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ORIGINAL ARTICLE
Year : 2022  |  Volume : 5  |  Issue : 3  |  Page : 80-87

The role of RAGE, MAPK and NF-κB pathway in the advanced glycation end-products induced HUVECs dysfunction


Department of Vascular Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China

Correspondence Address:
Dr. Dong-Lin Li
Department of Vascular Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou
China
Dr. Qian-Qian Zhu
Department of Vascular Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2589-9686.360874

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OBJECTIVE: The objective of this study was to investigate how receptor for advanced glycation end-products–mitogen-activated protein kinase–nuclear factor-kappa B (MAPK-NF-κB) pathway is involved in advanced glycation end-product (AGE)-induced human umbilical venous endothelial cell (HUVEC) dysfunction. MATERIALS AND METHODS: HUVECs were cultured with AGEs, anti-RAGE, inhibitors of MAPK or NF-κB respectively. Then we detected endothelial nitric oxide synthase (eNOS) activation, nitric oxide (NO) concentration, cell migration ability, and RAGE expression of HUVECs. RESULTS: AGEs depressed eNOS activation, decreased NO concentration, impaired endothelial cell (EC) migration, and upregulated RAGE expression, which could be recovered by p38 inhibitor and extracellular regulated protein kinases (ERK) inhibitor. However, these effects could not be recovered by NF-κB inhibitor. CONCLUSIONS: AGEs increase RAGE expression and decrease NO release and migration of HUVECs through RAGE-MAPK pathway, but not NF-κB pathway.


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