PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
26593276-5	2016	We found that lithium chloride (LiCl), a widely used GSK3 inhibitor and the mainstay treatment for bipolar disorder, reinforced the LPS adaptive response by enhancing both downregulation of pro-inflammatory genes (inducible nitric oxide synthase, interleukin 1beta, interleukin 6, tumor necrosis factor alpha), and upregulation of genes typically associated to anti-inflammatory functions (interleukin 10 and MRC1).	Lithium Chloride	14-30	interleukin 1 beta	Homo sapiens	247-264	
31573051-13	2019	In addition, the results demonstrated that IL-21 treatment reduced the expression levels of proteins associated with the Wnt/beta-catenin signaling, whereas activation of Wnt/beta-catenin signaling with the LiCl agonist upregulated PD-L1, IL-1beta and TNF-alpha expression.	Lithium Chloride	207-211	interleukin 1 beta	Homo sapiens	239-247	
29049420-8	2017	Furthermore, DAPT and LiCl decreased production of IL-1beta, TNF-alpha, IL-6, iNOS, Cox2 and MCP-1; however, IL-10 expression was increased notably in LiCl treated cells.	Lithium Chloride	22-26	interleukin 1 beta	Homo sapiens	51-59	
26593276-5	2016	We found that lithium chloride (LiCl), a widely used GSK3 inhibitor and the mainstay treatment for bipolar disorder, reinforced the LPS adaptive response by enhancing both downregulation of pro-inflammatory genes (inducible nitric oxide synthase, interleukin 1beta, interleukin 6, tumor necrosis factor alpha), and upregulation of genes typically associated to anti-inflammatory functions (interleukin 10 and MRC1).	Lithium Chloride	32-36	interleukin 1 beta	Homo sapiens	247-264	
25746333-9	2015	We also found that lower viral replication after LiCl treatment was associated with the reduced mRNA levels of pro-inflammatory IL-8, IL-6, IL-1 beta, tumor necrosis factor alpha and decreased NF-kappaB nuclear translocation.	Lithium Chloride	49-53	interleukin 1 beta	Homo sapiens	140-149	
17988365-6	2007	In vitro exposure of monocytes to LiCl did not have the same effects as lithium treatment: the procedure decreased IL-1beta production and had minimal effects on IL-6 production.	Lithium Chloride	34-38	interleukin 1 beta	Homo sapiens	115-123	
24470226-8	2014	CONCLUSION: LiCl reduced catabolic events in IL-1beta-treated human articular chondrocytes and attenuated the severity of cartilage destruction in IL-1beta-treated mouse femoral head explants and in the knee joints of mice with surgically induced OA, acting via inhibition of the activities of the NF-kappaB, p38, and STAT-3 signaling pathways.	Lithium Chloride	12-16	interleukin 1 beta	Homo sapiens	45-53	
24470226-8	2014	CONCLUSION: LiCl reduced catabolic events in IL-1beta-treated human articular chondrocytes and attenuated the severity of cartilage destruction in IL-1beta-treated mouse femoral head explants and in the knee joints of mice with surgically induced OA, acting via inhibition of the activities of the NF-kappaB, p38, and STAT-3 signaling pathways.	Lithium Chloride	12-16	interleukin 1 beta	Homo sapiens	147-155