PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
24213508-5	2012	The apoptosis induced by AZM was partly through a caspase-dependent mechanism with an up-regulation of apoptotic protein cleavage PARP and caspase-3 products, as well as a down-regulation of anti-apoptotic proteins, Mcl-1, bcl-2 and bcl-X1.	Azithromycin	25-28	caspase 3	Homo sapiens	139-148	
30515223-11	2018	In addition, pretreatment of PDLSCs with AZM (10 mug/ml, 20 mug/ml) prevented TNF-alpha-induced apoptosis by decreasing caspase-8 and caspase-3 expression.	Azithromycin	41-44	caspase 3	Homo sapiens	134-143	
27916734-11	2017	SIGNIFICANCE: Azithromycin is an attractive treatment option for reducing airway epithelial cell apoptosis by improving the imbalance of Bax/Bcl-2 ratio and inhibiting Caspase-3 level in airway epithelium.	Azithromycin	14-26	caspase 3	Homo sapiens	168-177	
33607534-8	2021	RESULTS: AZT treatment alone inhibited cell viability, induced apoptosis and enhanced caspase 3/7 activity in both K562S and high MDR-1 (Pgp) expressing K562R cells.	Azithromycin	9-12	caspase 3	Homo sapiens	86-97	
33607534-9	2021	Moreover, combination of AZT/IMA suppressed cell viability, induced apoptosis and caspase3/7 activity more effectively and significantly compared to K562R cells treated with only IMA or AZT.	Azithromycin	25-28	caspase 3	Homo sapiens	82-92	
27916734-2	2017	In the present study, we hypothesized that azithromycin alleviated airway epithelium injury through inhibiting airway epithelium apoptosis via down regulation of caspase-3 and Bax/Bcl2 ratio in vivo and in vitro.	Azithromycin	43-55	caspase 3	Homo sapiens	162-171	
27916734-10	2017	In vitro, azithromycin significantly suppressed TGF-beta1-induced BEAS-2B cells apoptosis (P<0.05) and reversed TGF-beta1 elevated Caspase-3 mRNA level and Bax/Bcl-2 ratio (P<0.05).	Azithromycin	10-22	caspase 3	Homo sapiens	134-143