Li Xue-Dong, Liu Zhao-Yong, Chang Bo, Liu Dong-Xin, Chen Bin, Guo Chun, Wang Yun-Guo, Xu Jian-Kun, Huang Dong-Yang, Du Shi-Xin
Department of Orthopedics, the First Affiliated Hospital, Shantou University Medical College, Shantou, R.P. China.
Cell Physiol Biochem. 2011;28(2):367-76. doi: 10.1159/000331753. Epub 2011 Aug 16.
The Chinese medicinal herb, Panax notoginseng, has long been used to treat bone fractures and Panax notoginseng saponins (PNS) could promote bone formation. Here, we investigated whether PNS could promote osteogenesis of bone marrow stromal cells (BMSCs) through modulating the MAPK signaling pathways, which are implicated in BMSC osteogenesis. We found that PNS markedly increased the mineralization of BMSCs by alizarin red S assays and stimulate alkaline phosphatase activity of these cells. Additionally, PNS significantly increased the mRNA levels of alkaline phosphatase, core-binding factor a1, and bone sialoprotein while decreasing PPARγ2 mRNA levels. Furthermore, inhibitors of ERK, PD98059, and p38, SB203580 inhibited the osteogenesis-potentiating effects by PNS. PNS stimulated the activation of ERK and p38 as evidenced by increased phosphorylation of these proteins, which was inhibited by PD98059 and SB203580. Our findings indicate that PNS could promote BMSC osteogenesis by activating the ERK and p38 signaling pathways.
中药三七长期以来被用于治疗骨折，三七总皂苷（PNS）能够促进骨形成。在此，我们研究了PNS是否可通过调节与骨髓间充质干细胞（BMSC）成骨作用相关的丝裂原活化蛋白激酶（MAPK）信号通路来促进BMSC的成骨作用。我们发现，通过茜素红S检测，PNS显著增加了BMSC的矿化，并刺激了这些细胞的碱性磷酸酶活性。此外，PNS显著增加了碱性磷酸酶、核心结合因子a1和骨唾液蛋白的mRNA水平，同时降低了PPARγ2 mRNA水平。此外，ERK抑制剂PD98059和p38抑制剂SB203580抑制了PNS的成骨增强作用。PNS刺激了ERK和p38的激活，这些蛋白的磷酸化增加证明了这一点，而这被PD98059和SB203580所抑制。我们的研究结果表明，PNS可通过激活ERK和p38信号通路促进BMSC的成骨作用。
