PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
32625095-10	2020	The correlational analysis between plasma of IL-6/TNF-alpha and metabolites suggested that acetylcholine, spermine, phenylalanine, threonine of plasma and phosphatidylcholine (36:4) of lung tissues were significantly associated with IL-6/TNF-alpha in CLP and CLP-ADMSCs groups.	Phosphatidylcholines	155-174	tumor necrosis factor	Rattus norvegicus	50-59	
32625095-10	2020	The correlational analysis between plasma of IL-6/TNF-alpha and metabolites suggested that acetylcholine, spermine, phenylalanine, threonine of plasma and phosphatidylcholine (36:4) of lung tissues were significantly associated with IL-6/TNF-alpha in CLP and CLP-ADMSCs groups.	Phosphatidylcholines	155-174	tumor necrosis factor	Rattus norvegicus	238-247	
23776397-12	2013	The treatment with PC or HC resulted in a significant attenuation on the increase in serum levels of TNF-alpha and IL-6, pro-inflammatory cytokines, while neither PC nor HC significantly attenuated serum levels of IL-10, anti-inflammatory cytokine.	Phosphatidylcholines	19-21	tumor necrosis factor	Rattus norvegicus	101-110	
17204250-4	2007	Treatment with TNF-alpha antibody or IL-1 receptor antagonist significantly attenuated infarction volume, sPLA2 IIA protein expression, PLA2 activity and significantly restored phosphatidylcholine levels after tMCAO.	Phosphatidylcholines	177-196	tumor necrosis factor	Rattus norvegicus	15-24	
21937953-9	2011	Phosphatidylcholine pretreatment reduced the plasma TNF-alpha and hippocampal NOx changes and prevented the decreased neurogenesis.	Phosphatidylcholines	0-19	tumor necrosis factor	Rattus norvegicus	52-61	
21937953-11	2011	Phosphatidylcholine supplementation did not reduce the overall extent of peripheral inflammatory activation, but efficiently counteracted the disturbed hippocampal neurogenesis by lowering circulating TNF-alpha concentrations.	Phosphatidylcholines	0-19	tumor necrosis factor	Rattus norvegicus	201-210	
19710104-8	2009	However, PC supplementation prevented the TNF-alpha-induced DNA fragmentation, cytochrome-c release and caspase-3 activity in control and CD hepatocytes.	Phosphatidylcholines	9-11	tumor necrosis factor	Rattus norvegicus	42-51	
19710104-10	2009	Furthermore, PC is identified as a new survival agent that reverses several TNFalpha-inducible responses that are likely to promote steatosis and necrosis.	Phosphatidylcholines	13-15	tumor necrosis factor	Rattus norvegicus	76-84	
17158358-2	2007	In this study we investigated the role of phosphatidylcholine-specific phospholipase C (PC-PLC) in silica-stimulated induction of TNF-alpha and IL-1beta and how PC-PLC activity is regulated by silica in a rat alveolar macrophage model.	Phosphatidylcholines	42-61	tumor necrosis factor	Rattus norvegicus	130-139	
7988135-21	1994	CONCLUSIONS: a) TNF-alpha alters the amounts of phosphatidylcholine, phosphatidylinositol, and possibly phosphatidylglycerol present in the lavage-accessible space of the isolated perfused rat lung.	Phosphatidylcholines	48-67	tumor necrosis factor	Rattus norvegicus	16-25	
10642356-4	2000	Cells isolated from rats given TNF-alpha had 26% lower levels of phosphatidylcholine compared with control.	Phosphatidylcholines	65-84	tumor necrosis factor	Rattus norvegicus	31-40	
9879668-0	1998	The inflammatory cytokines tumor necrosis factor alpha and interleukin-1beta stimulate phosphatidylcholine secretion in primary cultures of rat type II pneumocytes.	Phosphatidylcholines	87-106	tumor necrosis factor	Rattus norvegicus	27-54	
9879668-5	1998	These results suggest that tumor necrosis factor alpha or interleukin-1beta stimulate phosphatidylcholine secretion via protein kinase C activation in a Ca2+-independent manner.	Phosphatidylcholines	86-105	tumor necrosis factor	Rattus norvegicus	27-54	
9746498-5	1998	With phosphatidylcholine as substrate, TNF-alpha decreased both cytosolic and membrane-associated iPLA2 activities.	Phosphatidylcholines	5-24	tumor necrosis factor	Rattus norvegicus	39-48