Background The total flavonoids of rhizoma drynariae (TFRD) are the main active components of drynaria. In recent years, many studies have shown that TFRD can effectively increase bone mineral density in patients with osteoporosis, thereby promoting bone healing. However, the specific molecular mechanism of its effect is not yet fully understood.
Objective To explore the molecular mechanism of TFRD in multiplication response and differentiation of bone marrow mesenchymal stem cells (BMSCs) in rats.
Methods BMSCs from SD rats were obtained, cultured and identified. TFRD was added to the cell culture medium for intervention. According to the concentration of TFRD, BMSCs were divided into low concentration group (TFRD 0.1 mg/L), medium concentration group (TFRD 1.0 mg/L), high concentration group (TFRD 10.0 mg/L)and control group (without TFRD in the cell culture medium). The proliferation of BMSCs in each group was detected by CCK8 assay, the osteogenic differentiation of each group was detected by alizarin red staining, and the mRNA and protein expressions of β-catenin, RunX2 and PPARG in medium concentration group and control group were detected by RT-PCR and Western blot.
Results Compared with the control group, the absorbance level in the low concentration group, the medium concentration group and the high concentration group were significantly higher at different time points (all P＜0.05). The number of mineralized nodules in the medium concentration group was significantly higher than that in the other three groups (P＜0.05). The mRNA expressions of β-catenin and RunX2 and the protein expressions of β-catenin and RunX2 in the medium concentration group were also significantly higher than those in the control group, while the PPARG mRNA expression and the protein expression of PPARG were significantly lower than that in the control group (all P＜0.05).
Conclusion TFRD can promote cell proliferation and osteogenic differentiation of BMSCs, and the mechanism may be related to up-regulation of β-catenin and RunX2 expressions, and inhibition of PPARG expression.
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