PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
28191652-9	2017	GTN reduced all inflammatory mediators evaluated (TNF-alpha, COX-2, iNOS) and different from Celecoxib, it also decreased the protein levels of NF-kB and p-NF-kB.	goniothalamin	0-3	tumor necrosis factor	Mus musculus	50-59	
27797827-8	2017	Additionally, GTN suppressed production of IL-6, IL-17 and TNF-alpha in tumor tissue, as well as abrogated stromal immune cell activation and nuclear translocation of NF-kappaB.	goniothalamin	14-17	tumor necrosis factor	Mus musculus	59-68	
27797827-9	2017	Finally, in a tamoxifen inducible model of sporadic CRC, GTN-treated mice had significantly fewer tumors and decreased levels of IL-17A, IL-6, S100A9 and TNF-alpha protein within the tumors.	goniothalamin	57-60	tumor necrosis factor	Mus musculus	154-163	
26297443-6	2015	GTN (10, 30 and 100mg/kg) inhibited leukocyte migration in the peritonitis model and gene expression levels of IL-1beta, iNOS and TNF-alpha, as well as TNF-alpha protein levels, in LPS-stimulated macrophages, without affecting COX-2 gene expression levels.	goniothalamin	0-3	tumor necrosis factor	Mus musculus	130-139	
27016270-6	2016	In spontaneous-colitis using IL-10 deficient mice (C57BL/6 background), GTN prevented colitis development through downregulation of TNF-alpha, upregulation of SIRT-1 and inhibition of proliferation (PCNA index), without signs of toxicity after three months of treatment.	goniothalamin	72-75	tumor necrosis factor	Mus musculus	132-141	
26297443-6	2015	GTN (10, 30 and 100mg/kg) inhibited leukocyte migration in the peritonitis model and gene expression levels of IL-1beta, iNOS and TNF-alpha, as well as TNF-alpha protein levels, in LPS-stimulated macrophages, without affecting COX-2 gene expression levels.	goniothalamin	0-3	tumor necrosis factor	Mus musculus	152-161