PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
19172241-13	2009	Unlike Hextend, resuscitation with ethyl pyruvate prevented high serum TNF-alpha levels and blunted TNF-alpha responses in all the organs including the spleen.	ethyl pyruvate	35-49	tumor necrosis factor	Homo sapiens	71-80	
25867066-4	2015	We show that BV6/TNFalpha-induced cell death depends on ROS production, as several ROS scavengers such as butylated hydroxyanisole, N-acetylcysteine, alpha-tocopherol and ethyl pyruvate significantly rescue cell death.	ethyl pyruvate	171-185	tumor necrosis factor	Homo sapiens	17-25	
20969857-9	2011	Furthermore, immunostaining of A549 cells revealed that ethyl pyruvate inhibited the nuclear association of RelA after TNFalpha treatment.	ethyl pyruvate	56-70	tumor necrosis factor	Homo sapiens	119-127	
26677054-8	2016	Treating A549 cells with either EtOH or EtP significantly reduced the IL-1beta- or TNF-induced IL-8 release, whereas treating Huh7 cells did not significantly alter IL-6 release.	ethyl pyruvate	40-43	tumor necrosis factor	Homo sapiens	83-86	
20302967-8	2010	An immunoblot analysis revealed that ethyl pyruvate inhibited the nuclear translocation of RelA from 5 min of the treatment with TNFalpha.	ethyl pyruvate	37-51	tumor necrosis factor	Homo sapiens	129-137	
19172241-13	2009	Unlike Hextend, resuscitation with ethyl pyruvate prevented high serum TNF-alpha levels and blunted TNF-alpha responses in all the organs including the spleen.	ethyl pyruvate	35-49	tumor necrosis factor	Homo sapiens	100-109	
16814517-3	2006	Ethyl pyruvate specifically inhibits tumor necrosis factor-alpha production and decreases circulating levels of high-mobility group box-1 and nuclear factor-kappaB signaling pathways by specifically targeting its p65 subunit in animals with established endotoxemia or sepsis and in macrophage cultures.	ethyl pyruvate	0-14	tumor necrosis factor	Homo sapiens	37-64	
32029037-8	2019	Compared with the LPS group, the oxidative activities and inflammatory factors above were inhibited in EP group [MDA (mumol/L): 12.35+-2.21 vs. 45.95+-1.76, SOD (kU/L): 54.68+-1.42 vs. 40.73+-1.60, IL-6 (ng/L): 67.87+-2.61 vs. 338.92+-20.91, TNF-alpha (ng/L): 19.23+-1.80 vs. 180.69+-6.51], mitochondrial membrane potential and ATP level were significantly increased [mitochondrial membrane potential: (99.43+-0.25)% vs. (69.40+-0.75)%, ATP (x106 RLU): 0.19+-0.01 vs. 0.12+-0.05], the expression of mitochondrial fission protein was significantly decreased (DAPK-2/beta-actin: 0.03+-0.01 vs. 0.61+-0.02), mitochondrial fusion proteins were significantly increased (Mfn-1/beta-actin: 0.43+-0.04 vs. 0.17+-0.01, Mfn-2/beta-actin: 0.201+-0.004 vs. 0.001+-0.001), percentage of cell apoptosis was significantly decreased [(5.25+-0.17)% vs. (34.42+-0.64)%], the expressions of apoptotic proteins were significantly decreased (caspase-3/beta-actin: 0.25+-0.15 vs. 1.76+-0.01, caspase-9/beta-actin: 0.09+-0.02 vs. 1.52+-0.12, Cyt C/beta-actin: 0.001+-0.001 vs. 0.350+-0.030), and the expressions of anti-apoptotic proteins and PARP were significantly increased (Bcl-2/beta-actin: 0.500+-0.010 vs. 0.009+-0.004, Bcl-xL/beta-actin: 0.550+-0.010 vs. 0.009+-0.001, PARP/beta-actin: 0.94+-0.01 vs. 0.16+-0.13), with statistically significant differences (all P < 0.05).	ethyl pyruvate	103-105	tumor necrosis factor	Homo sapiens	242-251