PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31491943-10	2019	CONCLUSIONS: In rats with fructose-induced DM, dapagliflozin downregulates RAGE-induced NADPH oxidase expression in LECs via the inactivation of GLUTs and a reduction in ROS generation.	Fructose	26-34	advanced glycosylation end product-specific receptor	Rattus norvegicus	75-79	
34687200-12	2022	CONCLUSIONS: Fructose induced reactive oxygen species generation in the NTS of rats through GLUT5 and receptor for advanced glycation end products (RAGE) signaling, thus impairing the AKT-nNOS-NO signaling pathway and ultimately causing hypertension.	Fructose	13-21	advanced glycosylation end product-specific receptor	Rattus norvegicus	102-146	
34687200-12	2022	CONCLUSIONS: Fructose induced reactive oxygen species generation in the NTS of rats through GLUT5 and receptor for advanced glycation end products (RAGE) signaling, thus impairing the AKT-nNOS-NO signaling pathway and ultimately causing hypertension.	Fructose	13-21	advanced glycosylation end product-specific receptor	Rattus norvegicus	148-152	
31375034-1	2019	OBJECTIVE: Advanced glycation end products and their receptor - RAGE - in the adipose tissues contribute to metabolic derangements in fructose-fed rats.	Fructose	134-142	advanced glycosylation end product-specific receptor	Rattus norvegicus	64-68	
31375034-2	2019	However, it remains unclear whether fructose could cause endothelial cell damage via the activation of AGE-RAGE.	Fructose	36-44	advanced glycosylation end product-specific receptor	Rattus norvegicus	107-111	
31272030-0	2019	Fructose-induced AGEs-RAGE signaling in skeletal muscle contributes to impairment of glucose homeostasis.	Fructose	0-8	advanced glycosylation end product-specific receptor	Rattus norvegicus	22-26	
31272030-5	2019	In L6 rat skeletal muscle cells, chronic exposure to fructose induced AGEs accumulation and the cellular level of the receptor for AGEs (RAGE) and the effect was prevented by pharmacological inhibition of glycation.	Fructose	53-61	advanced glycosylation end product-specific receptor	Rattus norvegicus	137-141	
31272030-7	2019	We also observed a high level of AGEs in serum and gastrocnemius muscle of fructose-supplemented animals, associated with methylglyoxal accumulation and up regulated expression of RAGE in gastrocnemius muscle.	Fructose	75-83	advanced glycosylation end product-specific receptor	Rattus norvegicus	180-184	
31272030-9	2019	Inhibition of AGEs-RAGE axis counteracted fructose-mediated glucose intolerance without affecting energy metabolism.	Fructose	42-50	advanced glycosylation end product-specific receptor	Rattus norvegicus	19-23	
28101123-1	2017	BACKGROUND: The AGE-RAGE-oxidative stress (AROS) axis is involved in the onset and progression of metabolic syndrome induced by a high-fructose diet (HFD).	Fructose	135-143	advanced glycosylation end product-specific receptor	Rattus norvegicus	20-24	
25105541-0	2015	DNA aptamer raised against advanced glycation end products (AGEs) improves glycemic control and decreases adipocyte size in fructose-fed rats by suppressing AGE-RAGE axis.	Fructose	124-132	advanced glycosylation end product-specific receptor	Rattus norvegicus	161-165	
25105541-6	2015	Our present study suggests that AGE-aptamer could improve glycemic control and prevent adipocyte remodeling in fructose-fed rats partly by suppressing the AGE-RAGE-mediated oxidative stress generation.	Fructose	111-119	advanced glycosylation end product-specific receptor	Rattus norvegicus	159-163	
24040205-10	2013	The protein expression of the receptor for AGEs (RAGE) and NF-kappaB were also significantly increased in the aorta of fructose fed rats.	Fructose	119-127	advanced glycosylation end product-specific receptor	Rattus norvegicus	49-53