PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
28688762-5	2017	In this study, we investigated the effects of Trx1 on NADPH oxidase in human umbilical vein endothelial cells (HUVECs), whose ROS level is mainly produced by NADPH oxidase, especially Nox4 isoform.	Reactive Oxygen Species	126-129	thioredoxin	Homo sapiens	46-50	
28688762-6	2017	Our data demonstrated that Trx decreased NADPH oxidase activity, ROS production and ICAM-1 expression in ox-LDL treated HUVECs.	Reactive Oxygen Species	65-68	thioredoxin	Homo sapiens	27-30	
28688762-9	2017	Transient transfection of Nox4 and p22phox significantly increased intracellular ROS generation, which could be blocked by Trx overexpression.	Reactive Oxygen Species	81-84	NADPH oxidase 4	Homo sapiens	26-30	
28688762-9	2017	Transient transfection of Nox4 and p22phox significantly increased intracellular ROS generation, which could be blocked by Trx overexpression.	Reactive Oxygen Species	81-84	cytochrome b-245 alpha chain	Homo sapiens	35-42	
28688762-9	2017	Transient transfection of Nox4 and p22phox significantly increased intracellular ROS generation, which could be blocked by Trx overexpression.	Reactive Oxygen Species	81-84	thioredoxin	Homo sapiens	123-126	
28688762-11	2017	These results suggest that Trx suppresses NADPH oxidase activity in vascular endothelia under pathological conditions and may prevent the initiation of atherosclerosis by attenuating exceeding ROS production.	Reactive Oxygen Species	193-196	thioredoxin	Homo sapiens	27-30