PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
25811992-7	2015	We demonstrated that ABL treatment significantly reduced neurological deficits and cerebral infarct volume by inhibiting tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) expression in ischemic cerebral tissue and OGD-treated BV2 cells.	lauric acid	21-24	tumor necrosis factor	Mus musculus	121-148	
10429660-5	1999	6,6"-Diester-trehaloses and 4,4"-diester-trehaloses of C8 to C12 fatty acids, 6,6"-diamide-trehaloses of C8 to C14 fatty acids, and n-dodecyl-beta-D-maltoside all inhibited TNF-alpha release in a dose-dependent manner.	lauric acid	61-76	tumor necrosis factor	Mus musculus	173-182	
25811992-7	2015	We demonstrated that ABL treatment significantly reduced neurological deficits and cerebral infarct volume by inhibiting tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) expression in ischemic cerebral tissue and OGD-treated BV2 cells.	lauric acid	21-24	tumor necrosis factor	Mus musculus	150-159	
25811992-8	2015	Mechanistic studies suggested that the observed decrease in TNF-alpha and IL-1beta expression was attributable to the ABL-induced suppression of the expression of nuclear factor-kappa B (NF-kappaB) and Toll-like receptor 4 (TLR4).	lauric acid	118-121	tumor necrosis factor	Mus musculus	60-69	
25811992-9	2015	We further found that miR-155 promoted TNF-alpha and IL-1beta expression by upregulating TLR4 and downregulating the expression of suppressor of cytokine signaling 1 (SOCS1) and myeloid differentiation primary response gene 88 (MyD88), while ABL exerted an inhibitory effect on miR-155-mediated gene expression.	lauric acid	242-245	tumor necrosis factor	Mus musculus	39-48