Cyanidin-3-rutinoside protects INS-1 pancreatic ß cells against high glucose-induced glucotoxicity by apoptosis.
Z Naturforsch C J Biosci
; 73(7-8): 281-289, 2018 Jul 26.
Article
em En
| MEDLINE
| ID: mdl-29924740
ABSTRACT
Exposure to high levels of glucose may cause glucotoxicity, leading to pancreatic ß cell dysfunction, including cell apoptosis and impaired glucose-stimulated insulin secretion. The aim of this study was to explore the effect of cyanidin-3-rutinoside (C3R), a derivative of anthocyanin, on glucotoxicity-induced apoptosis in INS-1 pancreatic ß cells. Glucose (30 mM) treatment induced INS-1 pancreatic ß cell death, but glucotoxicity and apoptosis significantly decreased in cells treated with 50 µM C3R compared to that observed in 30 mM glucose-treated cells. Furthermore, hyperglycemia increased intracellular reactive oxygen species (ROS), lipid peroxidation, and nitric oxide (NO) levels, while C3R treatment reduced these in a dose-dependent manner. C3R also increased the activity of antioxidant enzymes, markedly reduced the expression of pro-apoptotic proteins (such as Bax, cytochrome c, caspase 9 and caspase 3), and increased the expression of the anti-apoptotic protein, Bcl-2, in hyperglycemia-exposed cells. Finally, cell death was examined using annexin V/propidium iodide staining, which revealed that C3R significantly reduced high glucose-induced apoptosis. In conclusion, C3R may have therapeutic effects against hyperglycemia-induced ß cell damage in diabetes.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Células Secretoras de Insulina
/
Glucose
/
Antocianinas
Limite:
Animals
Idioma:
En
Ano de publicação:
2018
Tipo de documento:
Article