淫羊藿对破骨细胞骨吸收功能及机制研究进展

Progress on Effect of Epimedii Folium on Osteoclastic Resorption Function and its Mechanism

实验研究发现淫羊藿具有抑制破骨细胞骨吸收作用,其作用机制可能与降低破骨细胞内Ca2+浓度;提高破骨细胞代谢速率,并降低破骨细胞线粒体膜电势和细胞间ATP促进凋亡;抑制TNF-α的表达,促进TGF-β1的表达,抑制破骨细胞的生成,减少骨质丢失;抑制破骨细胞骨架F-actin环的构建及其调控蛋白PAK和Rho GTPases的表达,减弱破骨细胞与骨组织的锚定和在骨组织表面的附着;促进OPG基因表达,提高OPG/RANKL比值,抑制破骨细胞的形成和活性;抑制p38、JNK信号传导通路,抑制破骨细胞形成,影响骨吸收,并通过抑制ERK的磷酸化,降低转录因子蛋白家族NF-κB的活化而抑制破骨细胞生长;通过雌激素样作用调节下丘脑-垂体-性腺轴系统功能平衡,产生补肾健骨作用。作者从多个层面对淫羊藿抑制破骨细胞骨吸收作用机制进行阐述,为其进一步研究提供基础。

Researches have found that epimedii folium inhibits osteoclast resorption function.Its possible mechanism may rely on many factors：reducing Ca2＋ lever in the osteoclast;increasing osteoclast metabolic rate,reducing the membrane potential of osteoclasts mitochondria and intercellular ATP to promote its apoptosis;inhibiting TNF-α,increasing TGF-β1 to inhibit osteoclast formation and reduce bone loss;inhibiting cytoskeleton F-actin ring constructing and the expression of PAK and Rho GTPases,reducing attachment of osteoclast in the bone tissue;promoting OPG gene expression and improving OPG/RANKL ratio to inhibit the formation and activity of osteoclasts;inhibiting p38 and JNK signal pathway to inhibit osteoclast formation,and reducing NF-κB via inhibite the phosphorylation of ERK to inhibit the activation of osteoclast growth;regulating the hypothalamus-pituitary-gonadal system via androgen-like effects. Epimedii folium shall be further investigated and the mechanism of inhibiting osteoclast resorption function shall be further research from several aspects.