PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
27573128-5	2016	The addition of Fasudil inhibited MSC-induced inflammatory signaling TLR-4/MyD88 and inflammatory molecule IFN-gamma, IL-1beta, and TNF-alpha but did not convert M1 microglia to M2 phenotype.	fasudil	16-23	tumor necrosis factor	Mus musculus	132-141	
27401064-9	2017	Fasudil intervention also inhibited TLR-2/4, p-NF-kappaB/p65, MyD88, interleukin-1beta, interleukin-6 and tumor necrosis factor-alpha for TLRs-NF-kappaB-MyD88 inflammatory cytokine axis and the induction of interleukin-10.	fasudil	0-7	tumor necrosis factor	Mus musculus	106-133	
26789651-7	2016	Neurotrophic factor BDNF and GDNF as well as immunomodulatory cytokine IL-10 in spinal cord were elevated in Fasudil-treated mice, while inflammatory cytokine IL-17, IL-1beta, IL-6, and TNF-alpha were obviously inhibited, accompanied by the decrease of inflammatory M1 iNOS and the increase of anti-inflammatory M2 Arg-1, providing a microenvironment that contributes to synaptic protection.	fasudil	109-116	tumor necrosis factor	Mus musculus	186-195	
26045742-9	2015	The expression of IL-1beta, TNF-alpha, TLR2 and p-NF-kappaB and iNOS were lower after fasudil treatment (P<0.05) while the expression of arginase1 was increased (P<0.05).	fasudil	86-93	tumor necrosis factor	Mus musculus	28-37	
25287052-5	2015	Fasudil also decreased levels of iNOS/NO, enhanced levels of Arg-1, and inhibited the TLR-4/NF-kappaB signaling and TNF-alpha, shifting M1 macrophage to M2 phenotype.	fasudil	0-7	tumor necrosis factor	Mus musculus	116-125	
24638037-5	2014	Administration of fasudil, a Rho-kinase inhibitor, significantly reduced the I/R-induced expression of the proinflammatory cytokines interleukin (IL)-6, C-C motif chemoattractant ligand 2 (CCL2), and tumor necrosis factor (TNF)-alpha, in leukocytes, compared with saline as the vehicle.	fasudil	18-25	tumor necrosis factor	Mus musculus	200-233	
25908255-4	2015	The administration of Fasudil exhibited neuroprotective effects against the dopaminergic neurons and improved the motor function recovery in the MPTP-PD mice, accompanied by the suppression of inflammatory responses (IL-1beta, TNF-alpha, NF-kappaB-p65 and TLR-2), and oxidative stress (iNOS and gp91Phox), which might be associated with the inhibition of ROCK and GSK-3beta activity.	fasudil	22-29	tumor necrosis factor	Mus musculus	227-236	
25263338-12	2014	In EAE mice, fasudil administration significantly decreased both CD11b(+)iNOS(+) and CD11b(+)TNF-alpha(+) M1 microglia, and increased CD11b(+)IL-10(+) M2 microglia.	fasudil	13-20	tumor necrosis factor	Mus musculus	93-102	
24311453-8	2014	Modeling a proinflammatory microglial phenotype by stimulation with LPS in vitro, Fasudil decreased the release of proinflammatory cytokines and chemokines TNFalpha, Il6, CCL2, CCL3, and CCL5 while CXCL1 release was only transiently suppressed.	fasudil	82-89	tumor necrosis factor	Mus musculus	156-164	
23232512-10	2012	Fasudil inhibited the expression of iNOS on microglia and p-NF-kappaB/p65 on astrocytes in spinal cords,  accompanied by the inhibition of inflammatory factors IL-1beta  and TNF-alpha.	fasudil	0-7	tumor necrosis factor	Mus musculus	174-183	
24405591-0	2014	[Inhibition of Fasudil on lipopolysaccharide-induced TNF-alpha and IL-1beta expressions through TLR4 pathway in murine BV-2 cells in vitro].	fasudil	15-22	tumor necrosis factor	Mus musculus	53-62	
24405591-7	2014	Fasudil attenuated NO production, and reduced the release of TNF-alpha and IL-1beta in LPS-stimulated BV-2 cells.	fasudil	0-7	tumor necrosis factor	Mus musculus	61-70	
24405591-9	2014	CONCLUSION: Fasudil can suppress the production of TNF-alpha, IL-1beta and NO of microglia cells induced by LPS, which may be associated with the down-regulation of TLR4 pathway.	fasudil	12-19	tumor necrosis factor	Mus musculus	51-60	
30779332-9	2019	Fasudil-modified MNCs inhibited the activation of inflammatory signaling p-NF-kB/P38, accompanied by the decrease of COX-2 and the increase of Arg-1 in spinal cord, as well as the reduction of IL-17, TNF-alpha, IL-6 and the elevation of IL-10 in cultured supernatant of splenocytes.	fasudil	0-7	tumor necrosis factor	Mus musculus	200-209	
16641138-6	2006	Moreover, we found that fasudil abolished extravascular infiltration of leukocytes as well as production of TNF-alpha and CXC chemokines in the liver of endotoxemic mice.	fasudil	24-31	tumor necrosis factor	Mus musculus	108-117	
16641138-8	2006	Our novel data document that fasudil is a potent inhibitor of endotoxin-induced expression of TNF-alpha and CXC chemokines as well as leukocyte infiltration and hepatocellular apoptosis in the liver.	fasudil	29-36	tumor necrosis factor	Mus musculus	94-103	
22994384-4	2012	Fasudil inhibited TLR-4, p-NF-kB/p65, and inflammatory cytokines (IL-1beta, IL-6, and TNF-alpha) and enhanced IL-10 production in spinal cords.	fasudil	0-7	tumor necrosis factor	Mus musculus	86-95	
21962807-9	2011	Furthermore, pretreatment of mice with fasudil inhibited LPS-induced increasing of TNF-alpha, IL-1beta mRNA expression (3 and 6 h) and AP-1/DNA binding activity (3 h) in blood cells.	fasudil	39-46	tumor necrosis factor	Mus musculus	83-92	
30236202-9	2018	Fasudil treatment significantly inhibited LPS-induced the secretion of NO, TNF-alpha and IL-6 and enhanced the production of IL-10 and IL-4.	fasudil	0-7	tumor necrosis factor	Mus musculus	75-84	
29554661-6	2018	RESULTS: The contents of pro-inflammatory cytokines interleukin (IL)-1beta, IL-6 and tumour necrosis factor (TNF)-alpha were inhibited by ALK, metformin or fasudil in diabetic db/db mice.	fasudil	156-163	tumor necrosis factor	Mus musculus	85-119