TY - JOUR
T1 - Chebulic acid inhibits advanced glycation end products-mediated vascular dysfunction by suppressing ROS via the ERK/Nrf2 pathway
AU - Nam, Mi Hyun
AU - Son, Won rak
AU - Yang, Sung Yong
AU - Lee, Young Seok
AU - Lee, Kwang Won
N1 - Funding Information:
This research was supported by a Korea University Grant (K1604281) and School of Life Sciences and Biotechnology for BK21 PLUS, Korea University. The authors thank the Institute of Biomedical Science & Food Safety, Korea University Food Safety Hall, for providing the equipment and facilities.
Publisher Copyright:
© 2017
Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2017/9
Y1 - 2017/9
N2 - 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.
AB - 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.
KW - Advanced glycation end products
KW - Inflammation
KW - Nuclear factor E2-related factor
KW - Oxidative stress
KW - Vascular dysfunction
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U2 - 10.1016/j.jff.2017.06.058
DO - 10.1016/j.jff.2017.06.058
M3 - Article
AN - SCOPUS:85021737868
SN - 1756-4646
VL - 36
SP - 150
EP - 161
JO - Journal of Functional Foods
JF - Journal of Functional Foods
ER -
