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Dioscin, a typical steroid saponin, has been reported to promote osteoblastic cell differentiation. However, the underling mechanisms remain to be elucidated. In the present study, it was identified that dioscin (0.5, 1, 5, 10 and 25 µg/ml) promoted MC3T3‑E1 cell proliferation and differentiation in a dose‑dependent manner. Western blot analysis showed that dioscin regulated autophagy‑associated protein expression in MC3T3‑E1 cells; it promoted the expression of apoptosis stimulated protein of p53‑2 (ASPP2), and inhibited the expression of nuclear factor (NF)‑κβ and microtubule‑associated protein 1 light chain 3β, in a concentration‑dependent manner. Caffeic acid phenethyl ester (CAPE) was used to inhibit the activation of NF‑κB and examine the effect of the ASPP2/NF‑κβ pathway on osteoblastic cell differentiation, proliferation and autophagy. It was identified that CAPE reversed the regulation of dioscin on osteoblastic cell differentiation, proliferation and autophagy. In conclusion, the present study revealed that dioscin promoted osteoblast proliferation and differentiation by inhibiting cell autophagy via the ASPP2/NF‑κβ pathway. These results are the first, to the best of our knowledge, to reveal the involvement of autophagy in the effects of dioscin on the prevention and therapy of osteoporosis.

Dioscin enhances osteoblastic cell differentiation and proliferation by inhibiting cell autophagy via the ASPP2/NF-κβ pathway