Department of Endocrinology, Huaihe Hospital of Henan University, Kaifeng, Henan Province, China.
J Cell Biochem. 2018 Sep;119(9):7310-7318. doi: 10.1002/jcb.27028. Epub 2018 May 24.
Gypenoside (GP) is one of the most pharmacologically active components in Gynostemma pentaphyllum and possesses neuroprotective, anticancer, anti-oxidant, anti-inflammatory, anti-diabetic, and anti-osteoarthritis effects. However, the involvement of GP the osteoclast differentiation has not yet been investigated. In the present study, we examined the effect of GP on receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast formation. Our results demonstrated that GP significantly inhibited the formation of osteoclast, as well as suppressed the expression of osteoclastogenesis-related marker proteins in RANKL-stimulated bone marrow macrophages (BMMs). For molecular mechanisms, GP inhibited RANKL-induced NF-κB and MAPK activation and AKT phosphorylation in BMMs. Collectively, these findings suggest that GP inhibits RANKL-induced osteoclastogenesis via regulating NF-κB, AKT, and MAPK signaling pathways. Therefore, GP may be a potential agent in the treatment of osteoclast-related diseases such as osteoporosis.
绞股蓝皂苷（GP）是绞股蓝中最具药理活性的成分之一，具有神经保护、抗癌、抗氧化、抗炎、抗糖尿病和抗骨关节炎作用。然而，GP 参与破骨细胞分化的情况尚未得到研究。在本研究中，我们研究了 GP 对核因子-κB 受体激活剂配体（RANKL）诱导的破骨细胞形成的影响。结果表明，GP 可显著抑制破骨细胞的形成，并抑制 RANKL 刺激的骨髓巨噬细胞（BMM）中破骨细胞生成相关标记蛋白的表达。在分子机制上，GP 抑制了 BMM 中 RANKL 诱导的 NF-κB 和 MAPK 激活以及 AKT 磷酸化。综上所述，这些发现表明 GP 通过调节 NF-κB、AKT 和 MAPK 信号通路抑制 RANKL 诱导的破骨细胞生成。因此，GP 可能是治疗骨质疏松症等与破骨细胞相关疾病的潜在药物。
