PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
22047130-9	2011	RESULTS: Diazoxide inhibited in vitro nitric oxide (NO), tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) production and inducible nitric oxide synthase (iNOS) expression by activated microglia without affecting cyclooxygenase-2 (COX-2) expression and phagocytosis.	Diazoxide	9-18	nitric oxide synthase 2, inducible	Mus musculus	170-174	
12856829-5	2003	The cellular resistance was acquired by iNOS-/- mice myocytes due to HS, SSI, CCPA, S-ENBA, pinacidil and diazoxide treatment, which was evidenced by reduction of LDH (U/L) release from 51.14 +/- 1.35 (iNOS-/-) to 42.20 +/- 1.01 (iNOS-/- + HS); 45.57 +/- 0.75 (iNOS-/- + SSI); 42.87 +/- 0.87 (iNOS-/- + CCPA); 43.21 +/- 0.70 (iNOS-/- + S-ENBA); 37.81 +/- 0.99 (iNOS-/- + Pin) and 36.79 +/- 0.68 (iNOS-/- + Diazo), p < 0.01.	Diazoxide	406-411	nitric oxide synthase 2, inducible	Mus musculus	40-44	
12856829-7	2003	Further, our data also suggest that pinacidil and diazoxide are more potent inducers of delayed cellular protection among others in iNOS-/- mice myocytes against sustained simulated ischemia.	Diazoxide	50-59	nitric oxide synthase 2, inducible	Mus musculus	132-136	
11708847-4	2001	We hypothesized that NO is an important trigger for the opening of mitoK(ATP) channels in the late phase of preconditioning and inducible nitric oxide synthase (iNOS) up-regulation via NF kappa B plays a critical role in diazoxide-induced cardioprotection.	Diazoxide	221-230	nitric oxide synthase 2, inducible	Mus musculus	128-159	
11708847-4	2001	We hypothesized that NO is an important trigger for the opening of mitoK(ATP) channels in the late phase of preconditioning and inducible nitric oxide synthase (iNOS) up-regulation via NF kappa B plays a critical role in diazoxide-induced cardioprotection.	Diazoxide	221-230	nitric oxide synthase 2, inducible	Mus musculus	161-165	
11708847-8	2001	Administration of 5-HD, a specific blocker of mitoK(ATP) channel or l -NAME, an inhibitor of iNOS before I/R, during diazoxide-pretreatment completely blocked the late cardioprotection against ischemia.	Diazoxide	117-126	nitric oxide synthase 2, inducible	Mus musculus	93-97	
12856829-5	2003	The cellular resistance was acquired by iNOS-/- mice myocytes due to HS, SSI, CCPA, S-ENBA, pinacidil and diazoxide treatment, which was evidenced by reduction of LDH (U/L) release from 51.14 +/- 1.35 (iNOS-/-) to 42.20 +/- 1.01 (iNOS-/- + HS); 45.57 +/- 0.75 (iNOS-/- + SSI); 42.87 +/- 0.87 (iNOS-/- + CCPA); 43.21 +/- 0.70 (iNOS-/- + S-ENBA); 37.81 +/- 0.99 (iNOS-/- + Pin) and 36.79 +/- 0.68 (iNOS-/- + Diazo), p < 0.01.	Diazoxide	106-115	nitric oxide synthase 2, inducible	Mus musculus	40-44	
11708847-11	2001	Diazoxide was totally inefffective in iNOS knockout mice.	Diazoxide	0-9	nitric oxide synthase 2, inducible	Mus musculus	38-42	
11708847-12	2001	These results suggest that diazoxide activates NF kappa B via PKC signaling pathway and that leads to iNOS up-regulation after 24 hours.	Diazoxide	27-36	nitric oxide synthase 2, inducible	Mus musculus	102-106