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目的 观察不同剂量卡托普利对抗小鼠维甲酸性骨质疏松的量效关系 ,探讨卡托普利抗骨质疏松的骨代谢作用特点及骨药理学作用机制。方法 用维甲酸 (10 5mg·kg-1)造成小鼠骨丢失为主的骨质疏松模型 4组 ,同时其中 3组再用 3种剂量卡托普利分别给药 ,实验过程监测体重 ,2wk后处死取肝、脾、胸腺称重 ,并取股骨进行骨干重、骨钙、磷、镁、锌、锰、硫及骨羟脯氨酸 (B HOP)的测定和比较。结果 维甲酸可造成小鼠骨丢失为主的骨质疏松 ,卡托普利可对抗维甲酸所致的小鼠骨横短径、骨基质的主要成分骨羟脯氨酸及骨矿物质的减少。结论 卡托普利可对抗维甲酸引起小鼠以骨钙、磷、镁和骨羟脯氨酸丢失为主的骨质疏松 ,其中尤以低剂量卡托普利 (6 2 5mg·kg-1)作用最显著
Objective To observe the dose-response relationship of captopril with different dosages against retinoic acid-induced osteoporosis in mice and to explore the mechanism of the effect of captopril on osteoporosis and bone pharmacology. Methods Four groups of osteoporosis mice were induced by retinoic acid (10 5 mg · kg-1). Three groups were given 3 doses of captopril respectively. The body weight, After sacrifice, the liver, spleen and thymus were weighed, and the bone weight, bone calcium, phosphorus, magnesium, zinc, manganese, sulfur and bone hydroxyproline (B HOP) were measured and compared. Results Retinoic acid can cause bone loss in mice mainly osteoporosis, captopril can be resistant to retinoic acid-induced mouse bone trabecular diameter, the main component of bone matrix hydroxyproline and bone mineral reduction . Conclusion Captopril can antagonize the retinoic acid caused by bone calcium, phosphorus, magnesium and bone hydroxyproline-based osteoporosis, especially low-dose captopril (62.5mg · kg-1 ) The most significant role