Publication: Protective effect of α-mangostin on high glucose induced endothelial cell apoptosis
Issued Date
2018-08-01
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2228835X
16863933
16863933
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2-s2.0-85049941513
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Mahidol University
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SCOPUS
Bibliographic Citation
Walailak Journal of Science and Technology. Vol.15, No.8 Special Issue (2018), 579-587
Suggested Citation
Kanjana Jittiporn, Primchanien Moongkarndi, Jutima Samer, Wisuda Suvitayavat Protective effect of α-mangostin on high glucose induced endothelial cell apoptosis. Walailak Journal of Science and Technology. Vol.15, No.8 Special Issue (2018), 579-587. Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/47514
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Title
Protective effect of α-mangostin on high glucose induced endothelial cell apoptosis
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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.