Blueberry anthocyanin extract significantly delayed the progression of diabetic cataracts. - GreenMedInfo Summary
Role of Blueberry Anthocyanin Extract in the Expression of SIRT1 and NF-κB in Rat Lens Epithelial Cells in Experimentally Induced DM.
Curr Eye Res. 2020 Jun 1. Epub 2020 Jun 1. PMID: 32478572
PURPOSE: To investigate the mechanism of the protective effects of blueberry anthocyanin extract (BAE) against oxidative stress and the roles of SIRT1 and NF-B in the pathogenesis of diabetic cataracts.
METHODS: Male SD rats were randomly divided into a control group (group A) and an experimental group. The rats in the experimental group were intraperitoneally injected with streptozotocin (STZ) (60 mg/kg). Rats with blood glucose levels≥16.7 mmol/L were considered to have DM. The rats in the experimental group were subdivided into group B (distilled water by oral gavage: 10 ml/kg/day), group C (5% blueberry anthocyanin extract by oral gavage: 10 ml/kg/day), and group D (15% blueberry anthocyanin extract by oral gavage: 10 ml/kg/day), with 15 rats in each group. At the end of 8 weeks, some biochemical parameters, including the expression of SIRT1 and NF-B by qRT-PCR and western blotting and the activity of SOD and GSH, were measured in lens epithelial cells (LECs).
RESULTS: The lenses of the rats in the control group appeared transparent during the entire 8-week period. Four weeks following STZ injection, cataracts gradually progressed in the experimental rats. SIRT1 expression was upregulated in groups B, C and D compared to the control group. However, the expression of NF-κB decreased in the experimental groups with increasing doses of BAE (p<0.05). Our study also showed that the activity of the SOD enzyme and GSH in the LECs of the rats in the experimental group increased with higher doses of BAE.
CONCLUSIONS: The results indicated that BAE significantly delayed the progression of diabetic cataracts in rats. These effects may be due to the dose-dependent antioxidant activity of BAE, which is mediated by enhanced SOD and GSH activities, SIRT1 expression and reduced NF-κB expression.