PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
32918847-0	2021	NLRP3 inflammasome-derived interleukin-1beta attenuates stress-induced gastric injury via the COX-2/PGE2 axis.	Dinoprostone	100-104	NLR family, pyrin domain containing 3	Mus musculus	0-5	
32918847-11	2021	PGE2 supplementation abolished the hypersensitivity in NLRP3-/- and caspase-1-/- mice through negative regulation of inflammatory cytokines.	Dinoprostone	0-4	NLR family, pyrin domain containing 3	Mus musculus	55-60	
32918847-12	2021	CONCLUSION: These results suggest that NLRP3 inflammasome-derived IL-1beta plays a protective role in stress-induced gastric injury via activation of the COX-2/PGE2 axis.	Dinoprostone	160-164	NLR family, pyrin domain containing 3	Mus musculus	39-44	
31141808-0	2020	Prostaglandin E2 Regulates Activation of Mouse Peritoneal Macrophages by Staphylococcus aureus through Toll-Like Receptor 2, Toll-Like Receptor 4, and NLRP3 Inflammasome Signaling.	Dinoprostone	0-16	NLR family, pyrin domain containing 3	Mus musculus	151-156	
31141808-7	2020	Our data demonstrate that S. aureus can induce macrophage TLR/mitogen-activated protein kinase/NF-kappaB signaling and that PGE2 treatment upregulates NLRP3/caspase-1 signaling activation.	Dinoprostone	124-128	NLR family, pyrin domain containing 3	Mus musculus	151-156	
31141808-8	2020	Thus, macrophage PGE2 secretion after S. aureus infection depends on bacterial lipoprotein maturation and macrophage receptors TLR2, TLR4, and NLRP3.	Dinoprostone	17-21	NLR family, pyrin domain containing 3	Mus musculus	143-148	
31141808-9	2020	Moreover, exogenous PGE2 regulates S. aureus-induced macrophage activation through TLRs and NLRP3 inflammasome signaling.	Dinoprostone	20-24	NLR family, pyrin domain containing 3	Mus musculus	92-97	
27666012-0	2016	Bone marrow stromal cells attenuate LPS-induced mouse acute liver injury via the prostaglandin E 2-dependent repression of the NLRP3 inflammasome in Kupffer cells.	Dinoprostone	81-98	NLR family, pyrin domain containing 3	Mus musculus	127-132	
27666012-2	2016	Bone marrow mesenchymal stem cells (BMSCs) attenuate sepsis through prostaglandin E 2 (PGE2) by increasing the interleukin-10 (IL-10) production of macrophages; moreover, NLRP3 inflammasome assembly is effectively regulated by IL-10 during infection.	Dinoprostone	68-85	NLR family, pyrin domain containing 3	Mus musculus	171-176	
27666012-7	2016	Furthermore, extracellular signal-regulated kinase 1 (ERK1) inhibitor reduced IL-10 production in KCs and blocked the inhibitory effect of PGE2 on the activation of the NLRP3 inflammasome.	Dinoprostone	139-143	NLR family, pyrin domain containing 3	Mus musculus	169-174	
27666012-8	2016	Our data reveal a novel mechanism of BMSC-mediated suppression of the activation of KCs through the secretion of PGE2 by BMSCs, which promotes KCs to secrete IL-10, leading to the inhibition of the NLRP3 inflammasome in KCs.	Dinoprostone	113-117	NLR family, pyrin domain containing 3	Mus musculus	198-203	
33413632-7	2021	MSC-derived PGE2 inhibited TGF-beta-activated kinase 1 (TAK1) signaling and NLRP3 inflammasome activation in liver macrophages to decrease the production of inflammatory cytokines.	Dinoprostone	12-16	NLR family, pyrin domain containing 3	Mus musculus	76-81	
29100270-4	2017	Meanwhile, NLRP3 and mPGES-1 were stimulated in NKCC2 positive tubules (thick ascending limb, TAL) paralleled with increased urinary PGE2 excretion.	Dinoprostone	133-137	NLR family, pyrin domain containing 3	Mus musculus	11-16