PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
12949732-4	2003	RESULTS: In the monocrotaline-induced rat model of sinusoidal obstruction syndrome, there was an early increase of matrix metalloproteinase-9 and a later, lower-magnitude increase of matrix metalloproteinase-2 in the liver.	Monocrotaline	16-29	matrix metallopeptidase 2	Rattus norvegicus	183-209	
19057128-12	2008	MMP-2 and MMP-9 expressions and activities in right ventricles increased significantly in monocrotaline-injected rats and captopril inhibited them.	Monocrotaline	90-103	matrix metallopeptidase 2	Rattus norvegicus	0-5	
12949732-8	2003	CONCLUSIONS: Monocrotaline causes depolymerization of F-actin in sinusoidal endothelial cells, which leads to increased expression of metalloproteinase-9 and matrix metalloproteinase-2 by sinusoidal endothelial cells.	Monocrotaline	13-26	matrix metallopeptidase 2	Rattus norvegicus	134-184	
31922224-9	2020	The results demonstrated that FMN significantly alleviated the changes of hemodynamics and pulmonary vascular morphology, and decreased the MCT-induced upregulations of TGFbeta1, MMP2 and MMP9 expression levels.	Monocrotaline	140-143	matrix metallopeptidase 2	Rattus norvegicus	179-183	
26638897-6	2016	These findings indicate that heparanase and MMP2 might play an important role in the development of MCT-induced cardiac hypertrophy.	Monocrotaline	100-103	matrix metallopeptidase 2	Rattus norvegicus	44-48