果糖二磷酸锶对糖皮质激素诱导的大鼠骨质疏松症的治疗作用

Therapeutic effect of strontium fructose 1,6-diphosphate(Sr-FDP) on glucocorticoid-induced osteoporosis in rats

目的:研究果糖二磷酸锶盐(Sr-FDP)对糖皮质激素诱导的大鼠继发性骨质疏松症的治疗作用。方法:应用肌肉注射地塞米松方法,建立大鼠继发性骨质疏松模型。口服不同剂量的Sr-FDP治疗8周,观察骨密度、骨生物力学、骨形态计量及骨代谢相关血清生化指标,综合评价Sr-FDP对糖皮质激素诱发的骨质疏松症的治疗效果。结果:肌肉注射地塞米松大鼠的骨密度、骨生物力学较正常组显著性下降,表明诱导大鼠骨质疏松模型成立。不同剂量Sr-FDP治疗均能显著增加模型大鼠的股骨与腰椎的骨密度、股骨干重与灰重,提高股骨和腰椎的骨强度,提高腰椎的骨小梁面积百分比及矿化沉积率,同时Sr-FDP对糖皮质激素引起的血清碱性磷酸酶及血抗酒石酸酸性磷酸酶5b活性的升高均有拮抗作用。结论:Sr-FDP能够促进骨形成,抑制骨吸收,对糖皮质激素诱导的大鼠骨质疏松症有明显的治疗作用。

Aim： To study the therapeutic effect of strontium fructose 1,6-diphosphate（Sr-FDP） on osteoporosis induced by glucocorticoid in rats. Methods： Osteoporosis rat model was developed successfully by intramuscular injection of dexamethasone for 8 weeks. Then treatment with oral dosing of Sr-FDP（ 110 mg/kg, 220 mg/kg and 440 mg/kg） was applied in the next 8 weeks, measurement of bones and mineral content, bone mineral density （BMD）, biomechanical properties of femur and lumbar vertebra, trabeeular histomorphology, biochemical assays of serum were recorded after the termination of therapy. Results： Compare with model group, treatment using Sr-FDP of middle and high doses markedly increased BMD, Biomechanical properties, trabecular areas, and mineral appositional rates. Meanwhile, it significantly decreased the levels of serum Alkaline phosphatase （ALP） and tartrate-resistant acid phosphatase 5b （TRACP 5b）. Conclusion： Sr-FDP, which enhances bone formation and slow bone resorption, could prevent osteoporosis in rats induced by glucocorticoid.