PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31608617-11	2020	The group co-administered with DHEA and aspirin showed significant increases in SOD, GST, CAT, GSH, Progesterone, Ca2+ ATPase, Na+ ATPase, H+ ATPase and significant reduction (p<0.05) in malondialdehyde, VEGF, TNF-alpha and estrogen as compared with the DHEA group.	Aspirin	40-47	vascular endothelial growth factor A	Rattus norvegicus	204-208	
31090331-4	2019	Through the study of network pharmacology,12 components of aspirin and Trichosanthis Fructus,including hydroxygenkwanin,quercetin and adenosine,were found to show the anti-platelet aggregation and anti-thrombosis mechanisms through9 common protein targets,such as SRC,RAC1,MAPK14,MAPK1,AKT1,and 14 common signaling pathways,such as VEGF signaling pathway.	Aspirin	59-66	vascular endothelial growth factor A	Rattus norvegicus	332-336	
31103824-9	2019	In the uterus, quercetin supplement to aspirin prevented the expression of VEGF and sFlt-1 mRNA.	Aspirin	39-46	vascular endothelial growth factor A	Rattus norvegicus	75-79	
31090331-5	2019	After the intervention with Trichosanthis Fructus pellets combined with aspirin pellets,the vascular endothslia growth factor(VEGF) signaling pathway can be activated to inhibit platelet aggregation and improve vascular endothelial function,and show the anti-platelet aggregation and anti-thrombosis mechanisms,which verify the results of the network pharmacology,and explain the anti-platelet aggregation and anti-thrombotic mechanisms of the combination of Trichosanthis Fructus pellets with aspirin pellets.	Aspirin	72-79	vascular endothelial growth factor A	Rattus norvegicus	126-130	
31090331-5	2019	After the intervention with Trichosanthis Fructus pellets combined with aspirin pellets,the vascular endothslia growth factor(VEGF) signaling pathway can be activated to inhibit platelet aggregation and improve vascular endothelial function,and show the anti-platelet aggregation and anti-thrombosis mechanisms,which verify the results of the network pharmacology,and explain the anti-platelet aggregation and anti-thrombotic mechanisms of the combination of Trichosanthis Fructus pellets with aspirin pellets.	Aspirin	494-501	vascular endothelial growth factor A	Rattus norvegicus	126-130	
18773975-3	2008	The reduction of growth factors such as transforming growth factor-alpha (TGF)-alpha and vascular endothelial cell growth factor (VEGF) by aspirin was determined by immunohistochemistry method.	Aspirin	139-146	vascular endothelial growth factor A	Rattus norvegicus	130-134	
29857294-12	2018	The higher expression of VEGFA in aspirin + PNS group verified the predicted potential protective targets of PNS.	Aspirin	34-41	vascular endothelial growth factor A	Rattus norvegicus	25-30	
29857294-13	2018	CONCLUSIONS: PNS may have protective function for aspirin-induced gastrointestinal injury through increasing VEGFA expression.	Aspirin	50-57	vascular endothelial growth factor A	Rattus norvegicus	109-114	
29219948-7	2018	In summary, ASA VI promotes angiogenesis of HUVECs in vitro via up-regulating the HIF-1alpha/VEGF pathway, and efficiently enhances the vascularization in regenerated tissue and facilitates wound healing in vivo.	Aspirin	12-15	vascular endothelial growth factor A	Rattus norvegicus	93-97	
18773975-4	2008	Administration of CAA produced significant protection against aspirin induced gastric toxicity by showing significant increase in PGE2, TGF-alpha, VEGF expression and accompanied by a significant inhibition of nitric oxide and regulating the levels of cytokines in rats.	Aspirin	62-69	vascular endothelial growth factor A	Rattus norvegicus	147-151	
12943528-12	2004	Overexpression of eNOS, VEGF and its receptor Flk-1 occurred early after azoxymethane administration in rat colonic tissue, even before morphological changes associated with tumour generation were observed, and aspirin prevented the overexpression of both eNOS and VEGF receptor Flk-1.	Aspirin	211-218	vascular endothelial growth factor A	Rattus norvegicus	24-28	
12943528-12	2004	Overexpression of eNOS, VEGF and its receptor Flk-1 occurred early after azoxymethane administration in rat colonic tissue, even before morphological changes associated with tumour generation were observed, and aspirin prevented the overexpression of both eNOS and VEGF receptor Flk-1.	Aspirin	211-218	vascular endothelial growth factor A	Rattus norvegicus	265-269