5-Bromoprotocatechualdehyde Combats against Palmitate Toxicity by Inhibiting Parkin Degradation and Reducing ROS-Induced Mitochondrial Damage in Pancreatic beta-Cells
- Authors
- Cha, Seon-Heui; Zhang, Chunying; Heo, Soo-Jin; Jun, Hee-Sook
- Issue Date
- Feb-2021
- Publisher
- MDPI
- Keywords
- 5-bromoprotocatechualdehyde; Diabetes; Polyphenol; Polysiphonia japonica; Seaweed; β-cell
- Citation
- ANTIOXIDANTS, v.10, no.2, pp.1 - 19
- Journal Title
- ANTIOXIDANTS
- Volume
- 10
- Number
- 2
- Start Page
- 1
- End Page
- 19
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/80367
- DOI
- 10.3390/antiox10020264
- ISSN
- 2076-3921
- Abstract
- Pancreatic β-cell loss is critical in diabetes pathogenesis. Up to now, no effective treatment has become available for β-cell loss. A polyphenol recently isolated from Polysiphonia japonica, 5-Bromoprotocatechualdehyde (BPCA), is considered as a potential compound for the protection of β-cells. In this study, we examined palmitate (PA)-induced lipotoxicity in Ins-1 cells to test the protective effects of BPCA on insulin-secreting β-cells. Our results demonstrated that BPCA can protect β-cells from PA-induced lipotoxicity by reducing cellular damage, preventing reactive oxygen species (ROS) overproduction, and enhancing glucose-stimulated insulin secretion (GSIS). BPCA also improved mitochondrial morphology by preserving parkin protein expression. Moreover, BPCA exhibited a protective effect against PA-induced β-cell dysfunction in vivo in a zebrafish model. Our results provide strong evidence that BPCA could be a potential therapeutic agent for the management of diabetes. © 2021 by the authors. Licensee MDPI, Basel, Switzerland.
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