Chebulic acid inhibits advanced glycation end products-mediated vascular dysfunction by suppressing ROS via the ERK/Nrf2 pathway

Mi Hyun Nam; Won rak Son; Sung Yong Yang; Young Seok Lee; Kwang Won Lee

doi:10.1016/j.jff.2017.06.058

Chebulic acid inhibits advanced glycation end products-mediated vascular dysfunction by suppressing ROS via the ERK/Nrf2 pathway

Mi Hyun Nam, Won rak Son, Sung Yong Yang, Young Seok Lee, Kwang Won Lee

Research output: Contribution to journal › Article › peer-review

16 Citations (Scopus)

Abstract

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.

Original language	English
Pages (from-to)	150-161
Number of pages	12
Journal	Journal of Functional Foods
Volume	36
DOIs	https://doi.org/10.1016/j.jff.2017.06.058
Publication status	Published - 2017 Sept

Bibliographical note

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.

Keywords

Advanced glycation end products
Inflammation
Nuclear factor E2-related factor
Oxidative stress
Vascular dysfunction

ASJC Scopus subject areas

Food Science
Medicine (miscellaneous)
Nutrition and Dietetics

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.jff.2017.06.058

Cite this

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title = "Chebulic acid inhibits advanced glycation end products-mediated vascular dysfunction by suppressing ROS via the ERK/Nrf2 pathway",

abstract = "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.",

keywords = "Advanced glycation end products, Inflammation, Nuclear factor E2-related factor, Oxidative stress, Vascular dysfunction",

author = "Nam, {Mi Hyun} and Son, {Won rak} and Yang, {Sung Yong} and Lee, {Young Seok} and Lee, {Kwang Won}",

note = "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: {\textcopyright} 2017 Copyright: Copyright 2017 Elsevier B.V., All rights reserved.",

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doi = "10.1016/j.jff.2017.06.058",

language = "English",

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journal = "Journal of Functional Foods",

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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

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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.

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KW - Nuclear factor E2-related factor

KW - Oxidative stress

KW - Vascular dysfunction

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Chebulic acid inhibits advanced glycation end products-mediated vascular dysfunction by suppressing ROS via the ERK/Nrf2 pathway

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

UN SDGs

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