补肾中药对绝经后骨质疏松症模型大鼠骨及肌肉组织Notch信号通路蛋白表达的影响

Effects of kidney-tonifying Chinese herbs on the protein expression of Notch signal pathway in bone and muscular tissues of the postmenopausal model rats with osteoporosis

目的:观察去卵巢骨质疏松症(OP)大鼠模型骨及肌肉组织Notch信号蛋白活性变化,探究补肾中药防治OP的分子生物学机制。方法:75只大鼠随机分为5组:正常组、假手术组、模型组、补肾中药组、福善美组,以去卵巢法建立绝经后OP大鼠模型,补肾中药组运用补肾中药干预8周后以双能X线骨密度分析仪检测骨密度,ELISA法检测血清OPG、RANKL,骨及肌组织HES1、JAG1以及Notch1蛋白表达。结果:与正常组比较,模型组骨密度及血清OPG明显减少(P<0.01),血清RANKL明显升高(P<0.01),骨及肌肉组织Notch信号蛋白表达明显减少(P<0.01);与模型组相比较,各治疗组骨密度、血清OPG及骨组织Noth信息蛋白均有不同程度的升高(P<0.05,P<0.01)。结论:OP的发生机制与Notch信号通路有关;补肾中药通过激活Notch信号传导通路,促成骨分化,抑制破骨活性,起到防治OP的作用。

Objective: To explore the molecular biological mechanism of the kidney-reinforcing herbs in preventing and treating osteoporosis by observing the activity changes of Notch signaling protein in bone and muscular tissues of the ovariectomized model rats with osteoporosis. Methods: Seventy-five rats were randomly divided into five group: normal group, sham operation group, model group, Fosamax group and kidney-tonifying Chinese herbs group, 15 in each group. Rats in kidneytonifying Chinese herbs group were intervened with kidney-reinforcing herbs for 8 weeks. Bone mineral density was determined by dual-energy X ray bone densitometer, and serum OPG, RANKL, bone and muscular tissue HES1, JAG1 and the protein expression of Notch1 were determined by ELISA method. Results: Compared with normal group, the bone mineral density and serum OPG were significantly decreased in model group(P<0.01), while serum RANKL was significantly increased(P<0.01), the Notch signal protein expression of bone and muscular tissues in model group was significantly decreased(P<0.01). The bone mineral density in each treatment group was increased with varying levels compared with model group(P<0.05, P<0.01). Conclusion: The mechanism of osteoporosis is related to Notch signal pathway. Kidney-reinforcing Chinese herbs has the effects of preventing osteoporosis by activating the Notch signal pathway, promoting the differentiation of osteoblast and suppressing the activity of osteoclast.