PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29567590-2	2018	In this study, we hypothesized that azithromycin (35 mg/kg orally) alleviated airway remodeling through suppression of epithelial-to-mesenchymal transition (EMT) via downregulation of transforming growth factor-beta 1 (TGF-beta1)/receptor for activated C-kinase1 (RACK1)/snail in mice.	Azithromycin	36-48	receptor for activated C kinase 1	Mus musculus	230-262	
29567590-2	2018	In this study, we hypothesized that azithromycin (35 mg/kg orally) alleviated airway remodeling through suppression of epithelial-to-mesenchymal transition (EMT) via downregulation of transforming growth factor-beta 1 (TGF-beta1)/receptor for activated C-kinase1 (RACK1)/snail in mice.	Azithromycin	36-48	receptor for activated C kinase 1	Mus musculus	264-269	
29567590-7	2018	Moreover, the increasing mRNA and protein expressions of TGF-beta1 and RACK1 and mRNA level of Snail in lung tissue were all significantly decreased in azithromycin-treated mice (P < 0.05).	Azithromycin	152-164	receptor for activated C kinase 1	Mus musculus	71-76	
29567590-8	2018	Taken together, our results suggest that azithromycin has the greatest effects on reducing airway remodeling by inhibiting TGF-beta1/RACK1/Snail signal and improving the EMT in airway epithelium.	Azithromycin	41-53	receptor for activated C kinase 1	Mus musculus	133-138