Puerarin promotes the proliferation and differentiation of MC3T3-E1 cells via microRNA‑106b by targeting receptor activator of nuclear factor‑κB ligand
- Zimei Shan
- Na Cheng
- Rong Huang
- Bin Zhao
- Yali Zhou
Published online on: October 31, 2017
Copyright: © Shan et al.
This is an open access article distributed under the terms of Creative Commons Attribution License.
Puerarin, an isoflavone-C-glucoside extracted from the root of Pueraria Labata (Willd.) Ohwi, is one of the most important crude herbs used in Chinese medicine for various medicinal purposes. Accumulating evidence has indicated that puerarin suppresses bone resorption and promotes bone formation. However, the molecular mechanism involved in puerarin‑associated bone formation is unclear. The present study aimed to investigate the molecular mechanism of puerarin‑induced osteoblast proliferation and differentiation. The study showed that puerarin treatment differentially affected cell proliferation in a time‑dependent manner. Notably, at a concentration of 20 µM, puerarin significantly promoted cell proliferation in comparison with the control (P<0.01). Furthermore, puerarin promoted MC3T3‑E1 cell differentiation at an appropriate concentration. In addition, miR‑106b was significantly upregulated in MC3T3‑E1 cells following treatment with 20 µM puerarin (P<0.01), and a known target for miR‑106b, receptor activator of nuclear factor‑κB ligand (RANKL) was demonstrated using the luciferase reporter assay. Furthermore, inhibition of miR‑106b significantly reversed the promotion of cell differentiation induced by puerarin in MC3T3‑E1 cells (P<0.01). In conclusion, the present study demonstrated that puerarin exerts its role in MC3T3‑E1 osteogenesis through miR‑106b by targeting RANKL. The findings suggest that puerarin may be considered a promising anti‑osteoporotic agent for the treatment of osteoporosis.