Publication: Water extract of mangosteen suppresses H<inf>2</inf>O<inf>2</inf>-induced endothelial apoptosis by inhibiting oxidative stress
Issued Date
2019-09-01
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22313354
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2-s2.0-85077439184
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Mahidol University
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SCOPUS
Bibliographic Citation
Journal of Applied Pharmaceutical Science. Vol.9, No.9 (2019), 010-016
Suggested Citation
Kanjana Jittiporn, Primchanien Moongkarndi, Jutima Samer, Sarawut Kumphune, Wisuda Suvitayavat Water extract of mangosteen suppresses H<inf>2</inf>O<inf>2</inf>-induced endothelial apoptosis by inhibiting oxidative stress. Journal of Applied Pharmaceutical Science. Vol.9, No.9 (2019), 010-016. doi:10.7324/JAPS.2019.90902 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/51433
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Title
Water extract of mangosteen suppresses H<inf>2</inf>O<inf>2</inf>-induced endothelial apoptosis by inhibiting oxidative stress
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Abstract
© 2019 Kanjana Jittiporn et al. Excessive production of reactive oxygen species (ROS) is a major cause of endothelial apoptosis. Mangosteen extract has been shown to possess antioxidant properties. Mangosteen is commonly extracted either with semi-polar solvent, yielding virtually pure α-mangostin, or with water, yielding a low α-mangostin concentration but including a wide variety of other polyphenols present in the fruit. However, the effect of a water extract of mangosteen (ME) on ROS induced cell death is not yet known. This study evaluated whether ME suppresses H2O2-induced endothelial cell death and ROS production in human endothelial cell lines. The concentrations of ME and H2O2 were determined by 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) assay. Intracellular ROS levels were determined by 2', 7' dichlorodihydrofluorescein diacetate assay, and cell death rates by MTT and Terminal deoxynucleotidyl transferase dUTP Nick-End Labeling assays. mitogen-activated protein kinase (MAPK) and apoptotic proteins were analyzed by western blot. Results showed that ME concentrations of 1, 5, and 10 μg/ml were non-toxic. ME significantly attenuated ROS formation and cell death, both in a dose-dependent manner. ME also reduced phosphorylation of p38 MAPK as well as cleavage of caspase 3 and poly(ADP-ribose) polymerase-1. In summary, ME demonstrates anti-apoptotic effects against H2O2-induced endothelial cell death by inhibiting ROS formation and suppressing p38 MAPK.