Open AccessProtective Effect of α-Mangostin on High Glucose Induced Endothelial Cell Apoptosis
Author(s) -
Kanjana Jittiporn,
Primchanien Moongkarndi,
Jutima Samer,
Wisuda Suvitayavat
Publication year - 2017
Publication title -
walailak journal of science and technology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.146
H-Index - 15
eISSN - 2228-835X
pISSN - 1686-3933
DOI - 10.48048/wjst.2018.3605
Subject(s) - apoptosis , umbilical vein , p38 mitogen activated protein kinases , reactive oxygen species , tunel assay , chemistry , oxidative stress , mapk/erk pathway , human umbilical vein endothelial cell , endothelial stem cell , microbiology and biotechnology , phosphorylation , biochemistry , biology , in vitro
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.