背景:越来越多的证据表明骨质疏松症的发生和发展与免疫系统功能失常而产生炎症反应直接关联。目的:总结了破骨细胞分化与形成的细胞分子机制,以及几种植物药及其对骨骼发挥保护作用机制,为今后发现更多通过抗炎产生抗骨质疏松作用的植物药,并使其可能成为安全、有效的抗骨质疏松症的食品或药物奠定基础。方法:以"(osteoporosis OR bone loss)AND lipopolysaccharide AND bone resorption;骨质疏松症;核因子κB受体激活剂配基;脂多糖;石斛;马齿苋;蛇葡萄;荆芥"为关键词检索PubM ed数据库和万方数据库,筛选出内容与骨质疏松、炎症及植物药相关的文献,选择在动物实验方面采用脂多糖诱导的小鼠模型的文献。经过筛查、分析,选择4篇较为代表性的文献,对这些植物药的作用机制进行探讨分析。结果与结论:体内实验中,通过计算机显微断层扫描和病理组织切片对小鼠股骨远端海绵骨构造进行分析,石斛、马齿苋、蛇葡萄、荆芥可以抑制脂多糖诱导的炎症性骨质疏松。体外实验中,这4种植物可以抑制破骨细胞分化从而降低骨吸收活性,发挥防治骨质疏松的作用。
The present study aimed at investigating the effects of Puerarin(PR), a major isoflavonoid isolated from the Chinese medicinal herb Puerariae radix, on bone metabolism and the underlying mechanism of action. The in vivo assay, female mice were ovariectomized(OVX), and the OVX mice were fed with a diet containing low, middle, and high doses of PR(2, 4, and 8 mg·d^(-1), respectively) or 17β-estradiol(E_2, 0.03 μg·d^(-1)) for 4 weeks. In OVX mice, the uterine weight declined, and intake of PR at any dose did not affect uterine weight, compared with the control. The total femoral bone mineral density(BMD) was significantly reduced by OVX, which was reversed by intake of the diet with PR at any dose, especially at the low dose. In the in vitro assay, RAW264.7 cells were used for studying the direct effect of PR on the formation of osteoclasts. PR reduced the formation of tartrate resistant acid phosphatase(TRAP)-positive multi-nucleated cells in the RAW 264.7 cells induced by receptor activator for nuclear factor-κB Ligand(RANKL). MC3T3-E1 cells were used for studying the effects of PR on the expression of osteoprotegerin(OPG) and RANKL m RNA expression in osteoblasts. The expression of OPG m RNA and RANKL m RNA was detected by RT-PCR on Days of 5, 7, 10, and 12 after PR exposure. PR time-dependently enhanced the expression of OPG m RNA and reduced the expression of RANKL m RNA in MC3T3-E1 cells. In conclusion, our results suggest that PR can effectively prevent bone loss in OVX mice without any hyperplastic effect on the uterus, and the antiosteoporosis activity of PR may be related to its effects on the formation of osteoclasts and the expression of RANKL OPG in osteoblasts.