Chebulic Acid Prevents Methylglyoxal-Induced Mitochondrial Dysfunction in INS-1 Pancreatic beta-Cells
DC Field | Value | Language |
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dc.contributor.author | Yoo, Hyun-jung | - |
dc.contributor.author | Hong, Chung-Oui | - |
dc.contributor.author | Ha, Sang Keun | - |
dc.contributor.author | Lee, Kwang-Won | - |
dc.date.accessioned | 2021-08-30T15:09:47Z | - |
dc.date.available | 2021-08-30T15:09:47Z | - |
dc.date.created | 2021-06-19 | - |
dc.date.issued | 2020-09 | - |
dc.identifier.issn | 2076-3921 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/53249 | - |
dc.description.abstract | To investigate the anti-diabetic properties of chebulic acid (CA) associated with the prevention of methyl glyoxal (MG)-induced mitochondrial dysfunction in INS-1 pancreatic beta-cells, INS-1 cells were pre-treated with CA (0.5, 1.0, and 2.0 mu M) for 48 h and then treated with 2 mM MG for 8 h. The effects of CA and MG on INS-1 cells were evaluated using the following: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay; glyoxalase 1 (Glo-1) expression via Western blot and enzyme activity assays; Nrf-2, nuclear factor erythroid 2-related factor 2 protein expression via Western blot assay; reactive oxygen species (ROS) production assay; mRNA expression of mitochondrial dysfunction related components (UCP2, uncoupling protein 2; VDAC1, voltage-dependent anion-selective channel-1; cyt c, cytochrome c via quantitative reverse transcriptase-PCR; mitochondrial membrane potential (MMP); adenosine triphosphate (ATP) synthesis; glucose-stimulated insulin secretion (GSIS) assay. The viability of INS-1 cells was maintained upon pre-treating with CA before exposure to MG. CA upregulated Glo-1 protein expression and enzyme activity in INS-1 cells and prevented MG-induced ROS production. Mitochondrial dysfunction was alleviated by CA pretreatment; this occurred via the downregulation of UCP2, VDAC1, and cyt c mRNA expression and the increase of MMP and ATP synthesis. Further, CA pre-treatment promoted the recovery from MG-induced decrease in GSIS. These results indicated that CA could be employed as a therapeutic agent in diabetes due to its ability to prevent MG-induced development of insulin sensitivity and oxidative stress-induced dysfunction of beta-cells. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | MDPI | - |
dc.subject | GLYCATION END-PRODUCTS | - |
dc.subject | HIGH GLUCOSE | - |
dc.subject | GLYOXALASE 1 | - |
dc.subject | APOPTOSIS | - |
dc.subject | MECHANISM | - |
dc.subject | NEUROPROTECTION | - |
dc.subject | ENHANCEMENT | - |
dc.subject | DEFENSE | - |
dc.subject | OBESITY | - |
dc.subject | STRESS | - |
dc.title | Chebulic Acid Prevents Methylglyoxal-Induced Mitochondrial Dysfunction in INS-1 Pancreatic beta-Cells | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Lee, Kwang-Won | - |
dc.identifier.doi | 10.3390/antiox9090771 | - |
dc.identifier.scopusid | 2-s2.0-85090810260 | - |
dc.identifier.wosid | 000581701600001 | - |
dc.identifier.bibliographicCitation | ANTIOXIDANTS, v.9, no.9 | - |
dc.relation.isPartOf | ANTIOXIDANTS | - |
dc.citation.title | ANTIOXIDANTS | - |
dc.citation.volume | 9 | - |
dc.citation.number | 9 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Pharmacology & Pharmacy | - |
dc.relation.journalResearchArea | Food Science & Technology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Chemistry, Medicinal | - |
dc.relation.journalWebOfScienceCategory | Food Science & Technology | - |
dc.subject.keywordPlus | GLYCATION END-PRODUCTS | - |
dc.subject.keywordPlus | HIGH GLUCOSE | - |
dc.subject.keywordPlus | GLYOXALASE 1 | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | MECHANISM | - |
dc.subject.keywordPlus | NEUROPROTECTION | - |
dc.subject.keywordPlus | ENHANCEMENT | - |
dc.subject.keywordPlus | DEFENSE | - |
dc.subject.keywordPlus | OBESITY | - |
dc.subject.keywordPlus | STRESS | - |
dc.subject.keywordAuthor | chebulic acid | - |
dc.subject.keywordAuthor | methylglyoxal | - |
dc.subject.keywordAuthor | INS-1 cells | - |
dc.subject.keywordAuthor | mitochondrial dysfunction | - |
dc.subject.keywordAuthor | insulin secretion | - |
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