PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
24198653-8	2013	Treatment of G-Re at 30 and 100 muM doses before I/R induction significantly prevented the decrease in hemodynamic parameters, ameliorated the electrocardiographic abnormality, and inhibited TNF-alpha level.	ginsenoside Re	13-17	tumor necrosis factor	Rattus norvegicus	191-200
34368872-8	2021	The results revealed that G-Re significantly inhibited the production of IL-6, TNF-alpha, nitric oxide (NO) and ROS in BV2 microglial cells, and that of NO in mouse primary microglia, without affecting cell viability.	ginsenoside Re	26-30	interleukin 6	Mus musculus	73-77
34368872-8	2021	The results revealed that G-Re significantly inhibited the production of IL-6, TNF-alpha, nitric oxide (NO) and ROS in BV2 microglial cells, and that of NO in mouse primary microglia, without affecting cell viability.	ginsenoside Re	26-30	tumor necrosis factor	Mus musculus	79-88
30978651-12	2019	Ginsenoside Re and schizandrin B are also potential substrates of NTCP, and their uptake mediated by NTCP was inhibited by the other components in SMF.	ginsenoside Re	0-14	solute carrier family 10 member 1	Homo sapiens	66-70
30978651-12	2019	Ginsenoside Re and schizandrin B are also potential substrates of NTCP, and their uptake mediated by NTCP was inhibited by the other components in SMF.	ginsenoside Re	0-14	solute carrier family 10 member 1	Homo sapiens	101-105
24054220-7	2014	Moreover, the heat-processed glucose-leucine mixture (major MRPs from the ginsenoside Re-leucine mixture) showed protective effects against cisplatin-induced oxidative renal damage in rats through the inhibition of caspase-3 activation.	ginsenoside Re	74-89	caspase 3	Rattus norvegicus	215-224
34764718-6	2021	Results: GK-1 possesses highest ginsenosides especially ginsenoside-Re amongst seven ginseng cultivars including (Chunpoong, Huangsuk, Kumpoong, K-1, Honkaejong, Gopoong, and Yunpoong).	ginsenoside Re	56-70	kallikrein 1-related peptidase b1	Mus musculus	9-13
31906464-0	2020	Ginsenoside Re Mitigates 6-Hydroxydopamine-Induced Oxidative Stress through Upregulation of GPX4.	ginsenoside Re	0-14	glutathione peroxidase 4	Homo sapiens	92-96
31906464-5	2020	In addition, ginsenoside Re induced the expression of the antioxidant protein glutathione peroxidase 4 (GPX4) but not catalase, glutathione peroxidase 1, glutathione reductase, or superoxide dismutase-1.	ginsenoside Re	13-27	glutathione peroxidase 4	Homo sapiens	78-102
31906464-5	2020	In addition, ginsenoside Re induced the expression of the antioxidant protein glutathione peroxidase 4 (GPX4) but not catalase, glutathione peroxidase 1, glutathione reductase, or superoxide dismutase-1.	ginsenoside Re	13-27	glutathione peroxidase 4	Homo sapiens	104-108
31906464-6	2020	Furthermore, upregulation of GPX4 by ginsenoside Re was mediated by phosphoinositide 3-kinase and extracellular signal-regulated kinase but not by p38 mitogen-activated protein kinase or c-Jun N-terminal kinase.	ginsenoside Re	37-51	glutathione peroxidase 4	Homo sapiens	29-33
31906464-8	2020	The GPX4 inhibitor (1S,3R)-RSL3 reversed ginsenoside Re-mediated inhibition of cellular damage in SH-SY5Y cells exposed to 6-OHDA, indicating that the neuronal activity of ginsenoside Re is due to upregulation of GPX4.	ginsenoside Re	41-55	glutathione peroxidase 4	Homo sapiens	4-8
31906464-8	2020	The GPX4 inhibitor (1S,3R)-RSL3 reversed ginsenoside Re-mediated inhibition of cellular damage in SH-SY5Y cells exposed to 6-OHDA, indicating that the neuronal activity of ginsenoside Re is due to upregulation of GPX4.	ginsenoside Re	41-55	glutathione peroxidase 4	Homo sapiens	213-217
31906464-8	2020	The GPX4 inhibitor (1S,3R)-RSL3 reversed ginsenoside Re-mediated inhibition of cellular damage in SH-SY5Y cells exposed to 6-OHDA, indicating that the neuronal activity of ginsenoside Re is due to upregulation of GPX4.	ginsenoside Re	172-186	glutathione peroxidase 4	Homo sapiens	4-8
31906464-8	2020	The GPX4 inhibitor (1S,3R)-RSL3 reversed ginsenoside Re-mediated inhibition of cellular damage in SH-SY5Y cells exposed to 6-OHDA, indicating that the neuronal activity of ginsenoside Re is due to upregulation of GPX4.	ginsenoside Re	172-186	glutathione peroxidase 4	Homo sapiens	213-217
31906464-9	2020	These findings suggest that ginsenoside Re-dependent upregulation of GPX4 reduces oxidative stress and thereby alleviates 6-OHDA-induced neuronal damage.	ginsenoside Re	28-42	glutathione peroxidase 4	Homo sapiens	69-73
31599782-7	2020	Compared with the MI group, Gin-Re treatment promoted AMPKalpha phosphorylation, decreased TGF-beta1 expression and attenuated Smad2/3 activation.	ginsenoside Re	28-34	transforming growth factor, beta 1	Rattus norvegicus	91-100
31599782-7	2020	Compared with the MI group, Gin-Re treatment promoted AMPKalpha phosphorylation, decreased TGF-beta1 expression and attenuated Smad2/3 activation.	ginsenoside Re	28-34	SMAD family member 2	Rattus norvegicus	127-134
31599782-8	2020	After Gin-Re treatment, the phosphorylation of FAK, PI3K p110alpha and Akt was enhanced in MI rats, while PI3K p110beta showed no difference compared with the MI group.	ginsenoside Re	6-12	protein tyrosine kinase 2	Rattus norvegicus	47-50
31599782-8	2020	After Gin-Re treatment, the phosphorylation of FAK, PI3K p110alpha and Akt was enhanced in MI rats, while PI3K p110beta showed no difference compared with the MI group.	ginsenoside Re	6-12	AKT serine/threonine kinase 1	Rattus norvegicus	71-74
31599782-8	2020	After Gin-Re treatment, the phosphorylation of FAK, PI3K p110alpha and Akt was enhanced in MI rats, while PI3K p110beta showed no difference compared with the MI group.	ginsenoside Re	6-12	phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit beta	Rattus norvegicus	111-119
31599782-9	2020	These results indicate that Gin-Re may improve MI-induced cardiac dysfunction and mitigate ventricular remodeling via regulation of the AMPK/TGF-beta1/Smad2/3 and FAK/PI3K p110alpha/Akt signaling pathways.	ginsenoside Re	28-34	transforming growth factor, beta 1	Rattus norvegicus	141-150
31599782-9	2020	These results indicate that Gin-Re may improve MI-induced cardiac dysfunction and mitigate ventricular remodeling via regulation of the AMPK/TGF-beta1/Smad2/3 and FAK/PI3K p110alpha/Akt signaling pathways.	ginsenoside Re	28-34	SMAD family member 2	Rattus norvegicus	151-158
31599782-9	2020	These results indicate that Gin-Re may improve MI-induced cardiac dysfunction and mitigate ventricular remodeling via regulation of the AMPK/TGF-beta1/Smad2/3 and FAK/PI3K p110alpha/Akt signaling pathways.	ginsenoside Re	28-34	protein tyrosine kinase 2	Rattus norvegicus	163-166
31599782-9	2020	These results indicate that Gin-Re may improve MI-induced cardiac dysfunction and mitigate ventricular remodeling via regulation of the AMPK/TGF-beta1/Smad2/3 and FAK/PI3K p110alpha/Akt signaling pathways.	ginsenoside Re	28-34	AKT serine/threonine kinase 1	Rattus norvegicus	182-185
30110677-11	2018	G-Re inhibited the inflammatory response by the reduction of the protein expression of cyclooxygenase-2 and inducible nitric oxide synthase.	ginsenoside Re	0-4	prostaglandin-endoperoxide synthase 2	Mus musculus	87-139
27080948-9	2016	G-Re administration also led to a decrease in cell death-related phospho-p38 protein levels, and had an antioxidative effect by reducing HO1 expression.	ginsenoside Re	0-4	mitogen-activated protein kinase 14	Mus musculus	73-76
27080948-9	2016	G-Re administration also led to a decrease in cell death-related phospho-p38 protein levels, and had an antioxidative effect by reducing HO1 expression.	ginsenoside Re	0-4	heme oxygenase 1	Mus musculus	137-140
22401937-8	2012	Treatment with Gin-Re inhibited secretion levels of inflammatory mediators such as tumor necrosis factor alpha (TNF alpha), and interleukin-1beta (IL-1beta) in LPS-stimulated murine macrophage Raw 264.7 cells.	ginsenoside Re	15-21	tumor necrosis factor	Mus musculus	83-110
22849695-12	2012	Ginsenoside Re (20 mg/kg) inhibited the activation of NF-kappaB in TNBS-treated mice.	ginsenoside Re	0-14	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	54-63
22401937-8	2012	Treatment with Gin-Re inhibited secretion levels of inflammatory mediators such as tumor necrosis factor alpha (TNF alpha), and interleukin-1beta (IL-1beta) in LPS-stimulated murine macrophage Raw 264.7 cells.	ginsenoside Re	15-21	tumor necrosis factor	Mus musculus	112-121
22401937-8	2012	Treatment with Gin-Re inhibited secretion levels of inflammatory mediators such as tumor necrosis factor alpha (TNF alpha), and interleukin-1beta (IL-1beta) in LPS-stimulated murine macrophage Raw 264.7 cells.	ginsenoside Re	15-21	interleukin 1 beta	Mus musculus	128-145
22401937-8	2012	Treatment with Gin-Re inhibited secretion levels of inflammatory mediators such as tumor necrosis factor alpha (TNF alpha), and interleukin-1beta (IL-1beta) in LPS-stimulated murine macrophage Raw 264.7 cells.	ginsenoside Re	15-21	interleukin 1 beta	Mus musculus	147-155
21704572-2	2011	Several types of saponins including G-Rg1, G-Rg2, G-F1, G-Rh1, and protopanaxatriol (PPT) may be the metabolites of G-Re according to reports from preclinical trials.	ginsenoside Re	116-120	TLE family member 2, transcriptional corepressor	Homo sapiens	43-48
20592135-1	2010	A single-chain variable fragment (scFv) antibody against ginsenoside Re (G-Re) have been successfully expressed in the silkworm larvae using Bombyx mori nucleopolyhedrovirus (BmNPV) bacmid DNA system.	ginsenoside Re	73-77	immunglobulin heavy chain variable region	Homo sapiens	34-38
17490654-0	2007	Non-genomic effects of ginsenoside-Re in endothelial cells via glucocorticoid receptor.	ginsenoside Re	23-37	nuclear receptor subfamily 3 group C member 1	Homo sapiens	63-86
17490654-1	2007	We demonstrated that ginsenoside-Re (Re), a pharmacological active component of ginseng, is a functional ligand of glucocorticoid receptor (GR) using competitive ligand-binding assay (IC(50)=156.6 nM; K(d)=49.7 nM) and reporter gene assay.	ginsenoside Re	21-35	nuclear receptor subfamily 3 group C member 1	Homo sapiens	115-138