Simple jQuery Dropdowns
Please use this identifier to cite or link to this item:
Full metadata record
DC FieldValueLanguage
dc.contributor.authorKanjana Jittipornen_US
dc.contributor.authorPrimchanien Moongkarndien_US
dc.contributor.authorJutima Sameren_US
dc.contributor.authorWisuda Suvitayavaten_US
dc.contributor.otherNaresuan Universityen_US
dc.contributor.otherMahidol Universityen_US
dc.identifier.citationWalailak Journal of Science and Technology. Vol.15, No.8 Special Issue (2018), 579-587en_US
dc.description.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.en_US
dc.rightsMahidol Universityen_US
dc.titleProtective effect of α-mangostin on high glucose induced endothelial cell apoptosisen_US
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.