Rosemarinic acid protects β-cell from STZ-induced cell damage via modulating NF-κβ pathway

Rosmarinic acid (RA), a natural ester phenolic compound, is known to have antioxidant and anti-inflammatory properties. RA has also been reported to exhibit a hypoglycemic effect; however, the mechanisms underlying this effect have yet to be investigated. Therefore, the present study focused on the anti-diabetic effects and mechanism of RA in INS-1 cells using in vitro model. Streptozotocin (STZ) at a concentration of 3 mM was applied to INS-1 cells for 4 h to create a diabetic model. The cells were pretreated for 24 h with various concentrations (1 and 2.5 mu M) of RA. The Cell viability, glucose-stimulated insulin secretion (GSIS), glucose uptake, lipid peroxidation, reactive oxygen species (ROS), apoptosis, and protein expression of Bcl-2, NF-kappa B, 1L-1 beta, and PARP were assessed. Results showed that STZ-treated INS-1 cells exhibited reduced cell viability, insulin release, insulin content, glucose uptake, and elevated MDA and ROS levels. Cells pretreated with RA maintained the function and morphology of beta-cells against STZ-induced damage. Moreover, RA sustained high protein expression levels of Bcl-2 and low expression levels of NF-kappa B, IL-1 beta, and PARP. In conclusion, RA preserved beta-cells function against STZ-induced damage by altering NF-kappa B and Bcl-2 pathways.

Automated summary

Rosmarinic acid (RA) exerts a protective effect against streptozotocin-induced beta-cell damage by modulating the NF-kappa B and Bcl-2 pathways.