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环孢素A影响脱钙骨基质诱导成骨的组织学观察
引用本文:袁亮,李靖年,张 彦.环孢素A影响脱钙骨基质诱导成骨的组织学观察[J].中国神经再生研究,2009,13(15):2818-2822.
作者姓名:袁亮  李靖年  张 彦
作者单位:大连医科大学附属第二医院,大连医科大学附属第二医院,大连医科大学附属第二医院
摘    要:背景:脱钙骨可用于成骨细胞的支架材料,机体组织对脱钙骨有一定的免疫排斥反应。 目的:观察环孢素A影响脱钙骨诱导成骨的组织学变化,探讨脱钙骨成为理想的骨移植材料的可行性。 设计、时间及地点:随机对照动物实验,于2007-03/2008-04在大连医科大学附属二院实验中心完成(国家分子生物学三级实验室)。 材料:用16只新西兰大白兔,分为4组,同种脱钙骨对照组和实验组,异种脱钙骨实验组和对照组,每组4只。环孢素注射液为北京诺华制药有限公司产品。 方法:制备脱钙骨,取自兔的脱钙骨命名为同种脱钙骨,取自犬的脱钙骨命名为异种脱钙骨。于兔的脊旁肌肉内植入相应脱钙骨制备物,每侧2处。实验组每天肌注含环孢素A的实验液2 mg/kg,对照组肌注对照液2 mg/kg,共4周。植入物标本进行苏木精-伊红染色,光镜观察。 主要观察指标:各组脱钙骨组织学观察结果。 结果:同种脱钙骨在所有动物中均引起了骨形成。环孢素A并没有改变同种脱钙骨诱导成骨的形态学。异种脱钙骨对照组在第4周时没有骨或软骨细胞生成。异种脱钙骨环孢素A实验组在第4周时有软骨、骨形成。 结论:环孢素A并没有改变同种脱钙骨诱导成骨的形态学。免疫反应抑制了异种脱钙骨的成骨,环孢素A可抵消这种抑制作用,环孢素A可提高异种脱钙骨治疗骨不连或骨缺损的成功率。

关 键 词:环孢菌素类  脱钙骨基质  成骨
修稿时间:3/9/2009 12:00:00 AM

Histological observation of cyclosporin A effects on ossification of demineralized bone matrix
Abstract:BACKGROUND: Demineralized bone can be used as the scaffolds of osteoblasts, and body tissue developed immunologic rejection to demineralized bone. OBJECTIVE: To investigate the histological changes of cyclosporin A (CSA) effect on ossification of demineralized bone, in addition, to explore the feasibility of demineralized bone served as ideal available bone substitute material. DESIGN, TIME AND SETTING: The randomized control experiment of animals was performed at the Experimental Center of Second Hospital of Dalian Medical University between March 2007 and April 2008. MATERIALS: Sixteen New Zealand rabbits were divided into the control and experimental group of homogenic decalcified bone, control and experimental group of heterogenous decalcified bone. CSA was produced by Beijing Novartis Pharmaceutical Co., Ltd. METHODS: Decalcified bone prepared from rabbits was served as homogenic decalcified bone, and decalcified bone prepared from dogs were served as heterogenous decalcified bone. Sixteen rabbits were randomly divided into 4 groups: the control and experimental group of homogenic decalcified bone, control and experimental group of heterogenous decalcified bone, with 4 rabbits in each group. Each rabbit was implanted with homogenic or heterogenous decalcified bone, respectively, 2 samples per side. 2 mg/kg CSA or 2 mg/kg placebo was intramuscular injected in the experimental or control groups for 4 weeks. Samples were examined by hematoxylin-eosin staining and light microscope. MAIN OUTCOME MEASURES: The histological observation of decalcified bone in each group. RESULTS: Homogenic allogeneic bone induced formation in all implants. CSA did not induce morphological changes of homogenic allogeneic bone. In the heterogenous decalcified bone treated group, at 4 weeks, there was no bone formation or chondrocytes production in the control group, but there was cartilage and bone formation in the experimental group. CONCLUSION: CSA did not alter the morphology of bone induction by homogenic allogeneic bone. Immunologic reactions may inhibit bone induction by heterogenous decalcified bone, which can be counteracted by treatment with CSA. CSA can increase the rate of nonunion or bone defect using heterogenous decalcified bone.
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