Volume 5, Issue 5, September 2017, Page: 162-172
The Effect of Mangiferin on Improving Endothelial Dysfunction by Inhibiting Endoplasmic Reticulum Stress to Alleviate Mitochondrial Fission
Yang Chen, Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, China; Jiangsu Key Laboratory of TCM Evaluation and Translational Research, China Pharmaceutical University, Nanjing, China
Yu-peng Chen, Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, China; Jiangsu Key Laboratory of TCM Evaluation and Translational Research, China Pharmaceutical University, Nanjing, China
Bao-lin Liu, Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, China; Jiangsu Key Laboratory of TCM Evaluation and Translational Research, China Pharmaceutical University, Nanjing, China
Kang Liu, Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, China; Jiangsu Key Laboratory of TCM Evaluation and Translational Research, China Pharmaceutical University, Nanjing, China
Fang Huang, Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, China; Jiangsu Key Laboratory of TCM Evaluation and Translational Research, China Pharmaceutical University, Nanjing, China
Zhi-xia Qiu, Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, China; Jiangsu Key Laboratory of TCM Evaluation and Translational Research, China Pharmaceutical University, Nanjing, China
Received: Jul. 23, 2017;       Accepted: Aug. 16, 2017;       Published: Aug. 31, 2017
DOI: 10.11648/j.ajcem.20170505.12      View  1688      Downloads  66
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.
Keywords
Mangiferin, Endoplasmic Reticulum Stress, Mitochondrial Dysfunction, Endothelial Dysfunction
To cite this article
Yang Chen, Yu-peng Chen, Bao-lin Liu, Kang Liu, Fang Huang, Zhi-xia Qiu, The Effect of Mangiferin on Improving Endothelial Dysfunction by Inhibiting Endoplasmic Reticulum Stress to Alleviate Mitochondrial Fission, American Journal of Clinical and Experimental Medicine. Vol. 5, No. 5, 2017, pp. 162-172. doi: 10.11648/j.ajcem.20170505.12
Copyright
Copyright © 2017 Authors retain the copyright of this article.
This article is an open access article distributed under the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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