Next Article in Journal
Lateral Membrane Heterogeneity Regulates Viral-Induced Membrane Fusion during HIV Entry
Previous Article in Journal
Exploration of ABA Responsive miRNAs Reveals a New Hormone Signaling Crosstalk Pathway Regulating Root Growth of Populus euphratica
Article Menu
Issue 5 (May) cover image

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2018, 19(5), 1484;

Alpha-Mangostin Improves Insulin Secretion and Protects INS-1 Cells from Streptozotocin-Induced Damage

2,* and 4,*
School of Pharmacy, Sungkyunkwan University, Suwon 16419, Korea
College of Pharmacy and Integrated Research Institute for Drug Development, Dongguk University-Seoul, Gyeonggi 10326, Korea
Institute of Pharmaceutical Sciences, College of Pharmacy, CHA University, Sungnam 13844, Korea
College of Korean Medicine, Gachon University, Seongnam 13120, Korea
These authors contributed equally to this work.
Authors to whom correspondence should be addressed.
Received: 3 April 2018 / Revised: 4 May 2018 / Accepted: 13 May 2018 / Published: 16 May 2018
(This article belongs to the Section Molecular Pathology, Diagnostics, and Therapeutics)
Full-Text   |   PDF [2759 KB, uploaded 16 May 2018]   |  


Alpha (α)-mangostin, a yellow crystalline powder with a xanthone core structure, is isolated from mangosteen (Garcinia mangostana), which is a tropical fruit of great nutritional value. The aim of the present study was to investigate the anti-diabetic effects of α-mangostin and to elucidate the molecular mechanisms underlying its effect on pancreatic beta (β)-cell dysfunction. To assess the effects of α-mangostin on insulin production, rat pancreatic INS-1 cells were treated with non-toxic doses of α-mangostin (1–10 μM) and its impact on insulin signaling was examined by Western blotting. In addition, the protective effect of α-mangostin against pancreatic β-cell apoptosis was verified by using the β-cell toxin streptozotocin (STZ). Our results showed that α-mangostin stimulated insulin secretion in INS-1 cells by activating insulin receptor (IR) and pancreatic and duodenal homeobox 1 (Pdx1) followed by phosphorylation of phospho-phosphatidylinositol-3 kinase (PI3K), Akt, and extracellular signal regulated kinase (ERK) signaling cascades, whereas it inhibited the phosphorylation of insulin receptor substrate (IRS-1) (Ser1101). Moreover, α-mangostin was found to restore the STZ-induced decrease in INS-1 cell viability in a dose-dependent manner. In addition, treatment of INS-1 cells with 50 μM STZ resulted in an increase in intracellular reactive oxygen species (ROS) levels, which was represented by the fluorescence intensity of 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA). This oxidative stress was decreased by co-treatment with 5 μM α-mangostin. Similarly, marked increases in the phosphorylation of P38, c-Jun N-terminal kinase (JNK), and cleavage of caspase-3 by STZ were decreased significantly by co-treatment with 5 μM α-mangostin. These results suggest that α-mangostin is capable of improving insulin secretion in pancreatic β-cells and protecting cells from apoptotic damage. View Full-Text
Keywords: alpha mangostin; glucose response; insulin secretion; streptozotocin alpha mangostin; glucose response; insulin secretion; streptozotocin

Graphical abstract

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Supplementary material


Share & Cite This Article

MDPI and ACS Style

Lee, D.; Kim, Y.-M.; Jung, K.; Chin, Y.-W.; Kang, K.S. Alpha-Mangostin Improves Insulin Secretion and Protects INS-1 Cells from Streptozotocin-Induced Damage. Int. J. Mol. Sci. 2018, 19, 1484.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top