Asperosaponin VI stimulates osteogenic differentiation of rat adipose-derived stem cells

Regen Ther. 2019 May 10:11:17-24. doi: 10.1016/j.reth.2019.03.007. eCollection 2019 Dec.

Abstract

In the aging population, the decrease on osteogenic differentiation resulted into a significant reduction in bone formation. Bone tissue engineering has been a successful technique for treatment of bone defects. It is reported that adipose-derived stem cells (ADSCs) have pluripotency to differentiate into adipocytes and osteoblasts. However little is revealed about the effect of the herbal medicine Asperosaponin VI (ASA VI) on ADSCs differentiation. In our study, we isolated and identified ADSCs from rats. We examined the effect of different concentrations of ASA VI in ADSCs on alkaline phosphatase (ALP) activity, calcium deposition, the expression of bone-related proteins and the release of inflammatory cytokines. Flowcytometry assay showed ADSCs were highly expressed CD44 and CD105, but hardly expressed CD34 and CD45, suggesting ADSCs were successfully isolated for follow-up experiments. ALP activity examination and Alizarin red (AR) stain showed that ASA VI enhanced the ALP activity and promoted matrix mineralization in ADSCs. In addition, bone-related protein OCN and RUNX2, and Smad2/3 phosphorylation was upregulated after ASA VI treatment in ADSCs. ELISA results showed that ASA VI blocked the release of TNF-α, IL-6 and IL-1β in ADSCs. Considering this results, we concluded that ASA VI promotes osteogenic differentiation of ADSCs through inducing the expression of bone-related proteins. These findings enriched the function of ASA VI as a regenerative medicine and shed new light for the treatment of bone defects in clinical research.

Keywords: ADSCs, adipose-derived stem cells; ALP, alkaline phosphatase; AR, alizarin red; ASA VI, Asperosaponin VI; Adipose-derived stem cells; Asperosaponin VI; Bone defects; MSCs, mesenchymal stem cells; OCN, osteocalcin; Osteogenic differentiation; PE, phycoerythrin; RUNX2, runt-related transcription factor 2.