PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
34266350-5	2021	Compared to the control group, increased BBB permeability, suppressed occludin expression, excessive release of inflammatory factors, and downregulation of kruppel-like factor 2 (KLF2) were observed in diabetic mice, all of which were dramatically reversed by Azilsartan treatment.	azilsartan	260-270	Kruppel-like factor 2 (lung)	Mus musculus	156-177	
34266350-5	2021	Compared to the control group, increased BBB permeability, suppressed occludin expression, excessive release of inflammatory factors, and downregulation of kruppel-like factor 2 (KLF2) were observed in diabetic mice, all of which were dramatically reversed by Azilsartan treatment.	azilsartan	260-270	Kruppel-like factor 2 (lung)	Mus musculus	179-183	
34266350-6	2021	In the in vitro experiments, elevated endothelial permeability and decreased expression of occludin and KLF2 were observed in high glucose-challenged endothelial cells, which were significantly alleviated by Azilsartan.	azilsartan	208-218	Kruppel-like factor 2 (lung)	Mus musculus	104-108	
34266350-7	2021	Lastly, the silencing of KLF2 abolished the protective effects of Azilsartan against the high glucose-induced expression of occludin and endothelial monolayer permeability in bEnd.3 brain endothelial cells.	azilsartan	66-76	Kruppel-like factor 2 (lung)	Mus musculus	25-29	
34266350-8	2021	Based on these observations, we concluded that Azilsartan protected against hyperglycemia-induced hyperpermeability of BBB via the KLF2/occludin axis.	azilsartan	47-57	Kruppel-like factor 2 (lung)	Mus musculus	131-135