摘要
目的探讨胰淀素对类固醇性骨质疏松大鼠骨代谢生化指标的影响。方法采用3月龄雌性Wistar大鼠地塞米松肌肉注射法建立类固醇性骨质疏松症动物模型,随机将32只分为:正常对照组、模型组、胰淀素治疗组、维生素D组,每组8只。12周后行骨密度及血尿生化检查。结果①骨密度:与模型组相比,胰淀素治疗组腰椎骨密度增加35%,股骨骨密度增加17%,其效果优于维生素D;②生化指标:胰淀素治疗组骨钙素、骨碱性磷酸酶明显升高,同时尿羟脯氨酸/肌酐、尿1型胶原羧基末端肽/肌酐、尿钙/肌酐、尿磷/肌酐均普遍降低。结论胰淀素可以有效地阻止糖皮质激素性骨质疏松大鼠的骨量丢失,不仅可以促进骨形成,同时还具有抑制骨吸收的作用。
Objective To investigate the effect of amylin (AMY) on bone metabolic biochemical indexes in glucocorticoid-induced osteoporosis(GIO) rats.Methods Four groups(n=8,each group) of female Wistar rats (3 months old) were respectively treated for 12 weeks as follows: Ⅰ ,normal control; Ⅱ ,desamethasone (DXM); Ⅲ DXM+AMY; IV DXM+Vitamin D3. By intramuscular injection of DXM lmg/kg twice a week during the first 8 weeks, the animal model of glucocorticoid induced osteopoprosis was established. After 12 weeks, BMD of the lumbar vertebrae and the femur were measured by DEXA. The bone markers of serum and urine were also determined. Results (1)After the treatment with AMY,bone mineral density (BMD) significantly increased by 35% at the lmnbar spine and by 17% at the femur (vs, DXM group) The BMD of the lumbar vertebrae was also higher in DXM+VitD than in DXM rats, but it was not different at the femur between these two groups.(2)The highest plasma BGP and BAP concentrations were measured in DEX+AMY rats. Simultaneously, urinary HOP/Cr, uCTX/Cr,uCa/Cr and uP/Cr were lower in DXM+AMY than in DXM rats. Conclusion AMY can effectively inhibit bone loss both by inhibiting resorption and by stimulating osteoblastic activity in GIO rats.
出处
《实用医药杂志》
2007年第3期337-339,共3页
Practical Journal of Medicine & Pharmacy
基金
南京军区总医院基金(2003034)
关键词
胰淀素
类固醇性骨质疏松
骨密度
骨代谢
Amylin Glueocorticoid-indueed osteoporosis Bone mineral density Bone metabolism