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高糖及糖基化终末产物对人脂肪干细胞成骨分化能力的影响
作者姓名:李冬松  李叔强  蔡 波  王 苹  冯 卫  刘建国
作者单位:1吉林大学第一医院骨关节外科,吉林省长春市 130021 2解放军第208医院特诊科,吉林省长春市 130061
基金项目:吉林省科技厅青年基金资助项目(20090130)。
摘    要:背景:因糖尿病条件下骨质代谢存在紊乱,对这类骨缺损的修复具有挑战性,研究糖尿病环境下脂肪干细胞的成骨特性将为其在特定环境下的应用提供理论基础。 目的:观察高糖、糖基化终末产物对人脂肪干细胞成骨分化能力的影响。 方法:选取27.5 mmol/L高糖、100 mg/L糖基化终末产物体外模拟糖尿病环境,干预人脂肪干细胞成骨分化;实验分为4组,每组设立6个样本。通过荧光染色检测脂肪干细胞诱导成骨21 d时的Ⅰ型胶原表达量,矿化结节染色观测各组中等量脂肪干细胞在14,21,28 d时矿化结节形成的数量。 结果与结论:21 d时,高糖联合糖基化终末产物组中Ⅰ型胶原荧光强度较正常组低2.76倍;5个视野下脂肪干细胞平均矿化结节数量与正常组、单纯高糖组、单纯糖基化终末产物组相比明显下降,差异有显著性意义(P < 0.01)。高糖及糖基化终末产物会抑制脂肪干细胞向成骨方向的同源分化,提示糖尿病环境下,高糖与糖基化终末产物的存在是导致脂肪干细胞成骨分化能力下降的不利因素。

关 键 词:高糖  糖基化终末产物  脂肪干细胞  Ⅰ型胶原  矿化结节  
收稿时间:2010-11-11

Effects of high glucose and advanced glycation end-products on osteogenic differentiation of human adipose-derived stromal cells in vitro
Authors:Li Dong-song  Li Shu-qiang  Cai Bo  Wang Ping  Feng Wei  Liu Jian-guo
Institution:1Department of Orthopedics, the First Hospital of Jilin University, Changchun  130021, Jilin Province, China
2Department of Special Diagnosis, the 208 Hospital of Chinese PLA, Changchun  130061, Jilin Province, China
Abstract:BACKGROUND:Bone metabolism disorder happens in diabetic environment, bone defects in which are difficult to repair. Study addressing osteogenic property of adipose-derived stroma cells (ADSCs) in diabetic environment provides theoretical basis for its application in certain environment. OBJECTIVE:To explore the effects of high glucose (HG) and advanced glycation end-products (AGEs) on osteogenic capacity of human ADSCs. METHODS:100 mg/L AGEs and 27.5 mmol/L HG were used to simulate in vitro diabetic environment and intervened ADSCs osteogenic differentiation. The cells were divided into 4 groups, with 6 samples in each group. The expression of type Ⅰ collagen was examined by fluorescent immunofluorescence at 21 days after osteogenic induction. The number of calcification nodes was counted under contrast phase microscopy at 14, 21 and 28 days.  RESULTS AND CONCLUSION:Fluorescent quantitation scan showed that the type Ⅰ collagen amount of the AGEs+HG treated group was 2.76 times lower than that of the control group. AGEs+HG reduced the number of ADSCs calcification nodes compared with the control, HG, and AGEs groups, the differences were statistical significant (P < 0.01). AGEs and HG exposure inhibit the cognate osteogenic differentiation of ADSCs, which suggest that AGEs and HG are unfavorable factors that reduce ADSCs osteogenic ability. 
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