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Inhibitory Effect of Arachis hypogaea (Peanut) and Its Phenolics against Methylglyoxal-Derived Advanced Glycation End Product Toxicity
Methylglyoxal (MGO) is a highly reactive dicarbonyl compound that causes endothelial dysfunction and plays important roles in the development of diabetic complications. Peanuts are rich in energy, minerals, and antioxidants. Here, we report the potential beneficial effects of peanuts, and particular...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5707686/ https://www.ncbi.nlm.nih.gov/pubmed/29113063 http://dx.doi.org/10.3390/nu9111214 |
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author | Park, Sin Hee Do, Moon Ho Lee, Jae Hyuk Jeong, Minsun Lim, Oh Kyung Kim, Sun Yeou |
author_facet | Park, Sin Hee Do, Moon Ho Lee, Jae Hyuk Jeong, Minsun Lim, Oh Kyung Kim, Sun Yeou |
author_sort | Park, Sin Hee |
collection | PubMed |
description | Methylglyoxal (MGO) is a highly reactive dicarbonyl compound that causes endothelial dysfunction and plays important roles in the development of diabetic complications. Peanuts are rich in energy, minerals, and antioxidants. Here, we report the potential beneficial effects of peanuts, and particularly the phenolic contents, against MGO-mediated cytotoxicity. Firstly, we optimized the extraction conditions for maximum yield of phenolics from peanuts by examining different processing methods and extraction solvents. To estimate the phenolic contents of peanut extracts, a simultaneous analysis method was developed and validated by ultra-high-performance liquid chromatography–tandem mass spectrometry. We found that roasted peanuts and their 80% methanol extracts showed the highest amount of total phenolics. Secondly, we evaluated the inhibitory effects of phenolics and peanut extracts against MGO-mediated cytotoxicity. Phenolics and peanut extracts were observed to inhibit advanced glycation end product (AGE) formation as well as to break preformed AGEs. Furthermore, pretreatment with peanut extracts significantly inhibited MGO-induced cell death and reactive oxygen species production in human umbilical vein endothelial cells. Peanut extracts prevented MGO-induced apoptosis by increasing Bcl-2 expression and decreasing Bax expression, and MGO-mediated activation of mitogen-activated protein kinases (MAPKs). In conclusion, the constituents of peanuts may prevent endothelial dysfunction and diabetic complications. |
format | Online Article Text |
id | pubmed-5707686 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-57076862017-12-05 Inhibitory Effect of Arachis hypogaea (Peanut) and Its Phenolics against Methylglyoxal-Derived Advanced Glycation End Product Toxicity Park, Sin Hee Do, Moon Ho Lee, Jae Hyuk Jeong, Minsun Lim, Oh Kyung Kim, Sun Yeou Nutrients Article Methylglyoxal (MGO) is a highly reactive dicarbonyl compound that causes endothelial dysfunction and plays important roles in the development of diabetic complications. Peanuts are rich in energy, minerals, and antioxidants. Here, we report the potential beneficial effects of peanuts, and particularly the phenolic contents, against MGO-mediated cytotoxicity. Firstly, we optimized the extraction conditions for maximum yield of phenolics from peanuts by examining different processing methods and extraction solvents. To estimate the phenolic contents of peanut extracts, a simultaneous analysis method was developed and validated by ultra-high-performance liquid chromatography–tandem mass spectrometry. We found that roasted peanuts and their 80% methanol extracts showed the highest amount of total phenolics. Secondly, we evaluated the inhibitory effects of phenolics and peanut extracts against MGO-mediated cytotoxicity. Phenolics and peanut extracts were observed to inhibit advanced glycation end product (AGE) formation as well as to break preformed AGEs. Furthermore, pretreatment with peanut extracts significantly inhibited MGO-induced cell death and reactive oxygen species production in human umbilical vein endothelial cells. Peanut extracts prevented MGO-induced apoptosis by increasing Bcl-2 expression and decreasing Bax expression, and MGO-mediated activation of mitogen-activated protein kinases (MAPKs). In conclusion, the constituents of peanuts may prevent endothelial dysfunction and diabetic complications. MDPI 2017-11-04 /pmc/articles/PMC5707686/ /pubmed/29113063 http://dx.doi.org/10.3390/nu9111214 Text en © 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Park, Sin Hee Do, Moon Ho Lee, Jae Hyuk Jeong, Minsun Lim, Oh Kyung Kim, Sun Yeou Inhibitory Effect of Arachis hypogaea (Peanut) and Its Phenolics against Methylglyoxal-Derived Advanced Glycation End Product Toxicity |
title | Inhibitory Effect of Arachis hypogaea (Peanut) and Its Phenolics against Methylglyoxal-Derived Advanced Glycation End Product Toxicity |
title_full | Inhibitory Effect of Arachis hypogaea (Peanut) and Its Phenolics against Methylglyoxal-Derived Advanced Glycation End Product Toxicity |
title_fullStr | Inhibitory Effect of Arachis hypogaea (Peanut) and Its Phenolics against Methylglyoxal-Derived Advanced Glycation End Product Toxicity |
title_full_unstemmed | Inhibitory Effect of Arachis hypogaea (Peanut) and Its Phenolics against Methylglyoxal-Derived Advanced Glycation End Product Toxicity |
title_short | Inhibitory Effect of Arachis hypogaea (Peanut) and Its Phenolics against Methylglyoxal-Derived Advanced Glycation End Product Toxicity |
title_sort | inhibitory effect of arachis hypogaea (peanut) and its phenolics against methylglyoxal-derived advanced glycation end product toxicity |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5707686/ https://www.ncbi.nlm.nih.gov/pubmed/29113063 http://dx.doi.org/10.3390/nu9111214 |
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