摘要
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 investigate the therapeutic effect of recombinant human parathyroid hormone(1-34)[rhPTH(1-34) ] on osteoporosis induced by glucocorticoid in rats. Methods The osteoporosis rat model was developed by intramusculr dexamethasone, and then rhPTH(1-34)5, 10, 20, and 40 μg/kg was subcutaneously injected once daily for 8 weeks. The dry weight and ash weight of bone, bone mineral density, bone biomechanical property, trabecular area, bone mineral deposition and the biochemistry of serum and urine related bone metabolites were measured after the termination of therapy. Results In rhPTH( 1-34)-treated rats, bone mass, bone biomechanical property, trabecular area, and bone depositon increased significantly, compared with the control group ( P < 0.05 - 0.001), but serum Ca and P had no marked change. Conclusions rhPTH(1-34) possesses remarkable therapeutic effect on glucocorticoid-induced osteoporosis in rats.
出处
《中国骨质疏松杂志》
CAS
CSCD
2004年第4期461-465,共5页
Chinese Journal of Osteoporosis
