Potential of delphinidin-3-rutinoside extracted from Solanum melongena L. as promoter of osteoblastic MC3T3-E1 function and antagonist of oxidative damage

• DOI: 10.1007/s00394-018-1618-0
• Publication Date: 2018-01-25T09:03:09Z
• Authors: Lavinia Casati; Francesca Pagani; Marta Fibiani; Roberto Lo Scalzo; Valeria Sibilia
• Keywords: 0301 basic medicine; 0303 health sciences; Osteoblasts; Cell Survival; Plant Extracts; Antioxidants; Cell Line; Anthocyanins; delphinidin-3-rutinoside; functional food component; osteoblastic MC3T3-E1 cells; oxidative stress; Mice; Oxidative Stress; 03 medical and health sciences; Animals; Solanum melongena; Cells, Cultured

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).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.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.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.