PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
17569628-3	2007	EGCG caused growth arrest at G1 stage of cell cycle through regulation of cyclin D1, cdk4, cdk6, p21/WAF1/CIP1 and p27/KIP1, and induced apoptosis through generation of reactive oxygen species and activation of caspase-3 and caspase-9.	epigallocatechin gallate	0-4	caspase 3	Mus musculus	211-220	
17981559-5	2008	In vivo, AsPC-1 xenografted tumors treated with EGCG showed significant reduction in volume, proliferation (Ki-67 and PCNA staining), angiogenesis (vWF, VEGF and CD31) and metastasis (MMP-2, MMP-7, MMP-9 and MMP-12) and induction in apoptosis (TUNEL), caspase-3 activity and growth arrest (p21/WAF1).	epigallocatechin gallate	48-52	caspase 3	Mus musculus	252-261	
17021948-7	2006	Furthermore, EGCG-treated transgenic mice showed increased number of motor neurons, diminished microglial activation, reduced immunohistochemical reaction of NF-kappaB and cleaved caspase-3 as well as reduced protein level of iNOS and NF-kappaB in the spinal cords.	epigallocatechin gallate	13-17	caspase 3	Mus musculus	180-189	
17451540-7	2007	Moreover, the effect of (-)-epigallocatechin gallate on the activation of caspase-3 was assessed by a colorimetric activity assay and western blotting.	epigallocatechin gallate	24-52	caspase 3	Mus musculus	74-83	
17451540-9	2007	Treatment with (-)-epigallocatechin gallate resulted in DNA fragmentation and induced the activation of caspase-3 in RAW 264.7 cell-derived osteoclasts.	epigallocatechin gallate	15-43	caspase 3	Mus musculus	104-113	
35409364-10	2022	Additionally, EGCG suppressed hypoxia-induced apoptosis of BV2 microglia with cleavage of poly (ADP-ribose) polymerase (PARP) and caspase-3.	epigallocatechin gallate	14-18	caspase 3	Mus musculus	130-139	
15375010-6	2005	Moreover, in skin from EGCG-treated ODC transgenic mice, caspase 3 (active form) was detected only in epidermal cells that possess very high levels of ODC protein.	epigallocatechin gallate	23-27	caspase 3	Mus musculus	57-66	
12205293-5	2002	Immunohistochemical analysis showed that topical applications of caffeine or EGCG increased apoptosis as measured by the number of caspase 3-positive cells in nonmalignant skin tumors by 87% or 72%, respectively, and in squamous cell carcinomas by 92% or 56%, respectively, but there was no effect on apoptosis in nontumor areas of the epidermis.	epigallocatechin gallate	77-81	caspase 3	Mus musculus	131-140	
15756018-8	2005	Treatment of EGCG-rich GTP in drinking water to 4T1 cells bearing BALB/c mice resulted in reduction of tumor growth accompanied with increase in Bax/Bcl-2 ratio, reduction in proliferating cell nuclear antigen and activation of caspase 3 in tumors.	epigallocatechin gallate	13-17	caspase 3	Mus musculus	228-237	
15756018-8	2005	Treatment of EGCG-rich GTP in drinking water to 4T1 cells bearing BALB/c mice resulted in reduction of tumor growth accompanied with increase in Bax/Bcl-2 ratio, reduction in proliferating cell nuclear antigen and activation of caspase 3 in tumors.	epigallocatechin gallate	23-26	caspase 3	Mus musculus	228-237	
31494133-5	2019	Besides, EGCG could down-regulate the expression of anti-apoptotic protein Bcl-2, and up-regulate the expression of pro-apoptotic proteins Bax and Caspase-3 in H22 cells.	epigallocatechin gallate	9-13	caspase 3	Mus musculus	147-156	
35287352-11	2022	Molecular docking results suggest that EGCG has a high affinity for the crystal structure of six targets (IL-6 (interleukin-6), TNF (tumor necrosis factor), Caspase3, MAPK3 (Mitogen-activated protein kinase 3), AKT1, and VEGFA (vascular endothelial growth factor)), and the experimental verification result showed levated expression of these 6 hub targets in the LPS group, but there is an obvious decrease in expression in the LPS + EGCG group.	epigallocatechin gallate	39-43	caspase 3	Mus musculus	157-165	
35287352-15	2022	The anti-inflammatory and anti-apoptotic effects of EGCG occur not only through direct binding to six target proteins (IL-6,TNF-alpha, Caspase3, MAPK3, AKT1, and VEGFA) but also by reducing their expression.	epigallocatechin gallate	52-56	caspase 3	Mus musculus	135-143	
29777127-5	2018	Moreover, in diabetic mice, EGCG preparation increased myocardial nuclear factor-kappa B and tumor necrosis factor-alpha in addition to pronounced overexpression of inducible nitric oxide synthase and active caspase-3.	epigallocatechin gallate	28-32	caspase 3	Mus musculus	208-217	
30840953-15	2019	Interestingly, compared with treatment with YC-1 or EGCG alone, more pronounced inhibition of ANGPTL4, caspase-3 and Nox1 were obtained when YC-1 and EGCG were administered simultaneously.	epigallocatechin gallate	52-56	caspase 3	Mus musculus	103-112	
30840953-15	2019	Interestingly, compared with treatment with YC-1 or EGCG alone, more pronounced inhibition of ANGPTL4, caspase-3 and Nox1 were obtained when YC-1 and EGCG were administered simultaneously.	epigallocatechin gallate	150-154	caspase 3	Mus musculus	103-112	
30310905-5	2018	EGCG induced breast cancer apoptotic cell death at 24 h, as evidenced by annexin V/PI, caspase 3, caspase 8 and caspase 9 activation.	epigallocatechin gallate	0-4	caspase 3	Mus musculus	87-96	
27889855-8	2017	Moreover, EGCG also decreased the expression of pro-apoptotic proteins (Bax, caspase-3), reduced the activity of the anti-inflammatory agent NF-kappaB and inhibited the oxidative stress by decreasing the levels of ROS and MDA and increasing the expression of MnSOD.	epigallocatechin gallate	10-14	caspase 3	Mus musculus	77-86	
28798484-5	2017	In particular, EGCG pretreatment significantly inhibited the H2O2-induced upregulation of cleaved forms of caspase-3, caspase-8, and caspase-9, Bax, CathepsinD, and downregulation of Bcl-2.	epigallocatechin gallate	15-19	caspase 3	Mus musculus	107-116	
28098182-11	2017	Administration of EGCG to diabetic mice showed significant elevation in serum cystatin C and neutrophil gelatinase-associated lipocalin, marked increase in oxidative stress and inflammatory states in addition to marked over expression of active caspase-3.	epigallocatechin gallate	18-22	caspase 3	Mus musculus	245-254	
26586942-6	2015	EGCG and TF-NPs were also found to be more effective than bulk TF/EGCG in inducing the cleavage of caspase-3 and caspase-9 and Bax/Bcl2 ratio in favor of apoptosis.	epigallocatechin gallate	66-70	caspase 3	Mus musculus	99-108	
23255902-10	2013	EGCG may inhibit the surrogate markers of proliferation and apoptosis (caspase 3) in A549 tumor xenografts in vivo.	epigallocatechin gallate	0-4	caspase 3	Mus musculus	71-80	
23605930-5	2011	Additionally, EGCG suppressed the DON-induced activation of caspase-3/7, which is an indicator of apoptosis.	epigallocatechin gallate	14-18	caspase 3	Mus musculus	60-71	
21633670-4	2011	EGCG combined with taxane also had an additive effect to increase the expression of apoptotic genes, (p53, p73, p21, and caspase 3) and the percent apoptosis observed in vitro and in tumor modeling studies in severe combined immunodeficient mice.	epigallocatechin gallate	0-4	caspase 3	Mus musculus	121-130	
26586942-6	2015	EGCG and TF-NPs were also found to be more effective than bulk TF/EGCG in inducing the cleavage of caspase-3 and caspase-9 and Bax/Bcl2 ratio in favor of apoptosis.	epigallocatechin gallate	0-4	caspase 3	Mus musculus	99-108	
25395675-5	2015	Mechanistically, prosurvival effects of EGCG treatment upon IR stress were regulated, at least in part, via the mitogen-activated protein kinase/BCL2 family/caspase 3 pathway.	epigallocatechin gallate	40-44	caspase 3	Mus musculus	157-166	
19122281-9	2009	Oral administration of EGCG (2 mg/kg or 6 mg/kg) for 4 weeks significantly improved the cognitive deficits in mice and elevated T-SOD and GSH-Px activities, decreased MDA contents in the hippocampus, and reduced the cell apoptosis index and expression of cleaved caspase-3 in the mouse hippocampus.	epigallocatechin gallate	23-27	caspase 3	Mus musculus	263-272