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腺嘌呤诱导肾性骨病大鼠模型的生物力学分析
引用本文:孟彦,贺宁,马岚,潘雪,韩霞,赵建荣,武素珍,左力. 腺嘌呤诱导肾性骨病大鼠模型的生物力学分析[J]. 肾脏病与透析肾移植杂志, 2020, 0(1): 31-35
作者姓名:孟彦  贺宁  马岚  潘雪  韩霞  赵建荣  武素珍  左力
作者单位:内蒙古医科大学附属医院肾内科;内蒙古医科大学药学院;北京大学人民医院肾内科
基金项目:国家自然科学基金资助项目(81960143,81960130,81870524);内蒙古自治区高等学校青年科技英才支持计划(NJYT-19-B34);第五批内蒙古“草原英才”基金内蒙古医科大学附属医院肾内科创新人才团队基金。
摘    要:目的:观察腺嘌呤诱导的慢性肾脏病(CKD)肾性骨病大鼠模型的腰椎及股骨的生物力学特点。方法:20只雄性SD大鼠分为正常对照组和CKD组。第6周末处死大鼠,行血清生化标志物检测,取股骨和第五腰椎做骨密度(BMD)及骨生物力学分析。结果:在第6周末,CKD组大鼠血清尿素氮、血清肌酐、血清无机磷、血清甲状旁腺激素较正常对照组均明显升高,血清钙明显降低。与正常对照组比较,CKD组的股骨和第五腰椎椎体BMD均明显降低。骨生物力学,股骨三点弯曲实验结果提示,CKD组大鼠的股骨结构力学指标和材料力学指标均明显降低;腰椎压缩实验结果提示,CKD组大鼠腰椎的结构力学指标和材料力学指标均明显降低。结论:腺嘌呤诱导的大鼠CKD模型能较好地模拟CKD时出现的高转运肾性骨病的生物力学特征,表现为皮质骨和松质骨材料力学和结构力学性能的下降,有望成为CKD肾性骨病模型的研究载体。

关 键 词:慢性肾脏病  慢性肾脏病矿物质和骨异常  肾性骨病  纤维性骨炎  生物力学

Biomechanical analyses of adenine-induced renal osteodystrophy in rat
MENG Yan,HE Ning,MA Lan,PAN Xue,HAN Xia,ZHAO Jianrong,WU Suzhen,ZUO Li. Biomechanical analyses of adenine-induced renal osteodystrophy in rat[J]. Chinese Journal of Nephrology, Dialysis & Transplantation, 2020, 0(1): 31-35
Authors:MENG Yan  HE Ning  MA Lan  PAN Xue  HAN Xia  ZHAO Jianrong  WU Suzhen  ZUO Li
Affiliation:(Division of Nephrology,the Attached Hospital of Inner Mongolia Medical University,Hohhot 010050,China;School of pharmacy,Inner Mongolia Medical University,Hohhot 010110,China;Division of Nephrology,the People's Hospital of Peking University,Beijing 100044,China)
Abstract:Objective:To investigate the bone biomechanical features of femur and the fifth lumbar vertebra in an adenine-induced renal osteodystrophy rat model of chronic kidney disease(CKD). Methodology:Twenty male Sprague Dawley rats of eleven weeks’ old were divided into two groups:(1) normal group,which were fed a diet without adenine;(2) CKD group,which were fed an 0.75% adenine diet for the initial 4 weeks and then adenine-free diet for the subsequent 2 weeks.Six weeks later,rats were subjected to euthanasia and serum was collected for biochemical marker tests.Bone mineral density(BMD) and bone biomechanical parameters were examined in femurs and the fifth lumbar vertebra. Results: At the end of the sixth week,serum creatinine,blood urea nitrogen,serum phosphorus and serum parathyroid hormone were significantly higher,and serum calcium was significantly lower,in the CKD group compared with the normal group.Total femur BMD and fifth lumbar vertebra BMD were lower significantly in CKD group than in normal group.For bone biomechanical tests,femur three-point bending tests indicated the femur indexes of both structural mechanics(maximum load,maximum displacement,stiffness,force energy) and materials mechanics(maximum stress,maximum strain,elastic modulus,toughness) in CKD group decreased significantly than in normal group,and lumbar compression tests indicated the fifth lumbar centrum indicators of both structural mechanics(maximum load,maximum displacement,stiffness,force energy) and materials mechanics(maximum stress,maximum strain,elastic modulus,toughness) in CKD group decreased significantly than in the normal group. Conclusion: Adenine-induced rat renal osteodystrophy model of CKD showed deteriorated properties of structural mechanics and materials mechanics in both cortical and trabecular bone,these features were in accordance with the actual clinical conditions.This model could be an appropriate medium in the study of renal osteodystrophy in CKD in the future.
Keywords:chronic kidney disease  chronic kidney disease-mineral and bone disorder  renal osteodystrophy  osteitis fibrosa  biomechanics
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