count	source_label	source_id	relationship	target_label	target_id	entity_type	solr_id	publication_id	sentences
4		IP:IPR011822	decreases	glycoursodeoxycholic acid	CHEBI:89929	ProteinFamily	2888fc5c-3c72-11f0-afc2-0050569a791b	10.1016/j.fct.2022.113208	Among conjugated BAs, Meth administration increased the levels of Tauro-β-muricholic acid (T-β-MCA), Taurochenodeoxycholic acid (TCDCA) and Tauroursodeoxycholic acid (TUDCA), and reduced the level of Glycocholic acid (GCA) and Glycoursodeoxycholic acid (GUDCA) in comparison with the control group (p-value<0.01).
4		FPLX:MYH	decreases	glycoursodeoxycholic acid	CHEBI:89929	ProteinFamily	37c68498-45a3-11f0-afc2-0050569a791b	10.3168/jds.2021-21204	Furthermore, MYH treatment significantly decreased the levels of glycoursodeoxycholic acid,d-sphingosine, dehydrocholic acid, palmitoyl carnitine, and glycocholic acid in the hepatic sample (P< 0.05).
2	glycoursodeoxycholic acid	CHEBI:89929	activates		CHEBI:16247	Chemical	82cff7be-d9be-11ee-b346-0050569a791b	10.1016/S0014-2999(98)00725-0	In agreement with previous studies (Hoffman et al., 1975;Poupon et al., 1976;Sama et al., 1982;Gurantz and Hofmann, 1984), ursodeoxycholic acid, tauroursodeoxycholic acid and glycoursodeoxycholic acid significantly increased biliary cholesterol, phospholipid, bilirubin and total Ca2+excretion during each infusion.
2	glycoursodeoxycholic acid	CHEBI:89929	activates		MESH:D002784	Phenotype	82cff7be-d9be-11ee-b346-0050569a791b	10.1016/S0014-2999(98)00725-0	In agreement with previous studies (Hoffman et al., 1975;Poupon et al., 1976;Sama et al., 1982;Gurantz and Hofmann, 1984), ursodeoxycholic acid, tauroursodeoxycholic acid and glycoursodeoxycholic acid significantly increased biliary cholesterol, phospholipid, bilirubin and total Ca2+excretion during each infusion.
2	glycoursodeoxycholic acid	CHEBI:89929	activates		MESH:D001663	Phenotype	82cff7be-d9be-11ee-b346-0050569a791b	10.1016/S0014-2999(98)00725-0	In agreement with previous studies (Hoffman et al., 1975;Poupon et al., 1976;Sama et al., 1982;Gurantz and Hofmann, 1984), ursodeoxycholic acid, tauroursodeoxycholic acid and glycoursodeoxycholic acid significantly increased biliary cholesterol, phospholipid, bilirubin and total Ca2+excretion during each infusion.
2		CHEBI:17864	inhibits	glycoursodeoxycholic acid	CHEBI:89929	Chemical	37c68498-45a3-11f0-afc2-0050569a791b	10.3168/jds.2021-21204	The gavaging of MFE-sweetened synbiotic yogurt increased the level of taurolithocholic acid 3-sulfate and decreased those of dehydrocholic acid and glycoursodeoxycholic acid.
1	glycoursodeoxycholic acid	CHEBI:89929	inhibits		UNIPROT:Q96RI1	Protein	ebd87cb6-ae93-11ec-840e-0050569a791b	PMCPMC8621166	Recent studies performed on HCD-rodents showed that intestinal FXR deficiency or direct FXR inhibition (via treatment with the FXR antagonist glycoursodeoxycholic acid [GUDCA]), decreased ATS and reduced the levels of circulating ceramides and cholesterol, all these results suggesting that intestinal FXR modulates intestinal ceramide production [137].
1	glycoursodeoxycholic acid	CHEBI:89929	activates		UNIPROT:P01584	Protein	54b5f31a-c8e7-11e5-9624-001a4ae51246	17805009	Both Glycoursodeoxycholic Acid and IL-10 Prevent Unconjugated Bilirubin-Induced Release of TNF-α and IL-1β, Whereas Only GUDCA Counteracts Unconjugated Bilirubin Suppression of IL-6 Secretion In previous experiments, we have demonstrated that significant levels of the proinflammatory cytokines TNF-α and IL-1β are released from cultured rat astrocytes after a short exposure to UCB, whereas IL-6 secretion is markedly prevented (6).
1	glycoursodeoxycholic acid	CHEBI:89929	inhibits		UNIPROT:P01584	Protein	54b5f31a-c8e7-11e5-9624-001a4ae51246	17805009	Both Glycoursodeoxycholic Acid and IL-10 Prevent Unconjugated Bilirubin-Induced Release of TNF-α and IL-1β, Whereas Only GUDCA Counteracts Unconjugated Bilirubin Suppression of IL-6 Secretion In previous experiments, we have demonstrated that significant levels of the proinflammatory cytokines TNF-α and IL-1β are released from cultured rat astrocytes after a short exposure to UCB, whereas IL-6 secretion is markedly prevented (6).
1	glycoursodeoxycholic acid	CHEBI:89929	activates		UNIPROT:P01375	Protein	54b5f31a-c8e7-11e5-9624-001a4ae51246	17805009	Both Glycoursodeoxycholic Acid and IL-10 Prevent Unconjugated Bilirubin-Induced Release of TNF-α and IL-1β, Whereas Only GUDCA Counteracts Unconjugated Bilirubin Suppression of IL-6 Secretion In previous experiments, we have demonstrated that significant levels of the proinflammatory cytokines TNF-α and IL-1β are released from cultured rat astrocytes after a short exposure to UCB, whereas IL-6 secretion is markedly prevented (6).
1	glycoursodeoxycholic acid	CHEBI:89929	activates		CHEBI:3098	Chemical	0f86aba0-c955-11ee-9133-0050569a1f61	10.1016/j.jpba.2022.115139	Glycochenodeoxycholic acid (GCDCA), glycodeoxycholic acid (GDCA), glycoursodeoxycholic acid (GUDCA), glycolithocholic acid (GLCA), taurochenodeoxycholic acid (TCDCA), taurodeoxycholic acid (TDCA), tauroursodeoxycholic acid (TUDCA) and taurolithocholic acid (TLCA) were synthesized via chemically linking the respective unconjugated bile acid with glycine or taurine, as described in our previous study[5].
1	glycoursodeoxycholic acid	CHEBI:89929	inhibits		MESH:D004249	Phenotype	bd8a75d2-bc3a-11e5-9b9d-001a4ae51247	PMC3602841	In cells isolated from a patient with non-dysplastic BE, Goldman et al. observed that replacement of hydrophobic bile acids with the more hydrophilic glycoursodeoxycholic acid (GUDCA) reduced DNA damage and oxidative stress, and thus GUDCA may possibly prevent EB progress to EAC (Goldman et al., 2010).
1	glycoursodeoxycholic acid	CHEBI:89929	inhibits		GO:0006915	Phenotype	957ab47e-6e02-11e6-b946-001a4ae51247	PMC5003190	Glycoursodeoxycholic acid inhibits apoptosis by blocking a key protease called caspase 3.
1	glycoursodeoxycholic acid	CHEBI:89929	activates		GO:0008219	Phenotype	11c307f4-bc2c-11e5-8abe-001a4ae51246	10.1016/j.neuro.2007.11.002	Glycoursodeoxycholic acid protects neurons from unconjugated bilirubin-induced cell death Apart from our own most recent studies showing that GUDCA is able to abrogate astroglial cell death (Fernandes et al., 2007b), there are no reports on the efficacy of this molecule to counteract the loss of cell membrane integrity characteristic of necrosis induced by an injurious stimulus.
1	glycoursodeoxycholic acid	CHEBI:89929	inhibits		FPLX:Protease	ProteinFamily	957ab47e-6e02-11e6-b946-001a4ae51247	PMC5003190	Glycoursodeoxycholic acid inhibits apoptosis by blocking a key protease called caspase 3.
1		MESH:D008687	increases	glycoursodeoxycholic acid	CHEBI:89929	Phenotype	aea242e8-c712-11ee-8b99-0050569a1f61	PMC10570704	"Lastly, metagenomic and meta-metabolomic analysis have shown that metformin increases the intestinal level of glycoursodeoxycholic acid while decreases the abundance of species of Bacteroides fragilis and, consequently, bile salt hydrolase activity in the intestine of individuals with T2D.55
        Unfortunately, if some of the beneficial effects of metformin on glucose metabolism are mediated by the GM, also some of its side effects may be due to GM alterations."
1		MESH:D008687	activates	glycoursodeoxycholic acid	CHEBI:89929	Phenotype	851742e4-ae95-11ec-840e-0050569a791b	PMCPMC8540512	Elbere et al. and Sun et al. found that metformin clinical benefits are partly mediated by bacteria-specific mechanisms such as glucose-SGLT1-sensing glucoregulatory pathway associated with Lactobacillus increase or B. fragilis—glycoursodeoxycholic acid (GUDCA)—intestinal farnesoid X receptor (FXR) [65,66].
1		MESH:D008687	increases	glycoursodeoxycholic acid	CHEBI:89929	Phenotype	ff6253d8-ae93-11ec-89b1-0050569a791b	PMCPMC8450894	Second, metformin treatment increases the levels of the BA glycoursodeoxycholic acid by inhibiting Bacteroides fragilis, thus improving insulin resistance by activating the FXR pathway (104).
1		MESH:D008687	increases	glycoursodeoxycholic acid	CHEBI:89929	Phenotype	4a7851ac-ae93-11ec-ae7b-0050569a1f61	PMCPMC8106557	Our team has reported that metformin treatment decreased the abundance of Bacteroides fragilis and increased the level of glycoursodeoxycholic acid (GUDCA) in the gut, thereby suppressing intestinal FXR signaling.
1		IP:IPR005556	activates	glycoursodeoxycholic acid	CHEBI:89929	ProteinFamily	851742e4-ae95-11ec-840e-0050569a791b	PMCPMC8540512	Elbere et al. and Sun et al. found that metformin clinical benefits are partly mediated by bacteria-specific mechanisms such as glucose-SGLT1-sensing glucoregulatory pathway associated with Lactobacillus increase or B. fragilis—glycoursodeoxycholic acid (GUDCA)—intestinal farnesoid X receptor (FXR) [65,66].
1		MESH:D001241	increases	glycoursodeoxycholic acid	CHEBI:89929	Phenotype	3cbd44f2-ab45-11e6-90f5-001a4ae51247	PMC4934856	Aspirin could increase the levels of glycoursodeoxycholic acid, glycocholic acid, and coprocholic acid, and increase the level of Glucose 1-phosphate, while WBH could not.
1		CHEBI:22868	inhibits	glycoursodeoxycholic acid	CHEBI:89929	Chemical	8aa9ec6a-c8dd-11e5-9ad8-001a4ae51247	16474011	[3H]taurochenodeoxycholic acid (10 Ci/mmol), [3H]glycochenodeoxycholic acid (11 Ci/mmol), [3H]ursodeoxycholic acid (12 Ci/mmol), [3H]tauroursodeoxycholic acid (10 Ci/mmol), [3H]glycoursodeoxycholic acid (11 Ci/mmol), [3H]taurodeoxycholic acid (29 Ci/mmol), and [3H]glycodeoxycholic acid (30 Ci/mmol) were synthesized by reductive tritiation of the Δ22 derivative of the corresponding bile salts (23).