Notoginsenoside R1 promotes differentiation of human alveolar osteoblasts in inflammatory microenvironment through inhibiting NF‑κB pathway and activating Wnt/β‑catenin pathway
Affiliations: Department of Oral and Maxillofacial Surgery, Jingmen Number 1 People's Hospital, Jingmen, Hubei 448000, P.R. China
- Published online on: September 25, 2020 https://doi.org/10.3892/mmr.2020.11537
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Alveolar bone is vital for dental implantation and periodontal treatment. Notoginsenoside R1 (NTR1) may promote the differentiation of human alveolar osteoblasts (HAOBs), but the underlying molecular mechanisms remain unclear. The present study investigated the pro‑differentiation function of NTR1 on HAOBs in order to find new methods of dental treatment. HAOBs were surgically obtained from dental patients and the cells were isolated, cultured and identified under an inverted phase contrast microscope. The cells were treated with different concentrations of NTR1 alone or further stimulated by TNF‑α. An alkaline phosphate (ALP) activity assay and alizarin red staining were performed to detect ALP activity and mineralization of the cells, respectively. Cell viability was assayed using an MTT assay. The expressions of osteogenic‑related factors and the factors associated with the NF‑κB and Wnt/β‑catenin pathways were examined by reverse transcription‑quantitative PCR or western blot analysis. Successfully passaged HAOBs presented blue granules and red calcium deposits after staining. The viability of HAOBs was unchanged following treatment with NTR1 at ≤20 µmol/l and/or TNF‑α, but slightly reduced by 40 µmol/l NTR1. TNF‑α‑induced decreases of calcium nodules and ALP activity were decreased by NTR1 in HAOBs. TNF‑α also regulated the expressions of runt‑related transcription factor 2, osteopontin (OPN), osteocalcin (OCN), p50, phosphorylated p65, AXIN2, Dickkopf‑related protein 1 and β‑catenin, while the regulatory effect was reversed by NTR1. NTR1 promoted the differentiation of HAOBs in the TNF‑α‑induced inflammatory microenvironment through inhibiting the NF‑κB pathway and activating the Wnt/β‑catenin pathway.