PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
33655586-12	2021	AZM can inhibit apoptosis and the expression of Bax and Cleaved caspase-3, 6, 9, and promote the expression of Bcl-2 (p < .001).	Azithromycin	0-3	BCL2 apoptosis regulator	Homo sapiens	111-116	
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	BCL2 apoptosis regulator	Homo sapiens	180-184	
27916734-10	2017	In vitro, azithromycin significantly suppressed TGF-beta1-induced BEAS-2B cells apoptosis (P&lt;0.05) and reversed TGF-beta1 elevated Caspase-3 mRNA level and Bax/Bcl-2 ratio (P&lt;0.05).	Azithromycin	10-22	BCL2 apoptosis regulator	Homo sapiens	163-168	
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	BCL2 apoptosis regulator	Homo sapiens	223-228	
33607534-11	2021	Based on qRT-PCR data, single AZT and combined AZT/IMA treatment also induced BAX/BCL-2 ratio significantly in both K562S and K562R cells.	Azithromycin	30-33	BCL2 apoptosis regulator	Homo sapiens	82-87	
33607534-11	2021	Based on qRT-PCR data, single AZT and combined AZT/IMA treatment also induced BAX/BCL-2 ratio significantly in both K562S and K562R cells.	Azithromycin	47-50	BCL2 apoptosis regulator	Homo sapiens	82-87	
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	BCL2 apoptosis regulator	Homo sapiens	141-146