Alpha-Mangostin Improves Insulin Secretion and Protects INS-1 Cells from Streptozotocin-Induced Damage
DC Field | Value | Language |
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dc.contributor.author | Lee, Dahae | - |
dc.contributor.author | Kim, Young-Mi | - |
dc.contributor.author | Jung, Kiwon | - |
dc.contributor.author | Chin, Young-Won | - |
dc.contributor.author | Kang, Ki Sung | - |
dc.date.available | 2020-02-27T11:40:40Z | - |
dc.date.created | 2020-02-07 | - |
dc.date.issued | 2018-05 | - |
dc.identifier.issn | 1422-0067 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/3834 | - |
dc.description.abstract | Alpha ()-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 -mangostin and to elucidate the molecular mechanisms underlying its effect on pancreatic beta ()-cell dysfunction. To assess the effects of -mangostin on insulin production, rat pancreatic INS-1 cells were treated with non-toxic doses of -mangostin (1-10 M) and its impact on insulin signaling was examined by Western blotting. In addition, the protective effect of -mangostin against pancreatic -cell apoptosis was verified by using the -cell toxin streptozotocin (STZ). Our results showed that -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, -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 M 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 M -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 M -mangostin. These results suggest that -mangostin is capable of improving insulin secretion in pancreatic -cells and protecting cells from apoptotic damage. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | MDPI | - |
dc.relation.isPartOf | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | - |
dc.subject | PANCREATIC BETA-CELL | - |
dc.subject | OXIDATIVE STRESS | - |
dc.subject | INDUCED APOPTOSIS | - |
dc.subject | NATURAL-PRODUCTS | - |
dc.subject | RESISTANCE | - |
dc.subject | RECEPTOR | - |
dc.subject | INHIBITION | - |
dc.subject | PROLIFERATION | - |
dc.subject | HYPERGLYCEMIA | - |
dc.subject | DYSFUNCTION | - |
dc.title | Alpha-Mangostin Improves Insulin Secretion and Protects INS-1 Cells from Streptozotocin-Induced Damage | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000435297000220 | - |
dc.identifier.doi | 10.3390/ijms19051484 | - |
dc.identifier.bibliographicCitation | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.19, no.5 | - |
dc.identifier.scopusid | 2-s2.0-85047152230 | - |
dc.citation.title | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | - |
dc.citation.volume | 19 | - |
dc.citation.number | 5 | - |
dc.contributor.affiliatedAuthor | Kang, Ki Sung | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | alpha mangostin | - |
dc.subject.keywordAuthor | glucose response | - |
dc.subject.keywordAuthor | insulin secretion | - |
dc.subject.keywordAuthor | streptozotocin | - |
dc.subject.keywordPlus | PANCREATIC BETA-CELL | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | INDUCED APOPTOSIS | - |
dc.subject.keywordPlus | NATURAL-PRODUCTS | - |
dc.subject.keywordPlus | RESISTANCE | - |
dc.subject.keywordPlus | RECEPTOR | - |
dc.subject.keywordPlus | INHIBITION | - |
dc.subject.keywordPlus | PROLIFERATION | - |
dc.subject.keywordPlus | HYPERGLYCEMIA | - |
dc.subject.keywordPlus | DYSFUNCTION | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Chemistry | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Chemistry, Multidisciplinary | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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