Please use this identifier to cite or link to this item:
http://repository.li.mahidol.ac.th/dspace/handle/123456789/47514
Title: | Protective effect of α-mangostin on high glucose induced endothelial cell apoptosis |
Authors: | Kanjana Jittiporn Primchanien Moongkarndi Jutima Samer Wisuda Suvitayavat Naresuan University Mahidol University |
Keywords: | Multidisciplinary |
Issue Date: | 1-Aug-2018 |
Citation: | Walailak Journal of Science and Technology. Vol.15, No.8 Special Issue (2018), 579-587 |
Abstract: | © 2018, Walailak University. All rights reserved. α-mangostin is a phenolic compound from pericarp of mangosteen. It has prominent anti-oxidant properties. Oxidative stress has been shown to be a major factor that disrupts cell functions including endothelium. High glucose (HG) induced ROS production plays a key role in endothelial cell apoptosis. However, the effect of α-mangostin on HG induced apoptosis has not been studied yet. This study demonstrates the effect of α-mangostin in HG induced human umbilical vein endothelial cells (HUVECs) apoptosis. The non-toxic dose of α-mangostin was determined using a MTT assay. Intracellular reactive oxygen species (ROS) and cell apoptosis were evaluated using DCF-DA and TUNEL assays, respectively. The signaling of α-mangostin was elucidated by western blotting. α-mangostin significantly and, dose-dependently, decreased HG induced ROS formation. Also, α-mangostin significantly attenuated HG induced endothelial cell apoptosis. In addition, α-mangostin suppressed HG induced apoptosis via JNK and p38-MAPK. According to our results, α-mangostin attenuated HG induced endothelial cell apoptosis through inhibition of phosphorylation of JNK and p38-MAPK. |
URI: | https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85049941513&origin=inward http://repository.li.mahidol.ac.th/dspace/handle/123456789/47514 |
ISSN: | 2228835X 16863933 |
Appears in Collections: | Scopus 2018 |
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.