Chebulic acid inhibits advanced glycation end products-mediated vascular dysfunction by suppressing ROS via the ERK/Nrf2 pathway
| Autor: | Young Seok Lee, Won rak Son, Kwang Won Lee, Sung Yong Yang, Mi Hyun Nam |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
MAPK/ERK pathway Endothelium Medicine (miscellaneous) Inflammation Pharmacology medicine.disease_cause Vascular dysfunction Endothelial activation 03 medical and health sciences chemistry.chemical_compound Glycation medicine TX341-641 Advanced glycation end products Nutrition and Dietetics Nutrition. Foods and food supply Chebulic acid 030104 developmental biology medicine.anatomical_structure chemistry Oxidative stress Nuclear factor E2-related factor Immunology medicine.symptom Intracellular Food Science |
| Zdroj: | Journal of Functional Foods, Vol 36, Iss, Pp 150-161 (2017) |
| ISSN: | 1756-4646 |
| Popis: | Advanced glycation end-products (AGEs) considered as a fatal mediator in the diabetic atherosclerotic pathology. In this study, we evaluated the effects of chebulic acid (CA) on anti-oxidant activities and its glycoaldehyde-induced AGEs (glycol-AGEs)-mediates systemic vascular dysfunction in endothelium, monocytes, and smooth muscle cells (SMC) co-culture condition. CA exhibited strong at free radical scavenging activity by blocking intracellular ROS formation in endothelium. They also suppressed endothelial activation by blocking the monocytes adhesion to endothelium, and pro-inflammatory cytokines, such as TNF-α, IL-1β, and IL-6 as well as enhancing anti-oxidant detoxification defensing mediators such as HO-1 and NQO1 expression, through ERK/Nrf2 signaling in HUVEC. Furthermore, CA administration provided powerful anti-inflammatory supplements to mice, and also has similar results by enhancing Nrf2, and their down-streamed mediators. These in vitro and in vivo studies indicated that CA attenuated glycol-AGEs-mediates vascular dysfunction by ameliorating AGEs-induced inflammation and oxidative stress via enhancing the detoxification defensing pathway of ERK/Nrf2. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect