PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
21496413-5	2011	In animal models and in vitro models, after treatment with Bosentan, a significant reduction of cytokine (TNF alpha, IFN gamma,IL-8, IL-4) levels was observed.	Bosentan	59-67	tumor necrosis factor	Homo sapiens	106-115	
19850966-4	2009	To elucidate the anti-inflammatory properties of the dual endothelin receptor antagonist bosentan that targets both endothelin receptor subtypes A (ET(A)R) and B (ET(B)R), its effect on the TNFalpha/ET-1/GM-CSF network was investigated.	Bosentan	89-97	tumor necrosis factor	Homo sapiens	190-198	
19850966-11	2009	Since bosentan impairs ET-1 autoregulation and TNFalpha-induced ET-1 release, as well as TNFalpha- and ET-1-induced GM-CSF release, the present data suggest therapeutic utility for bosentan in treating particularly the early stages of chronic inflammatory airway diseases.	Bosentan	6-14	tumor necrosis factor	Homo sapiens	47-55	
11238005-6	2001	Treatment of the animals with the ET receptor antagonist bosentan resulted in a substantial decrease in the concentrations of tumor necrosis factor-alpha, IL-4, IL-1beta, interferon-gamma, and ET-1 in bronchoalveolar lavage fluid.	Bosentan	57-65	tumor necrosis factor	Homo sapiens	126-153	
19850966-9	2009	ET-1- and TNFalpha-induced GM-CSF expression were both reduced by bosentan as well as by specific inhibition of either ET(A)R, ET(B)R, p38(MAPK) or ERK-1/-2.	Bosentan	66-74	tumor necrosis factor	Homo sapiens	10-18