Echinacoside suppresses dexamethasone-induced growth inhibition and apoptosis in osteoblastic MC3T3-E1 cells.

Glucocorticoids (GCs) are widely used to treat chronic diseases. Prolonged and/or overdose administration of GCs has many side-effects to human health including GC-induced osteoporosis (GIOP). In this investigation, the objective was to assess the influence that echinacoside (ECH) exerts upon dexamethasone-treated murine osteoblastic MC3T3-E1 cells. We found that ECH (5, 10, 20 and 40 mg/l) inhibited dexamethasone (1,000 nM)-suppressed cell viability as demonstrated by Cell Counting Kit-8 (CCK-8) assay. The dose of 10 mg/l was selected for the following experiments because this dose had a better effect than the dose of 5 mg/l, and the doses >10 mg/l had a similar effect as this dose. ECH (10 mg/l) or pifithrin-α (PFT-α) (a p53 inhibitor, 20 µM) suppressed dexamethasone-induced MC3T3-E1 apoptosis as illustrated by Annexin V/propidium iodide (PI) double-labeling flow cytometry analysis. ECH or PFT-α treatment also alleviated dexamethasone's action of inhibiting Bcl-2 expression as well as dexamethasone's action of stimulating on the expression of p53 and Bax. Moreover, lentivirus mediated-p53 overexpression reversed the effects of ECH in dexamethasone-treated MC3T3-E1 cells, suggesting that ECH induced anti-apoptotic effects in dexamethasone-treated osteoblasts via p53-dependent pathway. In summary, ECH has a protective effect against osteoblastic cell apoptosis induced by dexamethasone, suggesting that ECH may have potentials for clinical application in the treatment of GIOP.