中国组织工程研究 ›› 2014, Vol. 18 ›› Issue (20): 3122-3126.doi: 10.3969/j.issn.2095-4344.2014.20.002

• 骨组织构建 bone tissue construction • 上一篇    下一篇

2型糖尿病大鼠骨折愈合障碍与体内晚期糖基化终末产物的变化

刘振东1,刘亚江1,高敏伟1,黄祖发2,廖小军1,石  磊1   

  1. 中南大学湘雅三医院,1骨科,2普外科,湖南省长沙市  410013
  • 收稿日期:2014-02-19 出版日期:2014-05-14 发布日期:2014-05-14
  • 通讯作者: 黄祖发,中南大学湘雅三医院普外科,湖南省长沙市 410013
  • 作者简介:刘振东,男,1959年生,湖南省长沙市人,博士,中南大学湘雅医学院毕业,副教授,主要从事骨科创伤研究。
  • 基金资助:

    湖南省自然科学基金项目(05FJ3066),项目名称:2型糖尿病对骨再生与修复的影响

Impaired fracture healing and change of advanced glycation end products in vivo
in type 2 diabetes rats

Liu Zhen-dong1, Liu Ya-jiang1, Gao Min-wei1, Huang Zu-fa2, Liao Xiao-jun1, Shi Lei1   

  1. 1Department of Orthopedics, 2Department of General Surgery, the Third Xiangya Hospital of Central South University, Changsha 410013, Hunan Province, China
  • Received:2014-02-19 Online:2014-05-14 Published:2014-05-14
  • Contact: Huang Zu-fa, Department of General Surgery, the Third Xiangya Hospital of Central South University, Changsha 410013, Hunan Province, China
  • About author:Liu Zhen-dong, M.D., Associate professor, Department of Orthopedics, the Third Xiangya Hospital of Central South University, Changsha 410013, Hunan Province, China
  • Supported by:

    the Natural Science Foundation of Hunan Province, No. 05FJ3066

摘要:

背景:近年来,晚期糖基化终末产物在骨组织领域的作用日益受到重视,而糖代谢紊乱是引起晚期糖基化终末产物增加的主要原因之一。
目的:观察2型糖尿病大鼠体内晚期糖基化终末产物表达的变化,并探讨其与糖尿病骨折愈合障碍的关系。
方法:30只SD大鼠随机均分为2组,实验组制备2型糖尿病模型,对照组正常饲养。糖尿病模型制备成功后,所有大鼠建立左胫骨骨折牵引成骨模型,胫骨延长0.3 mm/d,持续14 d。
结果与结论:牵引结束后,X射线摄片显示实验组糖尿病模型大鼠骨折断端之间牵引骨痂形成较对照组明显减少;骨痂组织学检查表现为微骨柱排列紊乱,初始基质前沿浅染。ELISA法检测实验组血清和双侧骨痂组织中晚期糖基化终末产物水平较对照组明显升高(P < 0.01),骨钙素明显降低(P < 0.01)。提示2型糖尿病大鼠骨折牵引骨痂生成障碍,而骨组织中晚期糖基化终末产物水平增高可能是导致2型糖尿病骨折愈合障碍的原因。



中国组织工程研究
杂志出版内容重点:组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松组织工程


全文链接:

关键词: 组织构建, 骨组织工程, 2型糖尿病, 骨折愈合, 牵引成骨术, 骨钙素, 晚期糖基化终末产物, 湖南省自然科学基金

Abstract:

BACKGROUND: Increasing attention has been paid on the role of advanced glycation end products in bone tissue. Glucose metabolic disorder is one of the main reasons for the increase of advanced glycation end products.
OBJECTIVE: To observe the change of advanced glycation end products expressed in type 2 diabetes rats, and to investigate the relationship between impaired fracture healing and change of advanced glycation end products expression in vivo.
METHODS: Thirty Sprague-Dawley rats were randomly and equally divided into two groups: control group (normal feeding) and experimental group (high fat and sucrosum diet feeding to establish type 2 diabetes model). After diabetes models were established, the model of distraction osteogenesis in the left tibiae of all the rats was produced. Distraction was given 0.3 mm per day and continued for 14 days.
RESULTS AND CONCLUSION: After the traction was complete, callus formation in distraction gap was obviously reduced in experimental group compared with control group by X-ray examination. The array of microcolumn formation was disordered and the area of primary matrix front was catachromasis by histology examination. The enzyme-linked immunosorbent assay results showed that, the level of advanced glycation end products was obviously elevated (P < 0.01) while osteocalcin was obviously reduced (P < 0.01) in experimental group in comparison with control group. The formation of distraction callus was impaired in the process of fracture healing and blood of type 2 diabetes rats. The increase of advanced glycation end products may be one of the reasons that cause impaired fracture healing in diabetic rats.



中国组织工程研究
杂志出版内容重点:组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松组织工程


全文链接:

Key words: diabetes mellitus, model, animals, fracture healing, tibial fracture, osteocalcin, advanced glycation end products

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