PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
10956421-6	2000	Treatment of the cells with the general caspase inhibitor Boc-Asp(OMe)-Fluoromethylketone (BAF) completely inhibited caspase-3 activation in response to tBHP, and delayed, but did not prevent cell death.	tert-Butylhydroperoxide	153-157	caspase 3	Homo sapiens	117-126	
18845176-5	2008	Pretreatment of Hepa1c1c7 and HepG2 cells with puerarin significantly reduced t-BHP-induced caspase-3 activation and subsequent cell death.	tert-Butylhydroperoxide	78-83	caspase 3	Homo sapiens	92-101	
15728565-5	2005	Loss of mitochondrial membrane potential (Deltapsi(m)), release of cytochrome c, and activation of caspase 3 after tBH treatments all increased under the more oxidized conditions.	tert-Butylhydroperoxide	115-118	caspase 3	Homo sapiens	99-108	
11904147-2	2002	We report for the first time that procaspase 3 present in the anucleated mature human erythrocyte is activated under oxidative stress induced by t-butylhydroperoxide leading to impairment of the aminophospholipid translocase, PS externalization and increased erythrophagocytosis.	tert-Butylhydroperoxide	145-165	caspase 3	Homo sapiens	34-46	
11812934-8	2002	The results demonstrated that (1) the apoptotic effect of 4 out of 5 compounds could be detected in low concentrations of the drugs long before cell necrosis (tertiary-butyl-hydroperoxide-induced apoptosis was only detected at concentrations causing concomitant necrosis) and (2) among the markers evaluated, caspase 3 activation and nucleus and DNA analysis by flow cytometry were used to fulfil the compromise between reliability, sensitivity, and ease of performance, which are critical issues when screening for an apoptotic effect of newly developed drugs.	tert-Butylhydroperoxide	159-187	caspase 3	Homo sapiens	309-318	
10102293-6	1999	RESULTS: t-Butylhydroperoxide caused time- and dose-dependent activation of apoptosis in hRPE, indicated by characteristic morphologic changes; TUNEL-positive labeling; phosphatidylserine (PS) exposure; and procaspase 3, poly(ADP-ribose)polymerase, lamin, and tubulin cleavage.	tert-Butylhydroperoxide	9-29	caspase 3	Homo sapiens	207-219	
29926623-11	2016	Recombinant adiponectin protected HUVECs from apoptosis induced by t-BHP, which was correlated with the downregulation of p-JNK and active Caspase 3.	tert-Butylhydroperoxide	67-72	caspase 3	Homo sapiens	139-148	
33880054-11	2021	Results: Our results showed that hydrogen can inhibit inflammatory factors (ADAMTS5 and MMP13) and apoptosis factors (cleaved caspase-3, cytochrome c, and Bax) in TBHP-induced chondrocytes.	tert-Butylhydroperoxide	163-167	caspase 3	Homo sapiens	126-135	
32542535-6	2020	Exposure to 50 muM TBHP increased caspase 3/7 activity, an indicator of apoptosis, after 8 and 24 h. Antioxidant treatment markedly reduced TBHP-stimulated caspase 3/7 activity, PGE2 release, and IL-6 release.	tert-Butylhydroperoxide	19-23	caspase 3	Homo sapiens	34-45	
32542535-6	2020	Exposure to 50 muM TBHP increased caspase 3/7 activity, an indicator of apoptosis, after 8 and 24 h. Antioxidant treatment markedly reduced TBHP-stimulated caspase 3/7 activity, PGE2 release, and IL-6 release.	tert-Butylhydroperoxide	140-144	caspase 3	Homo sapiens	34-45	
32542535-8	2020	These data suggest that TBHP-stimulated IL-6 release and caspase 3/7 activation were independent of PGE2 yet were interrupted by treatments with known antioxidant properties, providing new insight into relationships between PGE2, IL-6, and apoptosis under conditions of chemically induced cellular oxidation.	tert-Butylhydroperoxide	24-28	caspase 3	Homo sapiens	57-68	
29362666-8	2017	Further study demonstrated that VCAF attenuated the apoptosis of t-BHP-treated HepG2 cells by suppressing the activation of caspase-3 and caspase-8.	tert-Butylhydroperoxide	65-70	caspase 3	Homo sapiens	124-133	
27030608-0	2016	Exendin-4 protects HUVECs from t-BHP-induced apoptosis via PI3K/Akt-Bcl-2-caspase-3 signaling.	tert-Butylhydroperoxide	31-36	caspase 3	Homo sapiens	74-83	
26989860-6	2016	Meanwhile, SCAD siRNA treatment triggered the same apoptosis as cardiomyocytes treated with tBHP, such as the increase in cell apoptotic rate, the activation of caspase3 and the decrease in the Bcl-2/Bax ratio, which showed that SCAD may play an important role in primary cardiomyocyte apoptosis.	tert-Butylhydroperoxide	92-96	caspase 3	Homo sapiens	161-169	
22980779-4	2012	The protective effect of WESP and their bioactive compounds in 0.2mM t-BHP-induced HepG2 cells may be associated with positive regulation of GSH levels and antioxidant enzymes, decrease in ROS formation and TBARS generation, increase in the mitochondria membrane potential and Bcl-2/Bax ratio, as well as decrease in caspase-3 activation.	tert-Butylhydroperoxide	69-74	caspase 3	Homo sapiens	317-326	
22610911-5	2013	In addition, pretreatment with ferulate markedly protected cells against t-BHP-induced apoptosis, as evidenced by decreased nuclear condensation, cytochrome c release, and caspase-3 cleavage and an increased Bax/Bcl-2 ratio.	tert-Butylhydroperoxide	73-78	caspase 3	Homo sapiens	172-181	
21046126-9	2011	Hence, Caco2 cells treated 20 h with the flavanols, especially PB2, and then submitted to an oxidative stress induced by a pro-oxidant, tert-butyl-hydroperoxide, showed a reduced ROS production, restricted activation of caspase 3 and higher viability than cells plainly submitted to the stressor.	tert-Butylhydroperoxide	136-160	caspase 3	Homo sapiens	220-229