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胰淀素治疗糖皮质激素性骨质疏松大鼠的实验研究
引用本文:孟萍,陆邦超,张忠辉,黄姝,乔飞. 胰淀素治疗糖皮质激素性骨质疏松大鼠的实验研究[J]. 第三军医大学学报, 2002, 24(10): 1214-1216
作者姓名:孟萍  陆邦超  张忠辉  黄姝  乔飞
作者单位:1. 第三军医大学附属西南医院内分泌科,重庆,400038
2. 卫生部北京医院,北京,100730
3. 解放军第81医院内科,南京,210002
摘    要:目的:探讨胰淀素对糖皮质激素性骨质疏松的治疗作用。方法:采用3月龄Wistar大鼠地塞米松肌注法建立糖皮质激素性骨质疏松症动物模型,随机分为4组:正常对照组、地塞米松组、胰淀素治疗组、维生素D组。12h后行骨密度、骨生物力学及血、尿生化检查。结果:①骨密度:与地塞米松组相比,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骨力学:胰淀素能显著提高类固醇大鼠股骨的生物力学性能。③生化指标:胰淀素治疗组骨钙素明显升高,同时尿羟脯氨酸/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。

关 键 词:胰淀素 糖皮质激素性骨质疏松 骨密度 生物力学
文章编号:1000-5404(2002)10-1214-03
修稿时间:2002-05-08

Experimental study on therapeutic effects of amylin on glucocorticoid induced osteoporosis in rats
MENG Ping,LU Bang chao,ZHANG Zhong hui,HUANG Shu,QIAO Fei. Experimental study on therapeutic effects of amylin on glucocorticoid induced osteoporosis in rats[J]. Acta Academiae Medicinae Militaris Tertiae, 2002, 24(10): 1214-1216
Authors:MENG Ping  LU Bang chao  ZHANG Zhong hui  HUANG Shu  QIAO Fei
Abstract:Objective To study the therapeutic effects of amylin (AMY) on glucocorticoid induced osteoporosis in rats. Methods Four groups of female Wistar rats (3 months old) were treated for 12 weeks as follows: normal control, dexamethasone (DXM), DXM+AMY, and DXM+Vitamin D3 groups. By intramuscular injection of DXM at 1 mg/kg twice a week during the first 8 weeks, the animal model of glucocorticoid induced osteopoprosis was made. After 12 weeks, bone mineral density (BMD) of the lumbar vertebrae and the femur were measured with DEXA. Bone biomechanics and bone markers in serum and urine were also determined. Results BMD was significantly increased by 35% in the lumbar spine and by 17% in the femur in AMY group than in DXM group, and that of the lumbar vertebrae in DXM+VitD was also obvious higher than in DXM rats, but no difference was seen in BMD of the femur between these 2 groups. Compared with DXM group, the biomechanical properties were markedly increased in DXM+AMY group. The highest plasma osteocalcin concentration was measured in DEX+AMY rats. Simultaneously, urinary HOP/Cr, uCa/Cr and uP/Crwere lower in DXM+AMY than in DXM rats. Conclusion These results indicate that AMY treatment inhibits bone loss both by inhibiting resorption and stimulating osteoblastic activity in GIO rats.
Keywords:amylin  glucocorticoid induced osteoporosis  bone mineral density  biomechanics
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