A
Ayako Ojima
Researcher at Kurume University
Publications - 17
Citations - 698
Ayako Ojima is an academic researcher from Kurume University. The author has contributed to research in topics: Glycation & RAGE (receptor). The author has an hindex of 14, co-authored 17 publications receiving 599 citations.
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Empagliflozin, an Inhibitor of Sodium-Glucose Cotransporter 2 Exerts Anti-Inflammatory and Antifibrotic Effects on Experimental Diabetic Nephropathy Partly by Suppressing AGEs-Receptor Axis
TL;DR: Empagliflozin could inhibit oxidative, inflammatory and fibrotic reactions in the kidney of diabetic rats partly via suppression of the AGE-RAGE axis, which might be a novel therapeutic target for tubulointerstitial damage in diabetic nephropathy.
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Glucagon-Like Peptide-1 Receptor Agonist Inhibits Asymmetric Dimethylarginine Generation in the Kidney of Streptozotocin-Induced Diabetic Rats by Blocking Advanced Glycation End Product–Induced Protein Arginine Methyltranferase-1 Expression
Ayako Ojima,Yuji Ishibashi,Takanori Matsui,Sayaka Maeda,Yuri Nishino,Masayoshi Takeuchi,Kei Fukami,Sho-ichi Yamagishi +7 more
TL;DR: It is suggested that GLP-1 receptor agonist may inhibit the AGE-RAGE-mediated ADMA generation by suppressing PRMT-1 expression via inhibition of ROS generation, thereby protecting against the development and progression of diabetic nephropathy.
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Sulforaphane reduces advanced glycation end products (AGEs)-induced inflammation in endothelial cells and rat aorta
TL;DR: It is demonstrated for the first time that sulforaphane could inhibit inflammation in A GEs-exposed HUVECs and AGEs-infused rat aorta partly by suppressing RAGE expression through its anti-oxidative properties.
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Dipeptidyl peptidase-4 deficiency protects against experimental diabetic nephropathy partly by blocking the advanced glycation end products-receptor axis.
Takanori Matsui,Sae Nakashima,Yuri Nishino,Ayako Ojima,Nobutaka Nakamura,Kazunari Arima,Kei Fukami,Seiya Okuda,Sho-ichi Yamagishi +8 more
TL;DR: It is suggested that DPP-4 deficiency could exert beneficial actions on type 1 diabetic nephropathy partly by blocking the AGE-RAGE axis and might be a novel therapeutic target for preventing diabetic neephropathy.
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Glucose-dependent insulinotropic polypeptide (GIP) inhibits signaling pathways of advanced glycation end products (AGEs) in endothelial cells via its antioxidative properties.
TL;DR: GIP could block the signal pathways of AGEs in HUVECs by reducing ROS generation and subsequent RAGE expression probably via GIP receptor-cyclic AMP axis.