PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
25086357-0	2014	Downregulation of cystathionine beta-synthase/hydrogen sulfide contributes to rotenone-induced microglia polarization toward M1 type.	Rotenone	78-86	cystathionine beta-synthase	Mus musculus	18-45	
25086357-6	2014	Moreover, the transcription and protein expression of cystathionine-beta-synthase (CBS), as well as hydrogen sulfide (H2S) production were decreased in rotenone-treated primary microglia.	Rotenone	152-160	cystathionine beta-synthase	Mus musculus	54-81	
25086357-6	2014	Moreover, the transcription and protein expression of cystathionine-beta-synthase (CBS), as well as hydrogen sulfide (H2S) production were decreased in rotenone-treated primary microglia.	Rotenone	152-160	cystathionine beta-synthase	Mus musculus	83-86	
25086357-7	2014	Elevating endogenous H2S via CBS over-expression in immortalized microglia not only reduced the expression of pro-inflammatory M1 genes, but also enhanced the anti-inflammatory M2 marker IL-10 production in response to rotenone stimulation as compared to vector-transfected cells.	Rotenone	219-227	cystathionine beta-synthase	Mus musculus	29-32	
25086357-9	2014	In addition, we observed reactive oxygen species (ROS) scavenger N-acetyl-l-cysteine reversed the down-regulation of CBS and H2S generation caused by rotenone in microglia.	Rotenone	150-158	cystathionine beta-synthase	Mus musculus	117-120	
25086357-11	2014	Taken together, these results reveal that probably via triggering ROS formation, rotenone suppressed the CBS-H2S pathway and thus promoted microglia polarization toward M1 pro-inflammatory phenotype.	Rotenone	81-89	cystathionine beta-synthase	Mus musculus	105-108