补肾中药对绝经后骨质疏松症大鼠肾组织Notch信号通路的影响

目的：本研究旨在观察去卵巢骨质疏松症大鼠模型肾组织Hes1、Jagged1和Notch1 mRNA及其编码蛋白HES1、Jagged1和Notch1的活性变化，探究补肾中药防治骨质疏松症的分子生物学机制。方法：将75只雌性SD大鼠随机分为正常组、假手术组、模型组、补肾复方组、福善美组，模型组采用切除雌性SD大鼠双侧卵巢的方式建立骨质疏松症模型，补肾复方组运用补肾复方对模型大鼠治疗8周，用福善美作为阳性药物对照组。8周后采用ELISA法检测各组肾组织HES1、Jagged1以及Notch1含量；RT-PCR检测各组Hes1、Jagged1和Notch1相对表达量。结果：与正常组相比，模型组肾组织Hes1、Jagged1和Notch1及其编码蛋白表达明显减少（P<0.01）；与模型组相比，补肾复方组和福善美组肾组织Hes1、Jagged1和Notch1及其编码蛋白的表达均明显增加（P<0.01）；结论：骨质疏松症的发生机制与Notch信号传导通路有关；补肾复方通过激活Notch信号传导通路，可以促进成骨细胞分化，抑制破骨细胞活性，起到防止骨质疏松症的作用。

Effects of Kidney-tonifying Chinese Herbs on Notch Signal Pathway in Kidney Tissues of Rats with Postmenopausal Osteoporosis

This study was aimed to observe the mRNA and protein expression of Hes1, Jagged1 and Notch1 in kidney tissues among osteoporosis rats of ovaries-removed, in order to discuss the molecular biological mechanism of kidney-tonifying Chinese herbs in the prevention and treatment of osteoporosis. A total of 75 female SD rats were randomly divided into the normal group, sham operation group, model group, kidney-tonifying compound group, and the Fosamax group. Both ovaries were removed in the female SD rat for the establishment of osteoporosis model. The kidney-tonifying compound was given for 8 weeks in the kidney-tonifying compound group. Fosamax was used as the positive control drug. Eight weeks later, ELISA and RT-PCR methods were used for the detection of contents and relative expressions of Hes1, Jagged1 and Notch1 in kidney tissues of each group. The results showed that compared with the normal group, the mRNA and protein expressions of Hes1, Jagged1 and Notch1 in kidney tissues were obviously reduced in the model group (P < 0.01). Compared with the model group, the mRNA and protein expressions of Hes1, Jagged1 and Notch1 in kidney tissues were obviously increased in the kidney-tonifying compound group and the Fosamax group (P < 0.01). It was concluded that the mechanism of osteoporosis was related to the Notch signal pathway. The kidney-tonifying compound activated the Notch signal pathway, promoted the osteoblast differentiation, and inhibited the osteoclast activity, for the prevention of osteoporosis.