PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30724800-6	2019	Celecoxib significantly reversed the CUMS-induced decrease and increase in the levels of serotonin (5-HT) and its metabolite (5-hydroxyindole acetic acid) in the prefrontal cortex, and attenuated the CUMS-induced increase in the levels of inflammatory markers such as interleukin-6 and tumor necrosis factor-alpha, and apoptosis marker caspase-3 in the prefrontal cortex.	Celecoxib	0-9	caspase 3	Mus musculus	336-345	
25109418-7	2014	Furthermore, celecoxib induced apoptosis via the loss of the mitochondrial transmembrane potential (DeltaPsim), the release of cytochrome c and AIF, and the activation of caspase-9 and caspase-3.	Celecoxib	13-22	caspase 3	Mus musculus	185-194	
24945311-11	2014	Incubation with celecoxib dose-dependently suppressed the CSC-like properties and enhanced the IR effect on the induction of apoptosis, as detected by TUNEL assay and staining for Caspase 3 and Annexin V.	Celecoxib	16-25	caspase 3	Mus musculus	180-189	
16902813-8	2006	Cxb (aerosol/oral) + Doc showed increased apoptosis mediated via increased Fas and caspase-3 (P < 0.001) expression as compared to untreated control.	Celecoxib	0-3	caspase 3	Mus musculus	83-92