led to envisage N-Acylethanolamine Acid Amidase (NAAA), the cysteine hydrolase mainly responsible for PEA degradation, as an attractive target for small molecule inhibitors.	palmidrol	90-93	N-acylethanolamine acid amidase	Homo sapiens	143-174
27915171-1	2017	The anti-inflammatory effects resulting from raising the levels of palmitoylethanolamide (PEA), an endogenous bioactive lipid, led to envisage N-Acylethanolamine Acid Amidase (NAAA), the cysteine hydrolase mainly responsible for PEA degradation, as an attractive target for small molecule inhibitors.	palmidrol	90-93	N-acylethanolamine acid amidase	Homo sapiens	176-180
28103941-7	2017	RESULTS: The acute BCCAO/R procedure is followed by increased brain tissue levels of the eCBs 2-arachidonoylglycerol and anandamide, palmitoylethanolamide, an avid ligand of PPAR-alpha, lipoperoxides, type 1 (CB1) and type 2 (CB2) cannabinoid receptors, and COX-2, and decreased brain tissue concentrations of docosahexaenoic acid (DHA), one of the major targets of lipid peroxidation.	palmidrol	133-154	cannabinoid receptor 1	Rattus norvegicus	209-212
28103941-7	2017	RESULTS: The acute BCCAO/R procedure is followed by increased brain tissue levels of the eCBs 2-arachidonoylglycerol and anandamide, palmitoylethanolamide, an avid ligand of PPAR-alpha, lipoperoxides, type 1 (CB1) and type 2 (CB2) cannabinoid receptors, and COX-2, and decreased brain tissue concentrations of docosahexaenoic acid (DHA), one of the major targets of lipid peroxidation.	palmidrol	133-154	cannabinoid receptor 2	Rattus norvegicus	226-229
28103941-7	2017	RESULTS: The acute BCCAO/R procedure is followed by increased brain tissue levels of the eCBs 2-arachidonoylglycerol and anandamide, palmitoylethanolamide, an avid ligand of PPAR-alpha, lipoperoxides, type 1 (CB1) and type 2 (CB2) cannabinoid receptors, and COX-2, and decreased brain tissue concentrations of docosahexaenoic acid (DHA), one of the major targets of lipid peroxidation.	palmidrol	133-154	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	258-263
28826538-7	2017	This has been best investigated for the endocannabinoid-like compounds palmitoylethanolamide and oleoylethanolamine acting at PPARalpha, and for phytocannabinoids or their derivatives activation acting at PPARgamma.	palmidrol	71-92	peroxisome proliferator activated receptor alpha	Homo sapiens	126-135
28861501-0	2017	Palmitoylethanolamide Modulates GPR55 Receptor Signaling in the Ventral Hippocampus to Regulate Mesolimbic Dopamine Activity, Social Interaction, and Memory Processing.	palmidrol	0-21	G protein-coupled receptor 55	Rattus norvegicus	32-37
28861501-5	2017	Materials and Methods: Using a combination of in vivo electrophysiology and behavioral pharmacological assays in rats, we tested whether intra-vHipp activation of GPR55 receptor transmission with the fatty acid amide, palmitoylethanolamide (PEA), a lipid neuromodulator with agonist actions at the GPR55 receptor, may modulate mesolimbic dopaminergic activity states.	palmidrol	218-239	G protein-coupled receptor 55	Rattus norvegicus	163-168
27693242-1	2016	N-Acylethanolamine acid amidase (NAAA) is a lysosomal enzyme, hydrolyzing various bioactive N-acylethanolamines with a preference for palmitoylethanolamide.	palmidrol	134-155	N-acylethanolamine acid amidase	Homo sapiens	0-31
27693242-1	2016	N-Acylethanolamine acid amidase (NAAA) is a lysosomal enzyme, hydrolyzing various bioactive N-acylethanolamines with a preference for palmitoylethanolamide.	palmidrol	134-155	N-acylethanolamine acid amidase	Homo sapiens	33-37
25598150-0	2016	The anti-inflammatory mediator palmitoylethanolamide enhances the levels of 2-arachidonoyl-glycerol and potentiates its actions at TRPV1 cation channels.	palmidrol	31-52	transient receptor potential cation channel subfamily V member 1	Homo sapiens	131-136
27649266-0	2016	N-palmitoylethanolamide in the anterior cingulate cortex attenuates inflammatory pain behaviour indirectly via a CB1 receptor-mediated mechanism.	palmidrol	0-23	cannabinoid receptor 1	Rattus norvegicus	113-116
27911411-4	2016	NAAA is a cysteine hydrolase that promotes inflammation by deactivating endogenous peroxisome proliferator-activated receptor (PPAR)-alpha agonists such as palmitoylethanolamide (PEA) and oleoylethanolamide (OEA).	palmidrol	156-177	N-acylethanolamine acid amidase	Homo sapiens	0-4
27911411-4	2016	NAAA is a cysteine hydrolase that promotes inflammation by deactivating endogenous peroxisome proliferator-activated receptor (PPAR)-alpha agonists such as palmitoylethanolamide (PEA) and oleoylethanolamide (OEA).	palmidrol	156-177	peroxisome proliferator activated receptor alpha	Homo sapiens	83-138
27720681-0	2016	Palmitoylethanolamide reduces inflammation and itch in a mouse model of contact allergic dermatitis.	palmidrol	0-21	itchy, E3 ubiquitin protein ligase	Mus musculus	47-51
27720681-2	2016	Palmitoylethanolamide (PEA), an endogenous anti-inflammatory molecule, acts by down-modulating MCs following activation of the cannabinoid CB2 receptor and peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	0-21	cannabinoid receptor 2 (macrophage)	Mus musculus	139-142
27720681-2	2016	Palmitoylethanolamide (PEA), an endogenous anti-inflammatory molecule, acts by down-modulating MCs following activation of the cannabinoid CB2 receptor and peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Mus musculus	156-204
27720681-2	2016	Palmitoylethanolamide (PEA), an endogenous anti-inflammatory molecule, acts by down-modulating MCs following activation of the cannabinoid CB2 receptor and peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Mus musculus	206-216
27720681-2	2016	Palmitoylethanolamide (PEA), an endogenous anti-inflammatory molecule, acts by down-modulating MCs following activation of the cannabinoid CB2 receptor and peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	23-26	cannabinoid receptor 2 (macrophage)	Mus musculus	139-142
27720681-2	2016	Palmitoylethanolamide (PEA), an endogenous anti-inflammatory molecule, acts by down-modulating MCs following activation of the cannabinoid CB2 receptor and peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	23-26	peroxisome proliferator activated receptor alpha	Mus musculus	156-204
27720681-2	2016	Palmitoylethanolamide (PEA), an endogenous anti-inflammatory molecule, acts by down-modulating MCs following activation of the cannabinoid CB2 receptor and peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	23-26	peroxisome proliferator activated receptor alpha	Mus musculus	206-216
27571266-1	2016	The membrane-associated enzyme NAPE-PLD (N-acyl phosphatidylethanolamine specific-phospholipase D) generates the endogenous cannabinoid arachidonylethanolamide and other lipid signaling amides, including oleoylethanolamide and palmitoylethanolamide.	palmidrol	227-248	N-acyl phosphatidylethanolamine phospholipase D	Homo sapiens	31-39
27571266-1	2016	The membrane-associated enzyme NAPE-PLD (N-acyl phosphatidylethanolamine specific-phospholipase D) generates the endogenous cannabinoid arachidonylethanolamide and other lipid signaling amides, including oleoylethanolamide and palmitoylethanolamide.	palmidrol	227-248	N-acyl phosphatidylethanolamine phospholipase D	Homo sapiens	41-97
27219328-0	2016	Palmitoylethanolamide Modulates Inflammation-Associated Vascular Endothelial Growth Factor (VEGF) Signaling via the Akt/mTOR Pathway in a Selective Peroxisome Proliferator-Activated Receptor Alpha (PPAR-alpha)-Dependent Manner.	palmidrol	0-21	vascular endothelial growth factor A	Homo sapiens	56-90
27219328-0	2016	Palmitoylethanolamide Modulates Inflammation-Associated Vascular Endothelial Growth Factor (VEGF) Signaling via the Akt/mTOR Pathway in a Selective Peroxisome Proliferator-Activated Receptor Alpha (PPAR-alpha)-Dependent Manner.	palmidrol	0-21	vascular endothelial growth factor A	Homo sapiens	92-96
27219328-0	2016	Palmitoylethanolamide Modulates Inflammation-Associated Vascular Endothelial Growth Factor (VEGF) Signaling via the Akt/mTOR Pathway in a Selective Peroxisome Proliferator-Activated Receptor Alpha (PPAR-alpha)-Dependent Manner.	palmidrol	0-21	AKT serine/threonine kinase 1	Homo sapiens	116-119
27219328-0	2016	Palmitoylethanolamide Modulates Inflammation-Associated Vascular Endothelial Growth Factor (VEGF) Signaling via the Akt/mTOR Pathway in a Selective Peroxisome Proliferator-Activated Receptor Alpha (PPAR-alpha)-Dependent Manner.	palmidrol	0-21	mechanistic target of rapamycin kinase	Homo sapiens	120-124
27219328-0	2016	Palmitoylethanolamide Modulates Inflammation-Associated Vascular Endothelial Growth Factor (VEGF) Signaling via the Akt/mTOR Pathway in a Selective Peroxisome Proliferator-Activated Receptor Alpha (PPAR-alpha)-Dependent Manner.	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Homo sapiens	148-196
27219328-0	2016	Palmitoylethanolamide Modulates Inflammation-Associated Vascular Endothelial Growth Factor (VEGF) Signaling via the Akt/mTOR Pathway in a Selective Peroxisome Proliferator-Activated Receptor Alpha (PPAR-alpha)-Dependent Manner.	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Homo sapiens	198-208
27616549-2	2016	Palmitoylethanolamide (PEA), an endogenous N-acylethanolamine, has been shown to be a neuroprotective and anti-inflammatory molecule, acting as a peroxisome proliferator activated receptor (PPAR)-alpha agonist.	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Mus musculus	190-201
27616549-2	2016	Palmitoylethanolamide (PEA), an endogenous N-acylethanolamine, has been shown to be a neuroprotective and anti-inflammatory molecule, acting as a peroxisome proliferator activated receptor (PPAR)-alpha agonist.	palmidrol	23-26	peroxisome proliferator activated receptor alpha	Mus musculus	190-201
26929026-0	2016	Palmitoylethanolamide Exerts Antiproliferative Effect and Downregulates VEGF Signaling in Caco-2 Human Colon Carcinoma Cell Line Through a Selective PPAR-alpha-Dependent Inhibition of Akt/mTOR Pathway.	palmidrol	0-21	vascular endothelial growth factor A	Homo sapiens	72-76
26929026-0	2016	Palmitoylethanolamide Exerts Antiproliferative Effect and Downregulates VEGF Signaling in Caco-2 Human Colon Carcinoma Cell Line Through a Selective PPAR-alpha-Dependent Inhibition of Akt/mTOR Pathway.	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Homo sapiens	149-159
26929026-0	2016	Palmitoylethanolamide Exerts Antiproliferative Effect and Downregulates VEGF Signaling in Caco-2 Human Colon Carcinoma Cell Line Through a Selective PPAR-alpha-Dependent Inhibition of Akt/mTOR Pathway.	palmidrol	0-21	AKT serine/threonine kinase 1	Homo sapiens	184-187
26929026-0	2016	Palmitoylethanolamide Exerts Antiproliferative Effect and Downregulates VEGF Signaling in Caco-2 Human Colon Carcinoma Cell Line Through a Selective PPAR-alpha-Dependent Inhibition of Akt/mTOR Pathway.	palmidrol	0-21	mechanistic target of rapamycin kinase	Homo sapiens	188-192
25598150-1	2016	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA) is an endogenous congener of anandamide and potentiates its actions at cannabinoid CB1 and CB2 receptors, and at transient receptor potential vanilloid type-1 (TRPV1) channels.	palmidrol	47-50	cannabinoid receptor 1	Homo sapiens	135-138
25598150-1	2016	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA) is an endogenous congener of anandamide and potentiates its actions at cannabinoid CB1 and CB2 receptors, and at transient receptor potential vanilloid type-1 (TRPV1) channels.	palmidrol	47-50	cannabinoid receptor 2	Homo sapiens	143-146
25598150-1	2016	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA) is an endogenous congener of anandamide and potentiates its actions at cannabinoid CB1 and CB2 receptors, and at transient receptor potential vanilloid type-1 (TRPV1) channels.	palmidrol	47-50	transient receptor potential cation channel subfamily V member 1	Homo sapiens	165-210
25598150-1	2016	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA) is an endogenous congener of anandamide and potentiates its actions at cannabinoid CB1 and CB2 receptors, and at transient receptor potential vanilloid type-1 (TRPV1) channels.	palmidrol	47-50	transient receptor potential cation channel subfamily V member 1	Homo sapiens	212-217
25598150-1	2016	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA) is an endogenous congener of anandamide and potentiates its actions at cannabinoid CB1 and CB2 receptors, and at transient receptor potential vanilloid type-1 (TRPV1) channels.	palmidrol	24-45	cannabinoid receptor 1	Homo sapiens	135-138
25598150-1	2016	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA) is an endogenous congener of anandamide and potentiates its actions at cannabinoid CB1 and CB2 receptors, and at transient receptor potential vanilloid type-1 (TRPV1) channels.	palmidrol	24-45	cannabinoid receptor 2	Homo sapiens	143-146
25598150-1	2016	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA) is an endogenous congener of anandamide and potentiates its actions at cannabinoid CB1 and CB2 receptors, and at transient receptor potential vanilloid type-1 (TRPV1) channels.	palmidrol	24-45	transient receptor potential cation channel subfamily V member 1	Homo sapiens	165-210
25598150-1	2016	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA) is an endogenous congener of anandamide and potentiates its actions at cannabinoid CB1 and CB2 receptors, and at transient receptor potential vanilloid type-1 (TRPV1) channels.	palmidrol	24-45	transient receptor potential cation channel subfamily V member 1	Homo sapiens	212-217
26769918-1	2016	The endogenous lipid amides, palmitoylethanolamide (PEA) and oleoylethanolamide (OEA), exert marked antinociceptive and anti-inflammatory effects in animal models by engaging nuclear peroxisome proliferator-activated receptor-alpha.	palmidrol	29-50	peroxisome proliferator activated receptor alpha	Rattus norvegicus	183-231
26930716-2	2016	One of these strategies lies in blockade of fatty acid amide hydrolase (FAAH) which catalyzes the degradation of endocannabinoids (anandamide [AEA], 2-arachidonoylglycerol [2-AG]) and endocannabinoid-like substances (N-oleoylethanolamine [OEA], N-palmitoylethanolamine [PEA]).	palmidrol	245-268	fatty acid amide hydrolase	Mus musculus	55-70
26930716-2	2016	One of these strategies lies in blockade of fatty acid amide hydrolase (FAAH) which catalyzes the degradation of endocannabinoids (anandamide [AEA], 2-arachidonoylglycerol [2-AG]) and endocannabinoid-like substances (N-oleoylethanolamine [OEA], N-palmitoylethanolamine [PEA]).	palmidrol	245-268	fatty acid amide hydrolase	Mus musculus	72-76
26930716-2	2016	One of these strategies lies in blockade of fatty acid amide hydrolase (FAAH) which catalyzes the degradation of endocannabinoids (anandamide [AEA], 2-arachidonoylglycerol [2-AG]) and endocannabinoid-like substances (N-oleoylethanolamine [OEA], N-palmitoylethanolamine [PEA]).	palmidrol	270-273	fatty acid amide hydrolase	Mus musculus	55-70
26930716-2	2016	One of these strategies lies in blockade of fatty acid amide hydrolase (FAAH) which catalyzes the degradation of endocannabinoids (anandamide [AEA], 2-arachidonoylglycerol [2-AG]) and endocannabinoid-like substances (N-oleoylethanolamine [OEA], N-palmitoylethanolamine [PEA]).	palmidrol	270-273	fatty acid amide hydrolase	Mus musculus	72-76
26769918-1	2016	The endogenous lipid amides, palmitoylethanolamide (PEA) and oleoylethanolamide (OEA), exert marked antinociceptive and anti-inflammatory effects in animal models by engaging nuclear peroxisome proliferator-activated receptor-alpha.	palmidrol	52-55	peroxisome proliferator activated receptor alpha	Rattus norvegicus	183-231
26370914-0	2015	Palmitoylethanolamide attenuates PTZ-induced seizures through CB1 and CB2 receptors.	palmidrol	0-21	cannabinoid receptor 1	Rattus norvegicus	62-65
27245900-2	2016	Since NAAA prefers anti-inflammatory and analgesic palmitoylethanolamide to other N-acylethanolamines as a substrate, its specific inhibitors are expected as a new class of anti-inflammatory and analgesic agents.	palmidrol	51-72	N-acylethanolamine acid amidase	Homo sapiens	6-10
26370914-0	2015	Palmitoylethanolamide attenuates PTZ-induced seizures through CB1 and CB2 receptors.	palmidrol	0-21	cannabinoid receptor 2	Rattus norvegicus	70-73
26263913-2	2015	The present study focused on inhibitors of the enzyme fatty acid amide hydrolase (FAAH), which catalyzes the degradation of endocannabinoids (anandamide, 2-arachidonoylglycerol) and endocannabinoid-like substances (N-oleoylethanolamine, N-palmitoylethanolamine).	palmidrol	237-260	fatty acid amide hydrolase	Homo sapiens	82-86
26102511-1	2015	N-Acylethanolamine acid amidase (NAAA) is a lysosomal cysteine hydrolase involved in the degradation of saturated and monounsaturated fatty acid ethanolamides (FAEs), a family of endogenous lipid signaling molecules that includes oleoylethanolamide (OEA) and palmitoylethanolamide (PEA).	palmidrol	259-280	N-acylethanolamine acid amidase	Homo sapiens	0-31
26297326-1	2015	RATIONALE: Fatty acid amide hydrolase (FAAH) inhibition elevates anandamide (AEA), which acts on cannabinoid (CB1 and CB2) receptors, as well as N-palmitoylethanolamide (PEA) and N-oleoylethanolamine (OEA), which act on peroxisome proliferator-activated receptor alpha (PPARalpha).	palmidrol	145-168	fatty-acid amide hydrolase-like	Rattus norvegicus	11-37
26297326-1	2015	RATIONALE: Fatty acid amide hydrolase (FAAH) inhibition elevates anandamide (AEA), which acts on cannabinoid (CB1 and CB2) receptors, as well as N-palmitoylethanolamide (PEA) and N-oleoylethanolamine (OEA), which act on peroxisome proliferator-activated receptor alpha (PPARalpha).	palmidrol	145-168	fatty-acid amide hydrolase-like	Rattus norvegicus	39-43
26297326-1	2015	RATIONALE: Fatty acid amide hydrolase (FAAH) inhibition elevates anandamide (AEA), which acts on cannabinoid (CB1 and CB2) receptors, as well as N-palmitoylethanolamide (PEA) and N-oleoylethanolamine (OEA), which act on peroxisome proliferator-activated receptor alpha (PPARalpha).	palmidrol	170-173	fatty-acid amide hydrolase-like	Rattus norvegicus	11-37
26297326-1	2015	RATIONALE: Fatty acid amide hydrolase (FAAH) inhibition elevates anandamide (AEA), which acts on cannabinoid (CB1 and CB2) receptors, as well as N-palmitoylethanolamide (PEA) and N-oleoylethanolamine (OEA), which act on peroxisome proliferator-activated receptor alpha (PPARalpha).	palmidrol	170-173	fatty-acid amide hydrolase-like	Rattus norvegicus	39-43
26102511-1	2015	N-Acylethanolamine acid amidase (NAAA) is a lysosomal cysteine hydrolase involved in the degradation of saturated and monounsaturated fatty acid ethanolamides (FAEs), a family of endogenous lipid signaling molecules that includes oleoylethanolamide (OEA) and palmitoylethanolamide (PEA).	palmidrol	259-280	N-acylethanolamine acid amidase	Homo sapiens	33-37
26102511-1	2015	N-Acylethanolamine acid amidase (NAAA) is a lysosomal cysteine hydrolase involved in the degradation of saturated and monounsaturated fatty acid ethanolamides (FAEs), a family of endogenous lipid signaling molecules that includes oleoylethanolamide (OEA) and palmitoylethanolamide (PEA).	palmidrol	282-285	N-acylethanolamine acid amidase	Homo sapiens	0-31
26102511-1	2015	N-Acylethanolamine acid amidase (NAAA) is a lysosomal cysteine hydrolase involved in the degradation of saturated and monounsaturated fatty acid ethanolamides (FAEs), a family of endogenous lipid signaling molecules that includes oleoylethanolamide (OEA) and palmitoylethanolamide (PEA).	palmidrol	282-285	N-acylethanolamine acid amidase	Homo sapiens	33-37
25951330-0	2015	Palmitoylethanolamide treatment reduces blood pressure in spontaneously hypertensive rats: involvement of cytochrome p450-derived eicosanoids and renin angiotensin system.	palmidrol	0-21	renin	Rattus norvegicus	146-151
25917763-6	2015	As could be expected, brain concentrations of AEA, palmitoylethanolamide (PEA) and oleoylethanolamide (OEA) were elevated in FAAH-null mice, while 2-arachidonoylglycerol (2-AG) concentrations remained unaltered.	palmidrol	51-72	fatty acid amide hydrolase	Mus musculus	125-129
25917763-6	2015	As could be expected, brain concentrations of AEA, palmitoylethanolamide (PEA) and oleoylethanolamide (OEA) were elevated in FAAH-null mice, while 2-arachidonoylglycerol (2-AG) concentrations remained unaltered.	palmidrol	74-77	fatty acid amide hydrolase	Mus musculus	125-129
25912618-1	2015	We have recently shown that PPAR alpha agonists induce N-oleoylethanolamide (OEA) and N-palmitoylethanolamide (PEA) biosynthesis.	palmidrol	86-109	peroxisome proliferator activated receptor alpha	Rattus norvegicus	28-38
25912618-1	2015	We have recently shown that PPAR alpha agonists induce N-oleoylethanolamide (OEA) and N-palmitoylethanolamide (PEA) biosynthesis.	palmidrol	111-114	peroxisome proliferator activated receptor alpha	Rattus norvegicus	28-38
25651941-9	2015	Application of OEA, palmitoylethanolamide (both PPARalpha mediated) or virodhamine (all 10 muM) decreased the OGD-induced increase in permeability during reperfusion.	palmidrol	20-41	peroxisome proliferator activated receptor alpha	Homo sapiens	48-57
26311517-4	2015	FINDINGS: Mice lacking FABP5 and FABP7, which exhibit highest affinities for endocannabinoids, possessed elevated levels of the endocannabinoid anandamide and the related N-acylethanolamines palmitoylethanolamide and oleoylethanolamide.	palmidrol	191-212	fatty acid binding protein 5, epidermal	Mus musculus	23-28
26311517-4	2015	FINDINGS: Mice lacking FABP5 and FABP7, which exhibit highest affinities for endocannabinoids, possessed elevated levels of the endocannabinoid anandamide and the related N-acylethanolamines palmitoylethanolamide and oleoylethanolamide.	palmidrol	191-212	fatty acid binding protein 7, brain	Mus musculus	33-38
25874594-1	2015	Fatty acid ethanolamides such as palmitoylethanolamide (PEA) and oleoylethanolamide (OEA) are lipid-derived mediators that potently inhibit pain and inflammation by ligating type-alpha peroxisome proliferator-activated receptors (PPAR-alpha).	palmidrol	33-54	peroxisome proliferator activated receptor alpha	Homo sapiens	230-240
25874594-1	2015	Fatty acid ethanolamides such as palmitoylethanolamide (PEA) and oleoylethanolamide (OEA) are lipid-derived mediators that potently inhibit pain and inflammation by ligating type-alpha peroxisome proliferator-activated receptors (PPAR-alpha).	palmidrol	56-59	peroxisome proliferator activated receptor alpha	Homo sapiens	230-240
25903129-5	2015	In this study, we found that the potency of GLP-1, not exendin 4, is specifically enhanced by the endocannabinoid-like lipids oleoylethanolamide (OEA) and 2-oleoylglycerol but not by stearoylethanolamide (SEA) or palmitoylethanolamide.	palmidrol	213-234	glucagon	Homo sapiens	44-49
25519724-2	2015	Accordingly, inhibition of fatty acid amide hydrolase (FAAH), a degrading enzyme of the endocannabinoids N-arachidonoylethanolamine (anandamide; AEA) and 2-arachidonoylglycerol (2-AG) as well as of the endocannabinoid-like substances N-oleoylethanolamine (OEA) and N-palmitoylethanolamine (PEA), can cause augmented endogenous cannabinoid tone.	palmidrol	265-288	fatty acid amide hydrolase	Homo sapiens	55-59
25855974-13	2015	In vivo insulin sensitivity decreased by 31.3+-12.1% (P&lt;0.05), concomitant with a decrease in plasma 2-arachidonoyl glycerol (from 39.1+-5.2 to 15.7+-2.0 nmol/L) but not anandamide, oleoyl ethanolamide, linoleoyl ethanolamide, or palmitoyl ethanolamide.	palmidrol	233-255	insulin	Canis lupus familiaris	8-15
25775474-5	2015	RESULTS: Rats on Hsn-2 PA diet had lower levels of anandamide with concomitant increase of its congener palmitoylethanolamide and its precursor PA into visceral adipose tissue phospholipids.	palmidrol	104-125	WNK lysine deficient protein kinase 1	Rattus norvegicus	17-22
25596343-7	2015	When HEK293 cells were metabolically labeled with N-[(14)C]palmitoylethanolamine lysophospholipid, the transient expression of GDE4 increased the [(14)C]palmitoylethanolamide level, while the knockdown of endogenous GDE4 decreased this level.	palmidrol	153-174	glycerophosphodiester phosphodiesterase domain containing 1	Homo sapiens	127-131
25519724-2	2015	Accordingly, inhibition of fatty acid amide hydrolase (FAAH), a degrading enzyme of the endocannabinoids N-arachidonoylethanolamine (anandamide; AEA) and 2-arachidonoylglycerol (2-AG) as well as of the endocannabinoid-like substances N-oleoylethanolamine (OEA) and N-palmitoylethanolamine (PEA), can cause augmented endogenous cannabinoid tone.	palmidrol	290-293	fatty acid amide hydrolase	Homo sapiens	55-59
24818658-0	2014	Palmitoylethanolamide normalizes intestinal motility in a model of post-inflammatory accelerated transit: involvement of CB1 receptors and TRPV1 channels.	palmidrol	0-21	cannabinoid receptor 1 (brain)	Mus musculus	121-124
25205418-1	2015	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA) acts via several targets, including cannabinoid CB1 and CB2 receptors, transient receptor potential vanilloid type-1 (TRPV1) ion channels, peroxisome proliferator-activated receptor alpha (PPAR alpha) and orphan G protein-coupled receptor 55 (GRR55), all involved in the control of intestinal inflammation.	palmidrol	24-45	cannabinoid receptor 1 (brain)	Mus musculus	100-103
25205418-1	2015	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA) acts via several targets, including cannabinoid CB1 and CB2 receptors, transient receptor potential vanilloid type-1 (TRPV1) ion channels, peroxisome proliferator-activated receptor alpha (PPAR alpha) and orphan G protein-coupled receptor 55 (GRR55), all involved in the control of intestinal inflammation.	palmidrol	24-45	cannabinoid receptor 2 (macrophage)	Mus musculus	108-111
25205418-1	2015	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA) acts via several targets, including cannabinoid CB1 and CB2 receptors, transient receptor potential vanilloid type-1 (TRPV1) ion channels, peroxisome proliferator-activated receptor alpha (PPAR alpha) and orphan G protein-coupled receptor 55 (GRR55), all involved in the control of intestinal inflammation.	palmidrol	24-45	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	123-168
25205418-1	2015	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA) acts via several targets, including cannabinoid CB1 and CB2 receptors, transient receptor potential vanilloid type-1 (TRPV1) ion channels, peroxisome proliferator-activated receptor alpha (PPAR alpha) and orphan G protein-coupled receptor 55 (GRR55), all involved in the control of intestinal inflammation.	palmidrol	24-45	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	170-175
25205418-1	2015	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA) acts via several targets, including cannabinoid CB1 and CB2 receptors, transient receptor potential vanilloid type-1 (TRPV1) ion channels, peroxisome proliferator-activated receptor alpha (PPAR alpha) and orphan G protein-coupled receptor 55 (GRR55), all involved in the control of intestinal inflammation.	palmidrol	24-45	peroxisome proliferator activated receptor alpha	Mus musculus	191-239
25205418-1	2015	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA) acts via several targets, including cannabinoid CB1 and CB2 receptors, transient receptor potential vanilloid type-1 (TRPV1) ion channels, peroxisome proliferator-activated receptor alpha (PPAR alpha) and orphan G protein-coupled receptor 55 (GRR55), all involved in the control of intestinal inflammation.	palmidrol	24-45	peroxisome proliferator activated receptor alpha	Mus musculus	241-251
25205418-1	2015	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA) acts via several targets, including cannabinoid CB1 and CB2 receptors, transient receptor potential vanilloid type-1 (TRPV1) ion channels, peroxisome proliferator-activated receptor alpha (PPAR alpha) and orphan G protein-coupled receptor 55 (GRR55), all involved in the control of intestinal inflammation.	palmidrol	47-50	cannabinoid receptor 1 (brain)	Mus musculus	100-103
25205418-1	2015	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA) acts via several targets, including cannabinoid CB1 and CB2 receptors, transient receptor potential vanilloid type-1 (TRPV1) ion channels, peroxisome proliferator-activated receptor alpha (PPAR alpha) and orphan G protein-coupled receptor 55 (GRR55), all involved in the control of intestinal inflammation.	palmidrol	47-50	cannabinoid receptor 2 (macrophage)	Mus musculus	108-111
25205418-1	2015	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA) acts via several targets, including cannabinoid CB1 and CB2 receptors, transient receptor potential vanilloid type-1 (TRPV1) ion channels, peroxisome proliferator-activated receptor alpha (PPAR alpha) and orphan G protein-coupled receptor 55 (GRR55), all involved in the control of intestinal inflammation.	palmidrol	47-50	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	123-168
25548106-8	2014	Pretreatment with oleoylethanolamide/ palmitoylethanolamide reduced plasma tumor necrosis factor-alpha levels after lipopolysaccharide, but only oleoylethanolamide significantly reduced brain tumor necrosis factor-alpha mRNA.	palmidrol	38-59	tumor necrosis factor	Rattus norvegicus	75-102
25548106-9	2014	Oleoylethanolamide and palmitoylethanolamide prevented lipopolysaccharide-induced nuclear transcription factor-kappaB (NF-kappaB)/IkappaBalpha upregulation in nuclear and cytosolic extracts, respectively, the expression of inducible isoforms of nitric oxide synthase, cyclooxygenase-2, and microsomal prostaglandin E2 synthase and the levels of prostaglandin E2.	palmidrol	23-44	NFKB inhibitor alpha	Rattus norvegicus	130-142
25548106-9	2014	Oleoylethanolamide and palmitoylethanolamide prevented lipopolysaccharide-induced nuclear transcription factor-kappaB (NF-kappaB)/IkappaBalpha upregulation in nuclear and cytosolic extracts, respectively, the expression of inducible isoforms of nitric oxide synthase, cyclooxygenase-2, and microsomal prostaglandin E2 synthase and the levels of prostaglandin E2.	palmidrol	23-44	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	268-284
25245162-3	2014	administration of the FAAH inhibitor URB597 increased hippocampal levels of the N-acylethanolamines palmitoylethanolamide and oleoylethanolamide, but not anandamide.	palmidrol	100-121	fatty-acid amide hydrolase-like	Rattus norvegicus	22-26
24952959-1	2014	Palmitoylethanolamide (PEA) is a peroxisome proliferator-activated receptor alpha (PPAR-alpha) ligand that exerts anti-inflammatory, analgesic and neuroprotective actions.	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Homo sapiens	33-81
24952959-1	2014	Palmitoylethanolamide (PEA) is a peroxisome proliferator-activated receptor alpha (PPAR-alpha) ligand that exerts anti-inflammatory, analgesic and neuroprotective actions.	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Homo sapiens	83-93
24952959-1	2014	Palmitoylethanolamide (PEA) is a peroxisome proliferator-activated receptor alpha (PPAR-alpha) ligand that exerts anti-inflammatory, analgesic and neuroprotective actions.	palmidrol	23-26	peroxisome proliferator activated receptor alpha	Homo sapiens	33-81
24952959-1	2014	Palmitoylethanolamide (PEA) is a peroxisome proliferator-activated receptor alpha (PPAR-alpha) ligand that exerts anti-inflammatory, analgesic and neuroprotective actions.	palmidrol	23-26	peroxisome proliferator activated receptor alpha	Homo sapiens	83-93
24952959-3	2014	Here, we review the impact of PEA administration in inflammatory and neurodegenerative settings and the differential role of FAAH and NAAA in controlling PEA levels.	palmidrol	154-157	fatty acid amide hydrolase	Homo sapiens	125-129
24952959-3	2014	Here, we review the impact of PEA administration in inflammatory and neurodegenerative settings and the differential role of FAAH and NAAA in controlling PEA levels.	palmidrol	154-157	N-acylethanolamine acid amidase	Homo sapiens	134-138
24818658-1	2014	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA), a naturally occurring acylethanolamide chemically related to the endocannabinoid anandamide, interacts with targets that have been identified in peripheral nerves controlling gastrointestinal motility, such as cannabinoid CB1 and CB2 receptors, TRPV1 channels and PPARalpha.	palmidrol	24-45	peroxisome proliferator activated receptor alpha	Mus musculus	317-326
24818658-1	2014	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA), a naturally occurring acylethanolamide chemically related to the endocannabinoid anandamide, interacts with targets that have been identified in peripheral nerves controlling gastrointestinal motility, such as cannabinoid CB1 and CB2 receptors, TRPV1 channels and PPARalpha.	palmidrol	47-50	cannabinoid receptor 1 (brain)	Mus musculus	275-278
24818658-1	2014	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA), a naturally occurring acylethanolamide chemically related to the endocannabinoid anandamide, interacts with targets that have been identified in peripheral nerves controlling gastrointestinal motility, such as cannabinoid CB1 and CB2 receptors, TRPV1 channels and PPARalpha.	palmidrol	47-50	cannabinoid receptor 2 (macrophage)	Mus musculus	283-286
24818658-1	2014	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA), a naturally occurring acylethanolamide chemically related to the endocannabinoid anandamide, interacts with targets that have been identified in peripheral nerves controlling gastrointestinal motility, such as cannabinoid CB1 and CB2 receptors, TRPV1 channels and PPARalpha.	palmidrol	47-50	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	298-303
24818658-1	2014	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA), a naturally occurring acylethanolamide chemically related to the endocannabinoid anandamide, interacts with targets that have been identified in peripheral nerves controlling gastrointestinal motility, such as cannabinoid CB1 and CB2 receptors, TRPV1 channels and PPARalpha.	palmidrol	47-50	peroxisome proliferator activated receptor alpha	Mus musculus	317-326
25384424-0	2015	N-Acylethanolamine-hydrolyzing acid amidase inhibition increases colon N-palmitoylethanolamine levels and counteracts murine colitis.	palmidrol	71-94	N-acylethanolamine acid amidase	Mus musculus	0-43
25384424-1	2015	N-Palmitoylethanolamine or palmitoylethanolamide (PEA) is an anti-inflammatory compound that was recently shown to exert peroxisome proliferator-activated receptor-alpha-dependent beneficial effects on colon inflammation.	palmidrol	0-23	peroxisome proliferator activated receptor alpha	Mus musculus	121-169
25384424-1	2015	N-Palmitoylethanolamine or palmitoylethanolamide (PEA) is an anti-inflammatory compound that was recently shown to exert peroxisome proliferator-activated receptor-alpha-dependent beneficial effects on colon inflammation.	palmidrol	27-48	peroxisome proliferator activated receptor alpha	Mus musculus	121-169
25384424-1	2015	N-Palmitoylethanolamine or palmitoylethanolamide (PEA) is an anti-inflammatory compound that was recently shown to exert peroxisome proliferator-activated receptor-alpha-dependent beneficial effects on colon inflammation.	palmidrol	50-53	peroxisome proliferator activated receptor alpha	Mus musculus	121-169
25205418-1	2015	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA) acts via several targets, including cannabinoid CB1 and CB2 receptors, transient receptor potential vanilloid type-1 (TRPV1) ion channels, peroxisome proliferator-activated receptor alpha (PPAR alpha) and orphan G protein-coupled receptor 55 (GRR55), all involved in the control of intestinal inflammation.	palmidrol	47-50	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	170-175
25205418-1	2015	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA) acts via several targets, including cannabinoid CB1 and CB2 receptors, transient receptor potential vanilloid type-1 (TRPV1) ion channels, peroxisome proliferator-activated receptor alpha (PPAR alpha) and orphan G protein-coupled receptor 55 (GRR55), all involved in the control of intestinal inflammation.	palmidrol	47-50	peroxisome proliferator activated receptor alpha	Mus musculus	191-239
25205418-1	2015	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA) acts via several targets, including cannabinoid CB1 and CB2 receptors, transient receptor potential vanilloid type-1 (TRPV1) ion channels, peroxisome proliferator-activated receptor alpha (PPAR alpha) and orphan G protein-coupled receptor 55 (GRR55), all involved in the control of intestinal inflammation.	palmidrol	47-50	peroxisome proliferator activated receptor alpha	Mus musculus	241-251
25135355-5	2014	Interestingly, intracerebroventricular (ICV) infusion of the PPARalpha activator palmitoylethanolamide (PEA) in HF-fed rats for 2weeks normalized spinal PPARalpha expression and activity without altering metabolic parameters.	palmidrol	81-102	peroxisome proliferator activated receptor alpha	Rattus norvegicus	61-70
25135355-5	2014	Interestingly, intracerebroventricular (ICV) infusion of the PPARalpha activator palmitoylethanolamide (PEA) in HF-fed rats for 2weeks normalized spinal PPARalpha expression and activity without altering metabolic parameters.	palmidrol	81-102	peroxisome proliferator activated receptor alpha	Rattus norvegicus	153-162
24818658-0	2014	Palmitoylethanolamide normalizes intestinal motility in a model of post-inflammatory accelerated transit: involvement of CB1 receptors and TRPV1 channels.	palmidrol	0-21	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	139-144
24818658-1	2014	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA), a naturally occurring acylethanolamide chemically related to the endocannabinoid anandamide, interacts with targets that have been identified in peripheral nerves controlling gastrointestinal motility, such as cannabinoid CB1 and CB2 receptors, TRPV1 channels and PPARalpha.	palmidrol	24-45	cannabinoid receptor 1 (brain)	Mus musculus	275-278
24818658-1	2014	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA), a naturally occurring acylethanolamide chemically related to the endocannabinoid anandamide, interacts with targets that have been identified in peripheral nerves controlling gastrointestinal motility, such as cannabinoid CB1 and CB2 receptors, TRPV1 channels and PPARalpha.	palmidrol	24-45	cannabinoid receptor 2 (macrophage)	Mus musculus	283-286
24818658-1	2014	BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA), a naturally occurring acylethanolamide chemically related to the endocannabinoid anandamide, interacts with targets that have been identified in peripheral nerves controlling gastrointestinal motility, such as cannabinoid CB1 and CB2 receptors, TRPV1 channels and PPARalpha.	palmidrol	24-45	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	298-303
24082036-0	2014	Palmitoylethanolamide improves colon inflammation through an enteric glia/toll like receptor 4-dependent PPAR-alpha activation.	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Homo sapiens	105-115
25191225-11	2014	In early clinical research, one PPARalpha agonist, palmitoylethanolamide (PEA), shows promise in relieving chronic pain.	palmidrol	51-72	peroxisome proliferator activated receptor alpha	Homo sapiens	32-41
24828120-1	2014	N-Acylethanolamine acid amidase (NAAA) is a cysteine hydrolase that catalyzes the hydrolysis of endogenous lipid mediators such as palmitoylethanolamide (PEA).	palmidrol	131-152	N-acylethanolamine acid amidase	Homo sapiens	0-31
24798679-1	2014	N-Acylethanolamine acid amidase (NAAA) is a cysteine amidase that hydrolyzes saturated or monounsaturated fatty acid ethanolamides, such as palmitoylethanolamide (PEA) and oleoylethanolamide (OEA).	palmidrol	140-161	N-acylethanolamine acid amidase	Homo sapiens	0-31
24798679-1	2014	N-Acylethanolamine acid amidase (NAAA) is a cysteine amidase that hydrolyzes saturated or monounsaturated fatty acid ethanolamides, such as palmitoylethanolamide (PEA) and oleoylethanolamide (OEA).	palmidrol	140-161	N-acylethanolamine acid amidase	Homo sapiens	33-37
24798679-1	2014	N-Acylethanolamine acid amidase (NAAA) is a cysteine amidase that hydrolyzes saturated or monounsaturated fatty acid ethanolamides, such as palmitoylethanolamide (PEA) and oleoylethanolamide (OEA).	palmidrol	163-166	N-acylethanolamine acid amidase	Homo sapiens	0-31
24798679-1	2014	N-Acylethanolamine acid amidase (NAAA) is a cysteine amidase that hydrolyzes saturated or monounsaturated fatty acid ethanolamides, such as palmitoylethanolamide (PEA) and oleoylethanolamide (OEA).	palmidrol	163-166	N-acylethanolamine acid amidase	Homo sapiens	33-37
24828120-1	2014	N-Acylethanolamine acid amidase (NAAA) is a cysteine hydrolase that catalyzes the hydrolysis of endogenous lipid mediators such as palmitoylethanolamide (PEA).	palmidrol	131-152	N-acylethanolamine acid amidase	Homo sapiens	33-37
24403170-1	2014	N-Acylethanolamine acid amidase (NAAA) is a cysteine amidase that preferentially hydrolyzes saturated or monounsaturated fatty acid ethanolamides (FAEs), such as palmitoylethanolamide (PEA) and oleoylethanolamide (OEA), which are endogenous agonists of nuclear peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	162-183	N-acylethanolamine acid amidase	Homo sapiens	0-31
24303983-8	2014	Furthermore, formalin-evoked nociceptive behaviour was associated with significant reductions in mPFC levels of endogenous PPARalpha ligands (N-palmitoylethanolamide and N-oleoylethanolamide) and a 70% reduction in PPARalpha mRNA but not protein expression.	palmidrol	142-165	peroxisome proliferator activated receptor alpha	Rattus norvegicus	123-132
24403170-1	2014	N-Acylethanolamine acid amidase (NAAA) is a cysteine amidase that preferentially hydrolyzes saturated or monounsaturated fatty acid ethanolamides (FAEs), such as palmitoylethanolamide (PEA) and oleoylethanolamide (OEA), which are endogenous agonists of nuclear peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	185-188	peroxisome proliferator activated receptor alpha	Homo sapiens	261-309
24602801-4	2014	Instead, palmitoylethanolamide (PEA) a member of the fatty acid ethanolamine family, is a novel non-steroidal, kidney friendly anti-inflammatory and anti-fibrotic agent with a well-documented safety profile, that may represent a potential candidate in treating CKD probably by a combination of pharmacological properties, including some activity at the peroxisome proliferator activated receptor alpha (PPAR-alpha).	palmidrol	9-30	peroxisome proliferator activated receptor alpha	Homo sapiens	353-401
24602801-4	2014	Instead, palmitoylethanolamide (PEA) a member of the fatty acid ethanolamine family, is a novel non-steroidal, kidney friendly anti-inflammatory and anti-fibrotic agent with a well-documented safety profile, that may represent a potential candidate in treating CKD probably by a combination of pharmacological properties, including some activity at the peroxisome proliferator activated receptor alpha (PPAR-alpha).	palmidrol	9-30	peroxisome proliferator activated receptor alpha	Homo sapiens	403-413
24602801-4	2014	Instead, palmitoylethanolamide (PEA) a member of the fatty acid ethanolamine family, is a novel non-steroidal, kidney friendly anti-inflammatory and anti-fibrotic agent with a well-documented safety profile, that may represent a potential candidate in treating CKD probably by a combination of pharmacological properties, including some activity at the peroxisome proliferator activated receptor alpha (PPAR-alpha).	palmidrol	32-35	peroxisome proliferator activated receptor alpha	Homo sapiens	353-401
24602801-4	2014	Instead, palmitoylethanolamide (PEA) a member of the fatty acid ethanolamine family, is a novel non-steroidal, kidney friendly anti-inflammatory and anti-fibrotic agent with a well-documented safety profile, that may represent a potential candidate in treating CKD probably by a combination of pharmacological properties, including some activity at the peroxisome proliferator activated receptor alpha (PPAR-alpha).	palmidrol	32-35	peroxisome proliferator activated receptor alpha	Homo sapiens	403-413
24440533-0	2014	Palmitoylethanolamide inhibits rMCP-5 expression by regulating MITF activation in rat chronic granulomatous inflammation.	palmidrol	0-21	chymase 1	Rattus norvegicus	31-37
24440533-0	2014	Palmitoylethanolamide inhibits rMCP-5 expression by regulating MITF activation in rat chronic granulomatous inflammation.	palmidrol	0-21	melanocyte inducing transcription factor	Rattus norvegicus	63-67
24440533-3	2014	In this study, we investigated the effects of palmitoylethanolamide (PEA), an anti-inflammatory and analgesic endogenous compound, on rMCP-5 mRNA expression and Microphtalmia-associated Transcription Factor (MITF) activation in the same model of chronic inflammation.	palmidrol	46-67	chymase 1	Rattus norvegicus	134-140
24433863-2	2014	A potent member of this class, (37), was found to inhibit FAAH centrally, elevate the brain levels of three fatty acid ethanolamides [FAAs: anandamide (AEA), oleoyl ethanolamide (OEA) and palmitoyl ethanolamide (PEA)], and was moderately efficacious in a rat model of neuropathic pain.	palmidrol	188-210	fatty-acid amide hydrolase-like	Rattus norvegicus	58-62
24433863-2	2014	A potent member of this class, (37), was found to inhibit FAAH centrally, elevate the brain levels of three fatty acid ethanolamides [FAAs: anandamide (AEA), oleoyl ethanolamide (OEA) and palmitoyl ethanolamide (PEA)], and was moderately efficacious in a rat model of neuropathic pain.	palmidrol	212-215	fatty-acid amide hydrolase-like	Rattus norvegicus	58-62
24403170-1	2014	N-Acylethanolamine acid amidase (NAAA) is a cysteine amidase that preferentially hydrolyzes saturated or monounsaturated fatty acid ethanolamides (FAEs), such as palmitoylethanolamide (PEA) and oleoylethanolamide (OEA), which are endogenous agonists of nuclear peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	185-188	peroxisome proliferator activated receptor alpha	Homo sapiens	311-321
24403170-1	2014	N-Acylethanolamine acid amidase (NAAA) is a cysteine amidase that preferentially hydrolyzes saturated or monounsaturated fatty acid ethanolamides (FAEs), such as palmitoylethanolamide (PEA) and oleoylethanolamide (OEA), which are endogenous agonists of nuclear peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	162-183	N-acylethanolamine acid amidase	Homo sapiens	33-37
24403170-1	2014	N-Acylethanolamine acid amidase (NAAA) is a cysteine amidase that preferentially hydrolyzes saturated or monounsaturated fatty acid ethanolamides (FAEs), such as palmitoylethanolamide (PEA) and oleoylethanolamide (OEA), which are endogenous agonists of nuclear peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	162-183	peroxisome proliferator activated receptor alpha	Homo sapiens	261-309
24403170-1	2014	N-Acylethanolamine acid amidase (NAAA) is a cysteine amidase that preferentially hydrolyzes saturated or monounsaturated fatty acid ethanolamides (FAEs), such as palmitoylethanolamide (PEA) and oleoylethanolamide (OEA), which are endogenous agonists of nuclear peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	162-183	peroxisome proliferator activated receptor alpha	Homo sapiens	311-321
24403170-1	2014	N-Acylethanolamine acid amidase (NAAA) is a cysteine amidase that preferentially hydrolyzes saturated or monounsaturated fatty acid ethanolamides (FAEs), such as palmitoylethanolamide (PEA) and oleoylethanolamide (OEA), which are endogenous agonists of nuclear peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	185-188	N-acylethanolamine acid amidase	Homo sapiens	0-31
24403170-1	2014	N-Acylethanolamine acid amidase (NAAA) is a cysteine amidase that preferentially hydrolyzes saturated or monounsaturated fatty acid ethanolamides (FAEs), such as palmitoylethanolamide (PEA) and oleoylethanolamide (OEA), which are endogenous agonists of nuclear peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	185-188	N-acylethanolamine acid amidase	Homo sapiens	33-37
23425575-3	2013	In the known metabolic pathway in mammals, anandamide and other bioactive N-acylethanolamines, such as palmitoylethanolamide and oleoylethanolamide, are biosynthesized from glycerophospholipids by a combination of Ca(2+)-dependent N-acyltransferase and N-acyl-phosphatidylethanolamine-hydrolyzing phospholipase D, and are degraded by fatty acid amide hydrolase.	palmidrol	103-124	N-acyl phosphatidylethanolamine phospholipase D	Homo sapiens	253-312
24312564-11	2013	The calcineurin inhibitor ciclosporin and the endogenous "entourage" compound palmitoylethanolamide potentiated the vasodilator response to 2-arachidonoylglycerol, disclosing TRPV1 activation of this monoacylglycerol at nanomolar concentrations.	palmidrol	78-99	transient receptor potential cation channel subfamily V member 1	Homo sapiens	175-180
23917217-2	2013	Palmitoylethanolamide (PEA) is a member of the fatty acid ethanolamine family with profound analgesic and anti-inflammatory effects, resulting from its ability to activate peroxisome proliferator activated receptor (PPAR)alpha.	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Rattus norvegicus	216-226
23917217-2	2013	Palmitoylethanolamide (PEA) is a member of the fatty acid ethanolamine family with profound analgesic and anti-inflammatory effects, resulting from its ability to activate peroxisome proliferator activated receptor (PPAR)alpha.	palmidrol	23-26	peroxisome proliferator activated receptor alpha	Rattus norvegicus	216-226
23578218-2	2013	Measurement of endocannabinoids and related compounds in PRP revealed the presence of a significant amount of anandamide, 2-arachidonoylglycerol, palmitoylethanolamide, and oleoylethanolamide.	palmidrol	146-167	proline rich protein HaeIII subfamily 1	Mus musculus	57-60
23991897-1	2013	N-Acylethanolamine acid amidase (NAAA) is a lysosomal cysteine hydrolase involved in the degradation of saturated and monounsaturated fatty acid ethanolamides (FAEs), a family of endogenous lipid agonists of peroxisome proliferator-activated receptor-alpha, which include oleoylethanolamide (OEA) and palmitoylethanolamide (PEA).	palmidrol	301-322	N-acylethanolamine acid amidase	Homo sapiens	0-31
23991897-1	2013	N-Acylethanolamine acid amidase (NAAA) is a lysosomal cysteine hydrolase involved in the degradation of saturated and monounsaturated fatty acid ethanolamides (FAEs), a family of endogenous lipid agonists of peroxisome proliferator-activated receptor-alpha, which include oleoylethanolamide (OEA) and palmitoylethanolamide (PEA).	palmidrol	301-322	N-acylethanolamine acid amidase	Homo sapiens	33-37
23991897-1	2013	N-Acylethanolamine acid amidase (NAAA) is a lysosomal cysteine hydrolase involved in the degradation of saturated and monounsaturated fatty acid ethanolamides (FAEs), a family of endogenous lipid agonists of peroxisome proliferator-activated receptor-alpha, which include oleoylethanolamide (OEA) and palmitoylethanolamide (PEA).	palmidrol	301-322	peroxisome proliferator activated receptor alpha	Homo sapiens	208-256
23991897-1	2013	N-Acylethanolamine acid amidase (NAAA) is a lysosomal cysteine hydrolase involved in the degradation of saturated and monounsaturated fatty acid ethanolamides (FAEs), a family of endogenous lipid agonists of peroxisome proliferator-activated receptor-alpha, which include oleoylethanolamide (OEA) and palmitoylethanolamide (PEA).	palmidrol	324-327	N-acylethanolamine acid amidase	Homo sapiens	0-31
23991897-1	2013	N-Acylethanolamine acid amidase (NAAA) is a lysosomal cysteine hydrolase involved in the degradation of saturated and monounsaturated fatty acid ethanolamides (FAEs), a family of endogenous lipid agonists of peroxisome proliferator-activated receptor-alpha, which include oleoylethanolamide (OEA) and palmitoylethanolamide (PEA).	palmidrol	324-327	N-acylethanolamine acid amidase	Homo sapiens	33-37
23991897-1	2013	N-Acylethanolamine acid amidase (NAAA) is a lysosomal cysteine hydrolase involved in the degradation of saturated and monounsaturated fatty acid ethanolamides (FAEs), a family of endogenous lipid agonists of peroxisome proliferator-activated receptor-alpha, which include oleoylethanolamide (OEA) and palmitoylethanolamide (PEA).	palmidrol	324-327	peroxisome proliferator activated receptor alpha	Homo sapiens	208-256
23206503-0	2013	Antiepileptic action of N-palmitoylethanolamine through CB1 and PPAR-alpha receptor activation in a genetic model of absence epilepsy.	palmidrol	24-47	cannabinoid receptor 1	Rattus norvegicus	56-59
23206503-0	2013	Antiepileptic action of N-palmitoylethanolamine through CB1 and PPAR-alpha receptor activation in a genetic model of absence epilepsy.	palmidrol	24-47	peroxisome proliferator activated receptor alpha	Rattus norvegicus	64-74
23206503-1	2013	N-palmitoylethanolamine (PEA), an endogenous fatty acid ethanolamide, plays a key role in the regulation of the inflammatory response and pain through, among others, activation of nuclear peroxisome proliferator-activated receptors (PPAR-alpha).	palmidrol	0-23	peroxisome proliferator activated receptor alpha	Rattus norvegicus	233-243
23206503-1	2013	N-palmitoylethanolamine (PEA), an endogenous fatty acid ethanolamide, plays a key role in the regulation of the inflammatory response and pain through, among others, activation of nuclear peroxisome proliferator-activated receptors (PPAR-alpha).	palmidrol	25-28	peroxisome proliferator activated receptor alpha	Rattus norvegicus	233-243
23964161-0	2013	Evolution in pharmacologic thinking around the natural analgesic palmitoylethanolamide: from nonspecific resistance to PPAR-alpha agonist and effective nutraceutical.	palmidrol	65-86	peroxisome proliferator activated receptor alpha	Homo sapiens	119-129
22705310-2	2013	FAAH KO mice and animals treated with FAAH inhibitors are impaired in their ability to hydrolyze AEA and other non-cannabinoid lipid signaling molecules, such as oleoylethanolamide (OEA) and palmitoylethanolamide (PEA).	palmidrol	191-212	fatty acid amide hydrolase	Mus musculus	0-4
22705310-2	2013	FAAH KO mice and animals treated with FAAH inhibitors are impaired in their ability to hydrolyze AEA and other non-cannabinoid lipid signaling molecules, such as oleoylethanolamide (OEA) and palmitoylethanolamide (PEA).	palmidrol	191-212	fatty acid amide hydrolase	Mus musculus	38-42
22705310-2	2013	FAAH KO mice and animals treated with FAAH inhibitors are impaired in their ability to hydrolyze AEA and other non-cannabinoid lipid signaling molecules, such as oleoylethanolamide (OEA) and palmitoylethanolamide (PEA).	palmidrol	214-217	fatty acid amide hydrolase	Mus musculus	0-4
22705310-2	2013	FAAH KO mice and animals treated with FAAH inhibitors are impaired in their ability to hydrolyze AEA and other non-cannabinoid lipid signaling molecules, such as oleoylethanolamide (OEA) and palmitoylethanolamide (PEA).	palmidrol	214-217	fatty acid amide hydrolase	Mus musculus	38-42
23218523-1	2013	Fatty acid ethanolamides (FAEs), which include palmitoylethanolamide (PEA) and oleoylethanolamide (OEA), are endogenous agonists of peroxisome proliferator-activated receptor-alpha (PPAR-alpha) and important regulators of the inflammatory response.	palmidrol	47-68	peroxisome proliferator activated receptor alpha	Mus musculus	132-180
23083124-0	2013	Activation and desensitization of TRPV1 channels in sensory neurons by the PPARalpha agonist palmitoylethanolamide.	palmidrol	93-114	LOW QUALITY PROTEIN: transient receptor potential cation channel subfamily V member 1	Cricetulus griseus	34-39
23083124-0	2013	Activation and desensitization of TRPV1 channels in sensory neurons by the PPARalpha agonist palmitoylethanolamide.	palmidrol	93-114	peroxisome proliferator-activated receptor alpha	Cricetulus griseus	75-84
23218523-1	2013	Fatty acid ethanolamides (FAEs), which include palmitoylethanolamide (PEA) and oleoylethanolamide (OEA), are endogenous agonists of peroxisome proliferator-activated receptor-alpha (PPAR-alpha) and important regulators of the inflammatory response.	palmidrol	47-68	peroxisome proliferator activated receptor alpha	Mus musculus	182-192
23218523-1	2013	Fatty acid ethanolamides (FAEs), which include palmitoylethanolamide (PEA) and oleoylethanolamide (OEA), are endogenous agonists of peroxisome proliferator-activated receptor-alpha (PPAR-alpha) and important regulators of the inflammatory response.	palmidrol	70-73	peroxisome proliferator activated receptor alpha	Mus musculus	132-180
23218523-1	2013	Fatty acid ethanolamides (FAEs), which include palmitoylethanolamide (PEA) and oleoylethanolamide (OEA), are endogenous agonists of peroxisome proliferator-activated receptor-alpha (PPAR-alpha) and important regulators of the inflammatory response.	palmidrol	70-73	peroxisome proliferator activated receptor alpha	Mus musculus	182-192
23241405-5	2013	Serum levels of FAAH substrates anandamide, palmitoylethanolamide (PEA), and oleoylethanolamide (OEA) were 1.4- to 2-fold higher in case of FAAH deficiency.	palmidrol	67-70	fatty acid amide hydrolase	Mus musculus	16-20
23394526-8	2013	Along this line palmitoylethanolamide (PEA) has attracted much attention because of its numerous pharmacological properties, particularly those related to the modulation of peripheral inflammation through the peroxisome proliferator activated receptor-alpha involvement.	palmidrol	16-37	peroxisome proliferator activated receptor alpha	Rattus norvegicus	209-257
23394526-8	2013	Along this line palmitoylethanolamide (PEA) has attracted much attention because of its numerous pharmacological properties, particularly those related to the modulation of peripheral inflammation through the peroxisome proliferator activated receptor-alpha involvement.	palmidrol	39-42	peroxisome proliferator activated receptor alpha	Rattus norvegicus	209-257
23302980-3	2013	In this study, we sought to verify whether the CB1 and CB2 cannabinoid receptor agonists anandamide and N-palmitoyl-ethanolamine (PEA), respectively, are able to induce peripheral antinociception via an adrenergic mechanism.	palmidrol	104-128	cannabinoid receptor 1	Rattus norvegicus	47-50
23302980-3	2013	In this study, we sought to verify whether the CB1 and CB2 cannabinoid receptor agonists anandamide and N-palmitoyl-ethanolamine (PEA), respectively, are able to induce peripheral antinociception via an adrenergic mechanism.	palmidrol	104-128	cannabinoid receptor 2	Rattus norvegicus	55-58
23302980-3	2013	In this study, we sought to verify whether the CB1 and CB2 cannabinoid receptor agonists anandamide and N-palmitoyl-ethanolamine (PEA), respectively, are able to induce peripheral antinociception via an adrenergic mechanism.	palmidrol	130-133	cannabinoid receptor 1	Rattus norvegicus	47-50
23302980-3	2013	In this study, we sought to verify whether the CB1 and CB2 cannabinoid receptor agonists anandamide and N-palmitoyl-ethanolamine (PEA), respectively, are able to induce peripheral antinociception via an adrenergic mechanism.	palmidrol	130-133	cannabinoid receptor 2	Rattus norvegicus	55-58
22429572-4	2012	Anandamide and palmitoylethanolamide relaxed the ophthalmic artery rings in time- and concentration-dependent manner stimulating the PPAR alpha (PPARalpha).	palmidrol	15-36	peroxisome proliferator activated receptor alpha	Bos taurus	133-143
23374874-0	2013	Molecular evidence for the involvement of PPAR-delta and PPAR-gamma in anti-inflammatory and neuroprotective activities of palmitoylethanolamide after spinal cord trauma.	palmidrol	123-144	peroxisome proliferator activator receptor delta	Mus musculus	42-52
23374874-0	2013	Molecular evidence for the involvement of PPAR-delta and PPAR-gamma in anti-inflammatory and neuroprotective activities of palmitoylethanolamide after spinal cord trauma.	palmidrol	123-144	peroxisome proliferator activated receptor gamma	Mus musculus	57-67
23573230-5	2013	Among those tested, the 200 microg/rat dose of URB597 was the only one that elevated the levels of the FAAH non-endocannabinoid and anti-inflammatory substrates, oleoylethanolamide (OEA) and palmitoylethanolamide (PEA), and of the endocannabinoid FAAH substrate, 2-arachidonoylglycerol, and fully inhibited thermal and tactile nociception, although in a manner blocked almost uniquely by TRPV1 antagonism.	palmidrol	214-217	fatty-acid amide hydrolase-like	Rattus norvegicus	103-107
22912404-5	2012	Infusion of NAEs (anandamide and palmitoylethanolamide) recapitulated increases in PPARgamma-mediated decreases in EE.	palmidrol	33-54	peroxisome proliferator activated receptor gamma	Mus musculus	83-92
23533304-0	2013	Palmitoylethanolamide is a disease-modifying agent in peripheral neuropathy: pain relief and neuroprotection share a PPAR-alpha-mediated mechanism.	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Mus musculus	117-127
22972997-0	2012	Peroxisome proliferator-activated receptor alpha mediates acute effects of palmitoylethanolamide on sensory neurons.	palmidrol	75-96	peroxisome proliferator activated receptor alpha	Mus musculus	0-48
22972997-2	2012	The effect of palmitoylethanolamide (PEA), a ligand for the peroxisome proliferator-activated receptor alpha (PPARalpha), was determined on the evoked-Ca2+ transient in the coculture condition.	palmidrol	14-35	peroxisome proliferator activated receptor alpha	Mus musculus	60-108
22972997-2	2012	The effect of palmitoylethanolamide (PEA), a ligand for the peroxisome proliferator-activated receptor alpha (PPARalpha), was determined on the evoked-Ca2+ transient in the coculture condition.	palmidrol	14-35	peroxisome proliferator activated receptor alpha	Mus musculus	110-119
22972997-2	2012	The effect of palmitoylethanolamide (PEA), a ligand for the peroxisome proliferator-activated receptor alpha (PPARalpha), was determined on the evoked-Ca2+ transient in the coculture condition.	palmidrol	37-40	peroxisome proliferator activated receptor alpha	Mus musculus	60-108
22972997-2	2012	The effect of palmitoylethanolamide (PEA), a ligand for the peroxisome proliferator-activated receptor alpha (PPARalpha), was determined on the evoked-Ca2+ transient in the coculture condition.	palmidrol	37-40	peroxisome proliferator activated receptor alpha	Mus musculus	110-119
22589443-4	2012	PEA-induced activation of p42/44 mitogen-activated protein kinase (MAPK) was determined by Western blot analysis using an antiphospho p42/44 MAPK antibody.	palmidrol	0-3	cyclin dependent kinase 20	Homo sapiens	26-29
22589443-4	2012	PEA-induced activation of p42/44 mitogen-activated protein kinase (MAPK) was determined by Western blot analysis using an antiphospho p42/44 MAPK antibody.	palmidrol	0-3	cyclin dependent kinase 20	Homo sapiens	134-137
22589443-10	2012	CONCLUSIONS: Our results demonstrate that PEA increases aqueous humor outflow through the TM pathway and these effects are mediated by GPR55 and PPARalpha receptors through activation of p42/44 MAPK.	palmidrol	42-45	G protein-coupled receptor 55	Homo sapiens	135-140
22589443-10	2012	CONCLUSIONS: Our results demonstrate that PEA increases aqueous humor outflow through the TM pathway and these effects are mediated by GPR55 and PPARalpha receptors through activation of p42/44 MAPK.	palmidrol	42-45	peroxisome proliferator activated receptor alpha	Homo sapiens	145-154
22589443-10	2012	CONCLUSIONS: Our results demonstrate that PEA increases aqueous humor outflow through the TM pathway and these effects are mediated by GPR55 and PPARalpha receptors through activation of p42/44 MAPK.	palmidrol	42-45	cyclin dependent kinase 20	Homo sapiens	187-190
22514334-2	2012	Brain enzymatic activity of FAAH and the endogenous levels of its substrates, anandamide (AEA; N-arachidonoylethanolamine), 2-arachidonoylglycerol (2-AG), and N-palmitoylethanolamine (PEA), were measured in control and ST4070-treated mice.	palmidrol	159-182	fatty acid amide hydrolase	Mus musculus	28-32
22514334-2	2012	Brain enzymatic activity of FAAH and the endogenous levels of its substrates, anandamide (AEA; N-arachidonoylethanolamine), 2-arachidonoylglycerol (2-AG), and N-palmitoylethanolamine (PEA), were measured in control and ST4070-treated mice.	palmidrol	184-187	fatty acid amide hydrolase	Mus musculus	28-32
22429572-4	2012	Anandamide and palmitoylethanolamide relaxed the ophthalmic artery rings in time- and concentration-dependent manner stimulating the PPAR alpha (PPARalpha).	palmidrol	15-36	peroxisome proliferator activated receptor alpha	Bos taurus	145-154
22429572-9	2012	These data support the view that anandamide and palmitoylethanolamide relax the ophthalmic artery in a time-dependent manner via the transcription factors PPARalpha suggesting a function for them in the physiological mechanisms of vascular regulation.	palmidrol	48-69	peroxisome proliferator activated receptor alpha	Bos taurus	155-164
22201038-3	2012	Cannabinoid compounds with analgesic activity such as palmitoylethanolamide (PEA) show low affinity to CB1 and CB2 receptors, yet selectively activate GPR55 receptors.	palmidrol	54-75	cannabinoid receptor 1	Rattus norvegicus	103-106
22860206-2	2012	A lysosomal enzyme referred to as N-acylethanolamine-hydrolyzing acid amidase (NAAA) catalyzes the same reaction with preference to palmitoylethanolamide, an endogenous analgesic and neuroprotective substance, and is therefore expected as a potential target of therapeutic drugs.	palmidrol	132-153	N-acylethanolamine acid amidase	Mus musculus	34-77
22860206-2	2012	A lysosomal enzyme referred to as N-acylethanolamine-hydrolyzing acid amidase (NAAA) catalyzes the same reaction with preference to palmitoylethanolamide, an endogenous analgesic and neuroprotective substance, and is therefore expected as a potential target of therapeutic drugs.	palmidrol	132-153	N-acylethanolamine acid amidase	Mus musculus	79-83
22201038-3	2012	Cannabinoid compounds with analgesic activity such as palmitoylethanolamide (PEA) show low affinity to CB1 and CB2 receptors, yet selectively activate GPR55 receptors.	palmidrol	54-75	cannabinoid receptor 2	Rattus norvegicus	111-114
22201038-3	2012	Cannabinoid compounds with analgesic activity such as palmitoylethanolamide (PEA) show low affinity to CB1 and CB2 receptors, yet selectively activate GPR55 receptors.	palmidrol	54-75	G protein-coupled receptor 55	Rattus norvegicus	151-156
22429826-0	2012	The association of N-palmitoylethanolamine with the FAAH inhibitor URB597 impairs melanoma growth through a supra-additive action.	palmidrol	19-42	fatty acid amide hydrolase	Mus musculus	52-56
22178921-1	2012	Palmitoylethanolamide (PEA), a peroxisome proliferator-activated receptor-alpha (PPAR-alpha) ligand, exerts antinociceptive and anti-inflammatory effects.	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Rattus norvegicus	31-79
22301508-0	2012	Multimodal stepped care approach with acupuncture and PPAR-alpha agonist palmitoylethanolamide in the treatment of a patient with multiple sclerosis and central neuropathic pain.	palmidrol	73-94	peroxisome proliferator activated receptor alpha	Homo sapiens	54-64
22178921-1	2012	Palmitoylethanolamide (PEA), a peroxisome proliferator-activated receptor-alpha (PPAR-alpha) ligand, exerts antinociceptive and anti-inflammatory effects.	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Rattus norvegicus	81-91
22178921-1	2012	Palmitoylethanolamide (PEA), a peroxisome proliferator-activated receptor-alpha (PPAR-alpha) ligand, exerts antinociceptive and anti-inflammatory effects.	palmidrol	23-26	peroxisome proliferator activated receptor alpha	Rattus norvegicus	31-79
22178921-1	2012	Palmitoylethanolamide (PEA), a peroxisome proliferator-activated receptor-alpha (PPAR-alpha) ligand, exerts antinociceptive and anti-inflammatory effects.	palmidrol	23-26	peroxisome proliferator activated receptor alpha	Rattus norvegicus	81-91
22916199-1	2012	N-acylethanolamine-hydrolyzing acid amidase (NAAA) is a lysosomal enzyme involved in biological deactivation of N-palmitoylethanolamide (PEA), which exerts anti-inflammatory and analgesic effects through the activation of nuclear receptor peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	112-135	N-acylethanolamine acid amidase	Mus musculus	0-43
22916199-1	2012	N-acylethanolamine-hydrolyzing acid amidase (NAAA) is a lysosomal enzyme involved in biological deactivation of N-palmitoylethanolamide (PEA), which exerts anti-inflammatory and analgesic effects through the activation of nuclear receptor peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	112-135	N-acylethanolamine acid amidase	Mus musculus	45-49
22916199-1	2012	N-acylethanolamine-hydrolyzing acid amidase (NAAA) is a lysosomal enzyme involved in biological deactivation of N-palmitoylethanolamide (PEA), which exerts anti-inflammatory and analgesic effects through the activation of nuclear receptor peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	palmidrol	112-135	peroxisome proliferator activated receptor alpha	Mus musculus	289-299
22457773-6	2012	RESULTS: Using LC-MS/MS, we measured a strong increase in arachidonoylethanolamide (AEA), oleoylethanolamide (OEA) and palmitoylethanolamide (PEA) levels in the denervation zone (dentate gyrus) 24 hours post lesion (hpl), whereas entorhinal cortex and CA1 region exhibited little if any changes.	palmidrol	142-145	carbonic anhydrase 1	Rattus norvegicus	252-255
22912680-8	2012	Treatment with PEA reduced MPTP-induced microglial activation, the number of GFAP-positive astrocytes and S100beta overexpression, and protected against the alterations of microtubule-associated protein 2a,b-, dopamine transporter-, nNOS- positive cells in the substantia nigra.	palmidrol	15-18	glial fibrillary acidic protein	Mus musculus	77-81
22912680-8	2012	Treatment with PEA reduced MPTP-induced microglial activation, the number of GFAP-positive astrocytes and S100beta overexpression, and protected against the alterations of microtubule-associated protein 2a,b-, dopamine transporter-, nNOS- positive cells in the substantia nigra.	palmidrol	15-18	S100 calcium binding protein A1	Mus musculus	106-114
22912680-8	2012	Treatment with PEA reduced MPTP-induced microglial activation, the number of GFAP-positive astrocytes and S100beta overexpression, and protected against the alterations of microtubule-associated protein 2a,b-, dopamine transporter-, nNOS- positive cells in the substantia nigra.	palmidrol	15-18	nitric oxide synthase 1, neuronal	Mus musculus	233-237
22912680-10	2012	Genetic ablation of peroxisome proliferator activated receptor (PPAR)-alpha in PPAR-alphaKO mice exacerbated MPTP systemic toxicity, while PEA-induced neuroprotection seemed be partially PPARalpha-dependent.	palmidrol	139-142	peroxisome proliferator activated receptor alpha	Mus musculus	187-196
23028630-6	2012	In addition, VNS reduced the amounts of endocannabinoids and increased N-palmitoylethanolamide, an endogenous ligand of the transcription factor PPARalpha (peroxisome proliferator-activated receptor alpha) in mesenteric adipose tissue but not in the hypothalamus.	palmidrol	71-94	peroxisome proliferator activated receptor alpha	Rattus norvegicus	145-154
23028630-6	2012	In addition, VNS reduced the amounts of endocannabinoids and increased N-palmitoylethanolamide, an endogenous ligand of the transcription factor PPARalpha (peroxisome proliferator-activated receptor alpha) in mesenteric adipose tissue but not in the hypothalamus.	palmidrol	71-94	peroxisome proliferator activated receptor alpha	Rattus norvegicus	156-204
20221904-0	2011	Palmitoylethanolamide protects dentate gyrus granule cells via peroxisome proliferator-activated receptor-alpha.	palmidrol	0-21	peroxisome proliferator activated receptor alpha	Mus musculus	63-111
21501143-3	2011	FAAH hydrolyses the endogenous endocannabinoid anandamide, as well as other non-cannabinoid ligands such as oleoylethanolamide (OEA) and palmitoylethanolamide (PEA).	palmidrol	160-163	fatty acid amide hydrolase	Homo sapiens	0-4
21801852-5	2011	While recombinant NAPE-PLD catalyzed direct release of N-palmitoylethanolamine from N-palmitoylethanolamine plasmalogen, the same reaction occurred in the brain homogenate of NAPE-PLD-deficient mice, suggesting that this reaction occurs through both the NAPE-PLD-dependent and -independent pathways.	palmidrol	55-78	N-acyl phosphatidylethanolamine phospholipase D	Mus musculus	18-26
21801852-5	2011	While recombinant NAPE-PLD catalyzed direct release of N-palmitoylethanolamine from N-palmitoylethanolamine plasmalogen, the same reaction occurred in the brain homogenate of NAPE-PLD-deficient mice, suggesting that this reaction occurs through both the NAPE-PLD-dependent and -independent pathways.	palmidrol	84-107	N-acyl phosphatidylethanolamine phospholipase D	Mus musculus	18-26
21801852-10	2011	In addition, we discovered that recombinant GDE1 has a weak activity to generate N-palmitoylethanolamine from its corresponding lyso pNAPE, suggesting that this enzyme is at least in part responsible for the lysophospholipase D activity.	palmidrol	81-104	glycerophosphodiester phosphodiesterase 1	Mus musculus	44-48
20801430-2	2011	Inhibition of FAAH increases levels of several endogenous substances in the brain, including the endocannabinoid anandamide and the noncannabinoid fatty acid ethanolamides oleoylethanolamide (OEA) and palmitoylethanolamide, which are ligands for alpha-type peroxisome proliferator-activated nuclear receptors (PPAR-alpha).	palmidrol	201-222	fatty-acid amide hydrolase-like	Rattus norvegicus	14-18
20801430-2	2011	Inhibition of FAAH increases levels of several endogenous substances in the brain, including the endocannabinoid anandamide and the noncannabinoid fatty acid ethanolamides oleoylethanolamide (OEA) and palmitoylethanolamide, which are ligands for alpha-type peroxisome proliferator-activated nuclear receptors (PPAR-alpha).	palmidrol	201-222	peroxisome proliferator activated receptor alpha	Rattus norvegicus	310-320
21864979-9	2011	These data suggest an important role for the endocannabinoid system in the vHip in FCA, whereby levels of 2-arachidonoylglycerol and the FAAH substrates palmitoylethanolamide and anandamide are increased in rats expressing FCA, and pharmacological inhibition of FAAH in the vHip enhances this form of endogenous analgesia via a CB(1) receptor-dependent mechanism.	palmidrol	153-174	fatty-acid amide hydrolase-like	Rattus norvegicus	137-141