应力缺失致骨质疏松大鼠成骨细胞细胞信号外调节激酶表达及通络生骨胶囊的影响*☆

背景：长期卧床患者和航天员应力缺失导致骨质疏松现象的发生，通络生骨胶囊具有促进骨生成的作用，可能干预应力缺失状态下骨质疏松的发生。目的：观察应力缺失型骨质疏松动物细胞信号外调节激酶的变化以及通络生骨胶囊对其改善作用。方法：SD大鼠40只随机分为对照组、模型组、药物高、药物低剂量组，除正常组外以鼠尾悬吊法制备动物应力缺失模型，药物高、低剂量组将通络生骨胶囊按0.6，1.2 g/kg剂量灌胃，1次/d，21 d后，取腿骨，观察骨形态变化及成骨细胞细胞信号外调节激酶的表达水平。结果与结论：应力缺失导致骨质疏松，对细胞信号外调节激酶总量无显著影响，但显著降低其磷酸化蛋白表达；通络生骨胶囊可显著改善应力造成的骨质疏松状态，但药物高剂量组对磷酸化的细胞信号外调节激酶的表达影响不显著，药物低剂量组则还降低其表达。说明应力缺失通过降低细胞信号外调节激酶磷酸化水平导致骨质疏松，通络生骨胶囊不是通过影响细胞信号外调节激酶通路改善应力缺失导致的骨质疏松的。

Stress absence effect on ERK42/44 expression and intervention of Tongluo Shenggu capsules

BACKGROUND: Stress absence induces osteoporosis in bedridden patients or astronauts. Tongluo Shenggu capsules can promote bone formation, which may affect stress absence-induced osteoporosis. OBJECTIVE: To investigate influence of stress absence on the expression of ERK42/44, and intervention of the Tongluo Shenggu capsules. METHODS: Totally 40 SD rats were randomly divided into normal control, model and high- and low-drug groups. Exception rats in the normal control group, all animals in other three groups were subjected to tail suspension test for preparing for stress absence models. Animals in the drug groups were administered Tongluo Shenggu capsule (0.6 or1.2 g/kg) once per day. After model preparation, animals were sacrificed, and bones of lower leg was taken out. Bone The norphological changes and expression of ERK was determined by western blot. RESULTS AND CONCLUSION: Stress absence induced osteoporosis and decreased the amount of phosphorylation ERK, but had little effect on the total ERK. Low-dose of Tongluo Shenggu capsules decreased the expression of ERK phosphorylation, but high-dose of drugs had marginal on ERK. Stress absence induced osteoporosis by decreasing the phosphorylation of ERK, and the bone formation improving effect of Tongluo Shenggu capsules is not by regulating ERK expression.