中国组织工程研究 ›› 2010, Vol. 14 ›› Issue (28): 5204-5207.doi: 10.3969/j.issn.1673-8225.2010.28.017

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

普伐他汀干预激素性股骨头坏死兔模型的组织学变化:大体和光镜下比较和印证

胡  敏1,赵宏斌2,董锡亮2,罗德军2,周  旭2   

  1. 1昆明学院医学院临床学科,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:2010-07-09 发布日期:2010-07-09
  • 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)。

Histological changes of a rabbit model of steroid-induced femoral head necrosis intervened by pravastatin: Comparison between general observation and light microscope

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

  1. 1 Clinical Speciality, the Medical College of Kunming University, Kunming 650032, Yunnan Province, China; 2 Department of Orthopedics, First Affiliated Hospital of Kunming Medical College, Kunming 650032, Yunnan Province, China
  • Online:2010-07-09 Published:2010-07-09
  • Contact: Zhao Hong-bin, Doctor, Associate professor, Department of Orthopedics, First Affiliated Hospital of Kunming Medical College, Kunming 650032, Yunnan Province, China 596829191@qq.com
  • About author:Hu Min, Associate professor, Clinical Speciality, the Medical College of Kunming University, Kunming 650032, Yunnan Province, China
  • Supported by:

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

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大体和光镜下的组织学改变,并进行相互比较和印证。
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。向实验组耳缘静脉注射大肠杆菌内毒素(10 μg/kg) 2次,注射间隔24 h。并于第2次注射大肠杆菌内毒素后,臀肌注射甲强龙(20 mg/kg)3次,注射间隔24 h,制备兔激素性股骨头缺血坏死模型。造模第5周,将造模成功的39只新西兰白兔以随机数字表法分配其中的36只至模型组和他汀组,每组18只。他汀组以普伐他汀(1.2 mg/kg)灌胃,1次/d;模型组和对照组以等体积的蒸馏水灌胃。造模后8,12,16周,取股骨头,分别进行大体和光镜观察。
结果与结论:大体观察及光镜观察显示模型组出现明显的骨坏死灶,骨髓腔内可见大量脂肪细胞增生;与模型组比较,他汀组骨细胞受损程度较轻,骨小梁密度较高,空骨陷窝比率较少,骨坏死面积和髓腔内脂肪细胞数量明显减少,骨坏死修复迹象明显。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, 兔, 激素性股骨头坏死, 组织学评价, 骨组织工程

Abstract:

BACKGROUND: Previous research has demonstrated that pravastatin promoted the repairing of steroid-induced femoral head necrosis via up-regulating expressions of endogenous bone morphogenetic protein-2, core-binding factor-α1, and vascular endothelial growth factor.
OBJECTIVE: To evaluate the histological changes of a rabbit model of steroid-induced femoral head necrosis intervened by pravastatin using general observation and light microscope.
METHODS: A total of 80 New Zealand white rabbits were randomly divided into normal control group (n=18) and experimental group (n=62). The experimental group was injected with escherichia coli endotoxin (10 μg/kg) into auricular vein twice, every 24-hour intervals; while, prednisolone (20 mg/kg) was injected into buttock three times, every 24-hour intervals to make steroid-induced femoral head necrosis model. At the fifth week, 36 out of 39 rabbits were equally divided into model group and pravastatin group. The pravastatin group was intragastrically administrated with pravastatin (1.2 mg/kg), once a day. Model and control groups were intragastrically administrated with the equal volume of saline. The femoral head was obtained at 8, 12, and 16 weeks and observed with general observation and light microscope.
RESULTS AND CONCLUSION: Gross observation and light microscopy demonstrated that a clear bone necrosis of femoral head was observed in the model group, and a large number of fat cell proliferation was found in the bone marrow cavity. As compared with model group, injured level of cells in the pravastatin group was mild, density of bone trabecula was high, ratio of bone lacuna was less, area of bone necrosis was decreased, number of adipocytes was reduced, and bone necrosis was well repaired. This suggested that pravastatin could effectively restore steroid-induced femoral head necrosis in the early stage.

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