4.7 Article

The potential mechanism of Fructus Ligustri Lucidi promoting osteogenetic differentiation of bone marrow mesenchymal stem cells based on network pharmacology, molecular docking and experimental identification

期刊

BIOENGINEERED
卷 13, 期 4, 页码 10640-10653

出版社

TAYLOR & FRANCIS INC
DOI: 10.1080/21655979.2022.2065753

关键词

Fructus Ligustri Lucidi; traditional Chinese medicine; bone marrow mesenchymal stem cells; osteogenic differentiation; PI3K; AKT signaling pathway; network pharmacology

资金

  1. National Natural Science Foundation of China [81772362]
  2. Excellent Youth Foundation of Heilongjiang Province of China [JQ2020H003]

向作者/读者索取更多资源

This study investigates the mechanism of Fructus Ligustri Lucidi (FLL) in promoting the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). By combining network pharmacological predictions and in vitro experiments, it is confirmed that FLL promotes BMSCs osteogenic differentiation by activating the PI3K/AKT signaling pathway. This research provides theoretical support for the clinical application of FLL in the treatment of bone formation deficiency.
Recent studies have shown that the differentiation of bone marrow mesenchymal stem cells (BMSCs) into osteogenic lineages can promotes bone formation and maintains bone homeostasis, which has become a promising therapeutic strategy for skeletal diseases such as osteoporosis. Fructus Ligustri Lucidi (FLL) has been widely used for the treatment of osteoporosis and other orthopedic diseases for thousands of years. However, whether FLL plays an anti-osteoporosis role in promoting the osteogenic differentiation of BMSCs, as well as its active components, targets, and specific molecular mechanisms, has not been fully elucidated. First, we obtained 13 active ingredients of FLL from the Traditional Chinese Medicine Systems Pharmacology (TCSMP) database, and four active ingredients without any target were excluded. Subsequently, 102 common drug-disease targets were subjected to protein-protein interaction (PPI) analysis, Gene Oncology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. The results of the three analyses were highly consistent, indicating that FLL promoted the osteogenic differentiation of BMSCs by activating the PI3K/AKT signaling pathway. Finally, we validated previous predictions using in vitro experiments, such as alkaline phosphatase (ALP) staining, alizarin red staining (ARS), and western blot analysis of osteogenic-related proteins. The organic combination of network pharmacological predictions with in vitro experimental validation comprehensively confirmed the reliability of FLL in promoting osteogenic differentiation of BMSCs. This study provides a strong theoretical support for the specific molecular mechanism and clinical application of FLL in the treatment of bone formation deficiency.

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