PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
32167222-9	2020	In addition, glyburide inhibited the expression of NLRP3, IL-18, and IL-1beta protein in lung tissues, and also suppressed NLRP3 inflammasome activation, including caspase-1 p10, active IL-1beta protein in lung tissues, IL-1beta, and IL-18 in BALF.	Glyburide	13-22	caspase 1	Mus musculus	164-173	
34052309-6	2021	Mechanistically, glibenclamide treatment blocked NLRP3 inflammasome activation evidenced by reduced expressions of NLRP3, activated caspase-1 and mature interleukin-1beta in glibenclamide co-treated mice compared with those in paraquat and maneb group mice.	Glyburide	17-30	caspase 1	Mus musculus	132-141	
25077824-19	2014	Furthermore, Nalp3 and Caspase-1 levels were markedly increased by high glucose plus LPS, and both proteins were significantly inhibited by glibenclamide treatment.	Glyburide	140-153	caspase 1	Mus musculus	23-32	
24907587-7	2014	Caspase-1 KO mice, IL-1R1 KO mice, A2A AR KO mice and WT mice treated with the KATP channel blocker, glyburide, were resistant to adenosine-induced anxiety-like behaviors.	Glyburide	101-110	caspase 1	Mus musculus	0-9	
24917577-7	2014	Fluvastatin-induced activation of the NLRP3/caspase-1 pathway was required for the development of insulin resistance in adipose tissue explants, an effect also prevented by glyburide.	Glyburide	173-182	caspase 1	Mus musculus	44-53	
35185385-4	2022	Meanwhile, the increased proteins of NLRP3 and Caspase-1/p20 after LPS instillation in lungs were downregulated by glibenclamide.	Glyburide	115-128	caspase 1	Mus musculus	47-56	
35185385-7	2022	In conclusion, glibenclamide alleviates the development of LPS-induced ALI in a mouse model via inhibiting the NLRP3/Caspase-1/IL-1beta signaling pathway, which might provide a new strategy for the treatment of LPS-induced ALI.	Glyburide	15-28	caspase 1	Mus musculus	117-126