补肾宁心方对小鼠绝经后骨质疏松的影响

作者	单位
王玉东	上海交通大学附属第六人民医院妇产科
李大金	复旦大学附属妇产科研究所生殖免疫
王文君	复旦大学附属妇产科研究所生殖免疫
朱影	复旦大学附属妇产科研究所生殖免疫

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中文摘要:

目的探讨补肾宁心方防治绝经后骨质疏松的作用。方法建立BALB/c小鼠绝经后骨质疏松模型,灌服补肾宁心方浓缩液(简称补肾方组),并以17β-雌二醇为阳性对照(简称E2组),以生理盐水为阴性对照(简称模型组)。12周后处死,取血测Th1/Th2型细胞因子;取椎骨(L3-4)和左股骨测骨密度(BMD);取右股骨行骨组织形态计量分析;胫骨提取总RNA,半定量RT-PCR分析护骨素(OPG)的mRNA表达。计算子宫对体重的比值,并行子宫组织切片观察。结果补肾方组的IFN-γ水平较模型组明显升高(P<0.01),而IL-4水平低于模型组(P<0.05)。补肾方组与E2组小鼠的BMD均改善,骨小梁面积增加,OPG mRNA表达增加;但补肾方组小鼠的子宫明显小于E2组(P<0.05),与模型组比较差异无显著性。结论补肾方能够选择性地防治绝经后骨质疏松,对子宫无或仅有轻微的刺激作用。其机制可能与调节Th1/Th2的偏移及提高OPG的表达,抑制破骨细胞的活性有关。

英文摘要:

ObjectiveTo investigate the preventive and therapeutic effect of Bushen Ningxin decoction （BSNX） on postmenopausal osteoporosis. Methods The BALB/c female mice postmenopausal osteoporosis model was established. The model mice were treated by BSNX, with 17β-estradiol （E₂） and normal saline as positive and negative control, respectively. All mice were sacrificed after 12 weeks’ treatment, the serum cytokines Th₁/Th₂, bone mineral density （BMD） of vertebrae （L3-4） and left femur were determined, and morphological quantitative analysis of bone tissue of right femurs was performed and osteoprotegerin （OPG） mRNA expression in tibia was detected by semi-quantitative RT-PCR. The ratio in weight of uterus to body was calculated, and uterine slice was gotten for histological observation. Results As compared with the negative control group, the level of interferon-γ （IFN-γ） was significantly increased （P<0.01） and interleukin-4 （IL-4） decreased （P<0.05）in the BSNX treated group. The BMD of mice were improved, area of bone trabecula and OPG mRNA expression were increased in the BSNX treated and E₂ treated group（P<0.01）. But the uterus in the former was significantly smaller than that in the latter（P<0.01）, while it was not significantly different to that in the negative control group. Conclusion BSNX can selectively prevent and cure the postmenopausal osteoporosis, it has no or slight stimulation on uterus. The mechanism may relate with its effects in regulating the deviation of Th₁/Th₂, enhancing the OPG expression and inhibiting the activity of osteoclasts.

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