The Effect of Mangiferin on Improving Endothelial Dysfunction by Inhibiting Endoplasmic Reticulum Stress to Alleviate Mitochondrial Fission

Yang Chen; Yu-peng Chen; Bao-lin Liu; Kang Liu; Fang Huang; Zhi-xia Qiu

doi:doi:10.11648/j.ajcem.20170505.12

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The Effect of Mangiferin on Improving Endothelial Dysfunction by Inhibiting Endoplasmic Reticulum Stress to Alleviate Mitochondrial Fission

Yang Chen, Yu-peng Chen, Bao-lin Liu, Kang Liu, Fang Huang, Zhi-xia Qiu

Published in American Journal of Clinical and Experimental Medicine (Volume 5, Issue 5)

Received: 23 July 2017 Accepted: 16 August 2017 Published: 31 August 2017

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Abstract

Microvascular and macrovascular diseases are important complications of metabolic diseases and affect the normal functioning of the human cardiovascular system. Endothelial dysfunction is the basic pathological tache of vascular diseases. This study aims to find out whether mangiferin can relieve endothelial dysfunction by inhibiting mitochondrial fission induced by endoplasmic reticulum stress. After being stimulated by palmitate, the expression of endoplasmic reticulum stress-related proteins Bip, p-PERK (RNA-like endoplasmic reticulum kinase) increased significantly. The endoplasmic reticulum stress was effectively inhibited after the treatment with mangiferin and the inhibition diminished after the knockout of AMPK (AMP-activated protein kinase) through AMPK siRNA interference, which demonstrated that AMPK was a key point for mangiferin action to exert its therapeutic effects. Under endoplasmic reticulum stress conditions, the influx of calcium ions from the endoplasmic reticulum into cytoplasm may lead to mitochondrial calcium ions overload and a large increase in mitochondrial ROS. As a result, mitochondrial fission was further promoted and apoptosis was induced. Mangiferin effectively improved the endothelial function by activating AMPK to inhibit the endoplasmic reticulum stress, maintaining the calcium homeostasis in mitochondria while inhibiting apoptosis by diminishing mitochondrial fission and ROS (Reactive Oxygen Specie) generation. In conclusion, mangiferin could maintain Ca²⁺ homeostasis in mitochondria under ER stress conditions, attenuate cell apoptosis induced by mitochondrial fission and ROS generation, and effectively improve the endothelial function by activating AMPK to inhibit endoplasmic reticulum stress.

Published in	American Journal of Clinical and Experimental Medicine (Volume 5, Issue 5)
DOI	10.11648/j.ajcem.20170505.12
Page(s)	162-172
Creative Commons	This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.
Copyright	Copyright © The Author(s), 2017. Published by Science Publishing Group

Keywords

Mangiferin, Endoplasmic Reticulum Stress, Mitochondrial Dysfunction, Endothelial Dysfunction

References

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APA Style

Yang Chen, Yu-peng Chen, Bao-lin Liu, Kang Liu, Fang Huang, et al. (2017). The Effect of Mangiferin on Improving Endothelial Dysfunction by Inhibiting Endoplasmic Reticulum Stress to Alleviate Mitochondrial Fission. American Journal of Clinical and Experimental Medicine, 5(5), 162-172. https://doi.org/10.11648/j.ajcem.20170505.12

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ACS Style

Yang Chen; Yu-peng Chen; Bao-lin Liu; Kang Liu; Fang Huang, et al. The Effect of Mangiferin on Improving Endothelial Dysfunction by Inhibiting Endoplasmic Reticulum Stress to Alleviate Mitochondrial Fission. Am. J. Clin. Exp. Med. 2017, 5(5), 162-172. doi: 10.11648/j.ajcem.20170505.12

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AMA Style

Yang Chen, Yu-peng Chen, Bao-lin Liu, Kang Liu, Fang Huang, et al. The Effect of Mangiferin on Improving Endothelial Dysfunction by Inhibiting Endoplasmic Reticulum Stress to Alleviate Mitochondrial Fission. Am J Clin Exp Med. 2017;5(5):162-172. doi: 10.11648/j.ajcem.20170505.12

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@article{10.11648/j.ajcem.20170505.12,
  author = {Yang Chen and Yu-peng Chen and Bao-lin Liu and Kang Liu and Fang Huang and Zhi-xia Qiu},
  title = {The Effect of Mangiferin on Improving Endothelial Dysfunction by Inhibiting Endoplasmic Reticulum Stress to Alleviate Mitochondrial Fission},
  journal = {American Journal of Clinical and Experimental Medicine},
  volume = {5},
  number = {5},
  pages = {162-172},
  doi = {10.11648/j.ajcem.20170505.12},
  url = {https://doi.org/10.11648/j.ajcem.20170505.12},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajcem.20170505.12},
  abstract = {Microvascular and macrovascular diseases are important complications of metabolic diseases and affect the normal functioning of the human cardiovascular system. Endothelial dysfunction is the basic pathological tache of vascular diseases. This study aims to find out whether mangiferin can relieve endothelial dysfunction by inhibiting mitochondrial fission induced by endoplasmic reticulum stress. After being stimulated by palmitate, the expression of endoplasmic reticulum stress-related proteins Bip, p-PERK (RNA-like endoplasmic reticulum kinase) increased significantly. The endoplasmic reticulum stress was effectively inhibited after the treatment with mangiferin and the inhibition diminished after the knockout of AMPK (AMP-activated protein kinase) through AMPK siRNA interference, which demonstrated that AMPK was a key point for mangiferin action to exert its therapeutic effects. Under endoplasmic reticulum stress conditions, the influx of calcium ions from the endoplasmic reticulum into cytoplasm may lead to mitochondrial calcium ions overload and a large increase in mitochondrial ROS. As a result, mitochondrial fission was further promoted and apoptosis was induced. Mangiferin effectively improved the endothelial function by activating AMPK to inhibit the endoplasmic reticulum stress, maintaining the calcium homeostasis in mitochondria while inhibiting apoptosis by diminishing mitochondrial fission and ROS (Reactive Oxygen Specie) generation. In conclusion, mangiferin could maintain Ca2+ homeostasis in mitochondria under ER stress conditions, attenuate cell apoptosis induced by mitochondrial fission and ROS generation, and effectively improve the endothelial function by activating AMPK to inhibit endoplasmic reticulum stress.},
 year = {2017}
}

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TY  - JOUR
T1  - The Effect of Mangiferin on Improving Endothelial Dysfunction by Inhibiting Endoplasmic Reticulum Stress to Alleviate Mitochondrial Fission
AU  - Yang Chen
AU  - Yu-peng Chen
AU  - Bao-lin Liu
AU  - Kang Liu
AU  - Fang Huang
AU  - Zhi-xia Qiu
Y1  - 2017/08/31
PY  - 2017
N1  - https://doi.org/10.11648/j.ajcem.20170505.12
DO  - 10.11648/j.ajcem.20170505.12
T2  - American Journal of Clinical and Experimental Medicine
JF  - American Journal of Clinical and Experimental Medicine
JO  - American Journal of Clinical and Experimental Medicine
SP  - 162
EP  - 172
PB  - Science Publishing Group
SN  - 2330-8133
UR  - https://doi.org/10.11648/j.ajcem.20170505.12
AB  - Microvascular and macrovascular diseases are important complications of metabolic diseases and affect the normal functioning of the human cardiovascular system. Endothelial dysfunction is the basic pathological tache of vascular diseases. This study aims to find out whether mangiferin can relieve endothelial dysfunction by inhibiting mitochondrial fission induced by endoplasmic reticulum stress. After being stimulated by palmitate, the expression of endoplasmic reticulum stress-related proteins Bip, p-PERK (RNA-like endoplasmic reticulum kinase) increased significantly. The endoplasmic reticulum stress was effectively inhibited after the treatment with mangiferin and the inhibition diminished after the knockout of AMPK (AMP-activated protein kinase) through AMPK siRNA interference, which demonstrated that AMPK was a key point for mangiferin action to exert its therapeutic effects. Under endoplasmic reticulum stress conditions, the influx of calcium ions from the endoplasmic reticulum into cytoplasm may lead to mitochondrial calcium ions overload and a large increase in mitochondrial ROS. As a result, mitochondrial fission was further promoted and apoptosis was induced. Mangiferin effectively improved the endothelial function by activating AMPK to inhibit the endoplasmic reticulum stress, maintaining the calcium homeostasis in mitochondria while inhibiting apoptosis by diminishing mitochondrial fission and ROS (Reactive Oxygen Specie) generation. In conclusion, mangiferin could maintain Ca2+ homeostasis in mitochondria under ER stress conditions, attenuate cell apoptosis induced by mitochondrial fission and ROS generation, and effectively improve the endothelial function by activating AMPK to inhibit endoplasmic reticulum stress.
VL  - 5
IS  - 5
ER  -

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Author Information

Yang Chen

Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, China
Yu-peng Chen

Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, China
Bao-lin Liu

Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, China
Kang Liu

Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, China
Fang Huang

Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, China
Zhi-xia Qiu

Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, China

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APA Style

Yang Chen, Yu-peng Chen, Bao-lin Liu, Kang Liu, Fang Huang, et al. (2017). The Effect of Mangiferin on Improving Endothelial Dysfunction by Inhibiting Endoplasmic Reticulum Stress to Alleviate Mitochondrial Fission. American Journal of Clinical and Experimental Medicine, 5(5), 162-172. https://doi.org/10.11648/j.ajcem.20170505.12

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ACS Style

Yang Chen; Yu-peng Chen; Bao-lin Liu; Kang Liu; Fang Huang, et al. The Effect of Mangiferin on Improving Endothelial Dysfunction by Inhibiting Endoplasmic Reticulum Stress to Alleviate Mitochondrial Fission. Am. J. Clin. Exp. Med. 2017, 5(5), 162-172. doi: 10.11648/j.ajcem.20170505.12

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AMA Style

Yang Chen, Yu-peng Chen, Bao-lin Liu, Kang Liu, Fang Huang, et al. The Effect of Mangiferin on Improving Endothelial Dysfunction by Inhibiting Endoplasmic Reticulum Stress to Alleviate Mitochondrial Fission. Am J Clin Exp Med. 2017;5(5):162-172. doi: 10.11648/j.ajcem.20170505.12

Copy | Download

@article{10.11648/j.ajcem.20170505.12,
  author = {Yang Chen and Yu-peng Chen and Bao-lin Liu and Kang Liu and Fang Huang and Zhi-xia Qiu},
  title = {The Effect of Mangiferin on Improving Endothelial Dysfunction by Inhibiting Endoplasmic Reticulum Stress to Alleviate Mitochondrial Fission},
  journal = {American Journal of Clinical and Experimental Medicine},
  volume = {5},
  number = {5},
  pages = {162-172},
  doi = {10.11648/j.ajcem.20170505.12},
  url = {https://doi.org/10.11648/j.ajcem.20170505.12},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajcem.20170505.12},
  abstract = {Microvascular and macrovascular diseases are important complications of metabolic diseases and affect the normal functioning of the human cardiovascular system. Endothelial dysfunction is the basic pathological tache of vascular diseases. This study aims to find out whether mangiferin can relieve endothelial dysfunction by inhibiting mitochondrial fission induced by endoplasmic reticulum stress. After being stimulated by palmitate, the expression of endoplasmic reticulum stress-related proteins Bip, p-PERK (RNA-like endoplasmic reticulum kinase) increased significantly. The endoplasmic reticulum stress was effectively inhibited after the treatment with mangiferin and the inhibition diminished after the knockout of AMPK (AMP-activated protein kinase) through AMPK siRNA interference, which demonstrated that AMPK was a key point for mangiferin action to exert its therapeutic effects. Under endoplasmic reticulum stress conditions, the influx of calcium ions from the endoplasmic reticulum into cytoplasm may lead to mitochondrial calcium ions overload and a large increase in mitochondrial ROS. As a result, mitochondrial fission was further promoted and apoptosis was induced. Mangiferin effectively improved the endothelial function by activating AMPK to inhibit the endoplasmic reticulum stress, maintaining the calcium homeostasis in mitochondria while inhibiting apoptosis by diminishing mitochondrial fission and ROS (Reactive Oxygen Specie) generation. In conclusion, mangiferin could maintain Ca2+ homeostasis in mitochondria under ER stress conditions, attenuate cell apoptosis induced by mitochondrial fission and ROS generation, and effectively improve the endothelial function by activating AMPK to inhibit endoplasmic reticulum stress.},
 year = {2017}
}

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TY  - JOUR
T1  - The Effect of Mangiferin on Improving Endothelial Dysfunction by Inhibiting Endoplasmic Reticulum Stress to Alleviate Mitochondrial Fission
AU  - Yang Chen
AU  - Yu-peng Chen
AU  - Bao-lin Liu
AU  - Kang Liu
AU  - Fang Huang
AU  - Zhi-xia Qiu
Y1  - 2017/08/31
PY  - 2017
N1  - https://doi.org/10.11648/j.ajcem.20170505.12
DO  - 10.11648/j.ajcem.20170505.12
T2  - American Journal of Clinical and Experimental Medicine
JF  - American Journal of Clinical and Experimental Medicine
JO  - American Journal of Clinical and Experimental Medicine
SP  - 162
EP  - 172
PB  - Science Publishing Group
SN  - 2330-8133
UR  - https://doi.org/10.11648/j.ajcem.20170505.12
AB  - Microvascular and macrovascular diseases are important complications of metabolic diseases and affect the normal functioning of the human cardiovascular system. Endothelial dysfunction is the basic pathological tache of vascular diseases. This study aims to find out whether mangiferin can relieve endothelial dysfunction by inhibiting mitochondrial fission induced by endoplasmic reticulum stress. After being stimulated by palmitate, the expression of endoplasmic reticulum stress-related proteins Bip, p-PERK (RNA-like endoplasmic reticulum kinase) increased significantly. The endoplasmic reticulum stress was effectively inhibited after the treatment with mangiferin and the inhibition diminished after the knockout of AMPK (AMP-activated protein kinase) through AMPK siRNA interference, which demonstrated that AMPK was a key point for mangiferin action to exert its therapeutic effects. Under endoplasmic reticulum stress conditions, the influx of calcium ions from the endoplasmic reticulum into cytoplasm may lead to mitochondrial calcium ions overload and a large increase in mitochondrial ROS. As a result, mitochondrial fission was further promoted and apoptosis was induced. Mangiferin effectively improved the endothelial function by activating AMPK to inhibit the endoplasmic reticulum stress, maintaining the calcium homeostasis in mitochondria while inhibiting apoptosis by diminishing mitochondrial fission and ROS (Reactive Oxygen Specie) generation. In conclusion, mangiferin could maintain Ca2+ homeostasis in mitochondria under ER stress conditions, attenuate cell apoptosis induced by mitochondrial fission and ROS generation, and effectively improve the endothelial function by activating AMPK to inhibit endoplasmic reticulum stress.
VL  - 5
IS  - 5
ER  -

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