中国组织工程研究

中国组织工程研究 ›› 2010, Vol. 14 ›› Issue (37): 6861-6864.doi: 10.3969/j.issn.1673-8225.2010.37.005

• 组织构建实验造模 experimental modeling in tissue construction • 上一篇    下一篇

普伐他汀修复激素性股骨头坏死兔模型的超微结构评价

胡  敏1，赵宏斌2，董锡亮2，罗德军2，周  旭2   

  1. 1昆明学院医学院，云南省昆明市  650032；2昆明医学院第一附属医院骨科，云南省昆明市  650032
  • 出版日期:2010-09-10 发布日期:2010-09-10
  • 通讯作者: 赵宏斌，博士，副教授，昆明医学院第一附属医院骨科，云南省昆明市 650032 596829191@qq.com
  • 作者简介:胡敏，男，1971年生，云南省石屏县人，汉族，1995年昆明医学院毕业，副教授，主要从事骨坏死与骨质疏松方面的研究。
  • 基金资助:

    国家自然科学基金资助项目(30460162)。课题名称：云南彝药恒古骨伤愈合剂对兔坏死股骨头内VEGF和Cbfa1基因表达的影响及其MRI评价。

Ultra-structural evaluation of repairing steroid-induced avascular necrosis of femoral head with pravastatin in rabbits

Hu Min1, Zhao Hong-bin2, Dong Xi-liang2, Luo De-jun2, Zhou Xu2   

  1. 1 Medical College of Kunming University, Kunming  650032, Yunnan Province, China; 2 D epartment of Orthopedics, the First Affiliated Hospital of Kunming Medical College, Kunming  650032, Yunnan Province, China
  • Online:2010-09-10 Published:2010-09-10
  • Contact: Zhao Hong-bin, Doctor, Associate professor, Department of Orthopedics, the First Affiliated Hospital of Kunming Medical College, Kunming 650032, Yunnan Province, China 596829191@qq.com
  • About author:Hu Min, Associate professor, Medical College of Kunming University, Kunming 650032, Yunnan Province, China
  • Supported by:

     the National Natural Science Foundation of China, No. 30460162*

PDF

347

被引次数

12

摘要：

背景：研究表明普伐他汀可通过上调内源性骨形成蛋白2、核心结合因子α1和血管内皮生长因子等基因的表达从而产生促进激素性股骨头坏死兔模型坏死股骨头修复的作用。
目的：验证性观察普伐他汀干预激素性股骨头坏死兔模型的超微结构改变。
方法：将80只新西兰白兔按随机数字表法分为对照组18只，实验组62只。实验组制备兔激素性股骨头缺血坏死模型。造模第5周，以随机数字表法分配36只模型兔至模型组和他汀组，每组18只。他汀组以普伐他汀(1.2 mg/kg)1次/d灌胃，模型组和对照组以等体积的蒸馏水灌胃。造模后8，12，16周，截取股骨头行透射电镜观察。
结果与结论：透射电镜观察显示模型组骨细胞变性坏死严重，大部分骨陷窝内骨细胞消失，残存的骨细胞内脂肪沉积增多；与模型组比较，他汀组骨细胞受损程度较轻，形态基本正常，胞浆内脂肪沉积少。说明普伐他汀可有效促进早期激素性股骨头坏死兔模型坏死股骨头的修复。

关键词: 普伐他汀, 干预, 激素性股骨头坏死, 超微结构, 骨组织工程

Abstract:

BACKGROUND: Studies demonstrated that pravastatin can promote the repair of steroid-induced avascular necrosis of femoral head (SANFH) via up-regulating expressions of endogenous bone morphogenetic protein 2, core-binding factor α1 and vascular endothelial growth factor.
OBJECTIVE: To verify the ultra-structural changes of SANFH animal models after intervened by pravastatin.
METHODS: Totally 80 New Zealand white rabbits were randomly divided into a normal control group (n = 18) and experimental group (n = 62). Rabbits in the experimental group were prepared for SANFH models. At 5 weeks after model preparation, 36 rabbits in the model group were assigned into the model and pravastatin groups, with 18 animals in each group. Rabbits in the pravastatin group received intragastric administration with 1.2 mg/kg pravastatin, once per day, and the same volume of distilled water was given to those in the model and control groups. The femoral head specimens were observed under a transmission electron microscope at 8, 12 and 16 weeks after model preparation.
RESULTS AND CONCLUSION: Transmission electron microscopy showed that severe degeneration and necrosis could be found in the model group, most of osteocytes disappeared in the lacunae, and there were more fat deposition in the remnant osteocytes. Compared with the model group, the damage of osteocytes in the pravastatin group were slighter, the morphology of cells were normal with few fat deposition. The results demonstrated that pravastatin can effectively restore femoral head necrosis of rabbits of SANFH animal models in the early stage.

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