摘要
背景:骨超微结构的变化是骨质疏松发生的重要原因,是骨脆性的决定因素,因此骨超微结构的改变可以更直接反映骨质疏松情况。目的:观察阿伦磷酸钠对糖皮质激素作用下大鼠股骨远端松质骨超微结构的影响。方法:选取3.5月龄SPF级雌性SD大鼠30只,随机分为3组,对照组给等量生理盐水皮下注射、等量生理盐水灌胃;模型组给予皮下注射甲泼尼龙3.5mg/(kg·d),诱导糖皮质激素性骨质疏松模型;干预组在造模同时给予阿伦磷酸钠1.2mg/kg灌胃。实验期9周后,扫描电镜观察大鼠股骨远端松质骨超微结构改变。结果与结论:模型组大鼠骨小梁数目较其他各组减少且骨小梁变细、易断裂,微损伤增多,立体网状结构破坏;干预组大鼠较模型组大鼠骨小梁数量增加,骨吸收面减少,骨小梁表面胶原纤维排列规律紧凑、走向清晰。提示阿伦磷酸钠能有效改善糖皮质激素诱导骨质疏松大鼠股骨远端松质骨超微结构,具有对抗糖皮质激素性骨质疏松的作用。
BACKGROUND: Bone ultrastructural changes play an important role in osteoporosis, which is a determinative factor in bone fragility, thus, bone ultrastructural change can reflect osteoporosis. OBJECTIVE: To observe the effect of alendronate on the ultrastructural changes of distal femur cancellous bone in glucocorticoid (GC)-treated rats. METHODS: Totally 30 female Sprague-Dawley rats, 3.5 months old, were randomized into 3 groups according to the following treatment schedule: control group: received subcutaneous injection of saline and intragastric administration of same volume of saline; model group: osteoporosis was induced by subcutaneous injection with methylprednisolone 3.5 mg/(kg·d); and intervention group: treated with methylprednisolone in combination with alendronate by gavage. Nine weeks later, the ultrastructure of rat distal femur cancellous bone was observed by a scanning electron microscopy. RESULTS AND CONCLUSION: Compared to the other groups, the number of bone trabeculae in the model group was significantly decreased and the bone trabeculae became thin, fragile, discontinuous, micro-damage increased and network structures of bone trabeculae were destroyed. Compared to model group, the number of trabeculae in the intervention group was increased, resorption surface was decreased and the collagenous fibers were arranged orderly. Alendronate can effectively improve the ultrastructure of distal femur callecllous bone in glucocorticoid-treated rats.
出处
《中国组织工程研究与临床康复》
CAS
CSCD
北大核心
2010年第41期7609-7612,共4页
Journal of Clinical Rehabilitative Tissue Engineering Research