PUBLICATION
5-Bromoprotocatechualdehyde Combats against Palmitate Toxicity by Inhibiting Parkin Degradation and Reducing ROS-Induced Mitochondrial Damage in Pancreatic β-Cells
- Authors
- Cha, S.H., Zhang, C., Heo, S.J., Jun, H.S.
- ID
- ZDB-PUB-210213-4
- Date
- 2021
- Source
- Antioxidants (Basel, Switzerland) 10(2): (Journal)
- Registered Authors
- Keywords
- 5-bromoprotocatechualdehyde, Polysiphonia japonica, diabetes, polyphenol, seaweed, β-cell
- MeSH Terms
- none
- PubMed
- 33572166 Full text @ Antioxidants (Basel)
Citation
Cha, S.H., Zhang, C., Heo, S.J., Jun, H.S. (2021) 5-Bromoprotocatechualdehyde Combats against Palmitate Toxicity by Inhibiting Parkin Degradation and Reducing ROS-Induced Mitochondrial Damage in Pancreatic β-Cells. Antioxidants (Basel, Switzerland). 10(2):.
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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping