1. Potential of delphinidin-3-rutinoside extracted from Solanum melongena L. as promoter of osteoblastic MC3T3-E1 function and antagonist of oxidative damage.
- Author
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Casati L, Pagani F, Fibiani M, Lo Scalzo R, and Sibilia V
- Subjects
- Animals, Cell Line drug effects, Cell Survival, Cells, Cultured, Mice, Anthocyanins pharmacology, Antioxidants pharmacology, Osteoblasts drug effects, Oxidative Stress drug effects, Plant Extracts pharmacology, Solanum melongena
- Abstract
Purpose: Increasing evidence suggests the potential use of natural antioxidant compounds in the prevention/treatment of osteoporosis. This study was undertaken to investigate the effects of purified delphinidin-3-rutinoside (D3R), isolated from Solanum melongena L., on osteoblast viability and differentiation in basal conditions and its ability to protect MC3T3-E1 cells against oxidative damage induced by tert-butyl hydroperoxide (t-BHP)., Methods: MC3T3-E1 osteoblastic cells were treated with D3R (10
-11 -10-5 M for 24 h), followed by treatment with t-BHP (250 µM for 3 h). To test cell viability, MTT test was performed. Apoptotic cells were stained with Hoechst-33258 dye. Cytoskeleton rearrangement was stained with FICT-labelled phalloidin. Intracellular ROS production was measured using dichlorofluorescein CM-DCFA. The reduced glutathione to oxidized glutathione ratio (GSH/GSSG) contents was measured according to the OPT fluorimetric assay., Results: D3R (10-9 M) significantly increases viability of MC3T3-E1 cells and promotes osteoblast differentiation by increasing the expression of type I collagen, alkaline phosphatase and osteocalcin. Pre-treatment with D3R (10-9 M) significantly prevented t-BHP-induced osteoblastic dysfunction and changes in the cytoskeleton organization by decreasing intracellular ROS and preventing the reduction in GSH/GSSG. D3R did not significantly modify the expression of Osteoprotegerin/RANKL system activated by t-BHP suggesting a lack of effect of D3R on osteoblast/osteoclast crosstalk. D3R protective effects against t-BHP-induced osteoblastic dysfunction were mediated by the PI3K/Akt pathway since they were completely prevented by LY294002, a PI3K/Akt specific inhibitor., Conclusions: These findings indicate that D3R protects MC3T3-E1 cells from oxidative damage and suggest the potential utility of dietary D3R supplement to prevent osteoblast dysfunction in age-related osteoporosis.- Published
- 2019
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