Chebulic Acid Prevents Methylglyoxal-Induced Mitochondrial Dysfunction in INS-1 Pancreatic beta-Cells
- Authors
- Yoo, Hyun-jung; Hong, Chung-Oui; Ha, Sang Keun; Lee, Kwang-Won
- Issue Date
- 9월-2020
- Publisher
- MDPI
- Keywords
- chebulic acid; methylglyoxal; INS-1 cells; mitochondrial dysfunction; insulin secretion
- Citation
- ANTIOXIDANTS, v.9, no.9
- Indexed
- SCIE
SCOPUS
- Journal Title
- ANTIOXIDANTS
- Volume
- 9
- Number
- 9
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/53249
- DOI
- 10.3390/antiox9090771
- ISSN
- 2076-3921
- 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.
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Collections - Graduate School > Department of Biotechnology > 1. Journal Articles
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