PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
10788575-0	2000	Diethyldithiocarbamate enhances production of nitric oxide and TNF-alpha by lipopolysaccharide-stimulated rat Kupffer cells.	Ditiocarb	0-22	tumor necrosis factor	Rattus norvegicus	63-72	
10788575-2	2000	The purpose of this study was to evaluate if DDC was able to stimulate other potentially toxic mediators such as nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) using isolated rat Kupffer cells.	Ditiocarb	45-48	tumor necrosis factor	Rattus norvegicus	135-162	
10788575-2	2000	The purpose of this study was to evaluate if DDC was able to stimulate other potentially toxic mediators such as nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) using isolated rat Kupffer cells.	Ditiocarb	45-48	tumor necrosis factor	Rattus norvegicus	164-173	
10788575-4	2000	Interestingly, when Kupffer cells were stimulated by lipopolysaccharide (LPS), DDC (0-30 microM) enhanced the production of both NO and TNF-alpha in a concentration-dependent manner.	Ditiocarb	79-82	tumor necrosis factor	Rattus norvegicus	136-145	
10788575-7	2000	The enhanced effects of DDC on the release of NO and TNF-alpha from Kupffer cells was inhibited by N-acetyl-L-cysteine (an inhibitor of transcription factor NF-kappaB activation).	Ditiocarb	24-27	tumor necrosis factor	Rattus norvegicus	53-62	
10788575-10	2000	The stimulatory effect of DDC on both NO and TNF-alpha release was inhibited by H-7 (an inhibitor of protein kinase C) but not H-8 (an inhibitor of cAMP-dependent protein kinase).	Ditiocarb	26-29	tumor necrosis factor	Rattus norvegicus	45-54	
10788575-11	2000	These findings demonstrate that DDC enhances the production of NO and TNF-alpha by LPS-stimulated Kupffer cells and suggest that protein kinase C plays a critical role in mediating these effects of DDC.	Ditiocarb	32-35	tumor necrosis factor	Rattus norvegicus	70-79	
31391086-7	2019	Moreover, the enhancement of AAR caused by TNFalpha can be significantly strengthened by the pretreatment of diethyldithiocarbamate (DETC), a superoxide dismutase inhibitor, but attenuated by TNF-alpha receptor antagonist R-7050, superoxide scavenger PEG-SOD and NADPH oxidase inhibitor apocynin (Apo) in rats with OH.	Ditiocarb	109-131	tumor necrosis factor	Rattus norvegicus	43-51	
34422078-15	2021	Results: The pathohistological results demonstrated that DD could ameliorate DDC-induced CP in vivo, indicated by reduction of alpha-SMA, col-1, col-3, TNF-alpha, and IL-6.	Ditiocarb	77-80	tumor necrosis factor	Rattus norvegicus	152-161	
31391086-7	2019	Moreover, the enhancement of AAR caused by TNFalpha can be significantly strengthened by the pretreatment of diethyldithiocarbamate (DETC), a superoxide dismutase inhibitor, but attenuated by TNF-alpha receptor antagonist R-7050, superoxide scavenger PEG-SOD and NADPH oxidase inhibitor apocynin (Apo) in rats with OH.	Ditiocarb	133-137	tumor necrosis factor	Rattus norvegicus	43-51