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目的 观察重组人甲状旁腺激素(1-34)[recombinant human parathyroid hormone(1-34),rh-PTH(1-34)]对糖皮质激素引起的大鼠继发性骨质疏松症(OP)的治疗作用。方法 应用肌肉注射地塞米松(dexamethasone.DEX)方法,建立模拟糖皮质激素引起的继发性OP大鼠模型。给予皮下注射5、10、20和40μg·kg-1·d-1rhVTH(1-34)治疗8周。观察骨量、骨生物力学、骨形态计量及骨代谢相关血尿生化指标,综合评价PTH对糖皮质激素诱发OP的治疗效果。结果显示肌注地塞米松大鼠的骨量、骨生物力学较对照组显著性下降,表明诱导大鼠骨质疏松模型成立。不同剂量咖治疗均能显著增加模型大鼠的腰椎与股骨骨密度、股骨干重与灰重,提高股骨三点弯曲最大载荷、提高腰椎骨小梁面积百分比及矿化沉积率(P<0.05-0.001),并呈一定剂量效应关系。血钙、磷无明显变化。结论外源性PTH对糖皮质激素诱发的大鼠OP具有显著治疗作用。
Objective To observe the effect of recombinant human parathyroid hormone (1-34) and rh-PTH (1-34) on glucocorticoid-induced secondary osteoporosis in rats ) Of the therapeutic effect. Methods A rat model of secondary OP induced by glucocorticoid was established by intramuscular injection of dexamethasone (DEX). Subcutaneous injections of 5, 10, 20 and 40 μg · kg-1 · d-1 rhVTH (1-34) were given for 8 weeks. Observe the bone mass, bone biomechanics, bone morphometry and bone metabolism related to serum biochemical indicators, a comprehensive evaluation of PTH glucocorticoid-induced OP treatment. The results showed that the bone mass and bone biomechanics in the intramuscular dexamethasone group decreased significantly compared with the control group, indicating that the induced osteoporosis model was established. Different doses of coffee can significantly increase the lumbar and femoral bone mineral density, weight and weight of the femur, increase the maximum bending load of three points of the femur, increase trabecular area percentage and mineralization deposition rate (P <0.05) 0.001), and showed a dose-response relationship. Blood calcium, phosphorus no significant change. Conclusion Exogenous PTH has a significant therapeutic effect on glucocorticoid-induced OP in rats.