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作 者:李冬松[1] 李叔强[1] 王苹[1] 蔡波[2] 冯卫[1] 刘建国[1]
机构地区:[1]吉林大学第一医院骨关节外科,长春130021 [2]解放军208医院特诊科
出 处:《中华实验外科杂志》2010年第11期1592-1594,共3页Chinese Journal of Experimental Surgery
基 金:吉林省科技厅青年基金资助项目(20090130)
摘 要:目的 观察高糖、糖基化终末产物(AGEs)对人脂肪干细胞(ADSCs)成骨分化能力的影响.方法 选取27.5 mmoL/L高糖浓度、100 mg/L AGEs浓度体外模拟糖尿病环境 设立实验分组及对照组,每组实验样本数为6个.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(CNI)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时矿化结节形成的变化.结果 高糖及AGEs会抑制ADSCs向成骨方向的同源分化,在此过程中,ACEs的抑制作用要强于高糖,但小于高糖与AGEs的联合作用.21 d时,高糖联合AGEs组中CNI荧光强度较正常组低2.76倍 5个视野下ADSCs平均矿化结节数量(4.10±1.24)个与正常组比较明显下降,两组间差异有统计学意义(P<0.01).结论 糖尿病环境下,高糖与AGEs的存在是导致ADSCs成骨分化能力下降的不利因素.Objective To explore the effects of hyperglycemia and advanced glycation end-productes (AGEs) on osteogenesis of human adipose-derived stromal cells (ADSCs). Methods Human ADSCs were isolated and induced to the bone formation. 27.5 mmol/L high glucose concentration and 100 mg/L AGEs were used to simulate the diabetic environment. There were four groups in the present study, 6 specimens in each group. Through immunofluorescence detection and observation of calcification in each group,the different changes in CNI secretion and osteogeniesis ability were statistically analyzed. Results Hyperglycemia and AGEs prevented ADSCs cognate differentiation into bone. On the 21st day, the CNI amount in combination group was 2.76 times lower than the normal group, and the average calcification nodes were (4.10 ± 1.24). There was significant difference between two groups (P 〈0.01 ). Conclusion Hyperglycemia and AGEs had a deleterious effect on osteogenesis ability of ADSCs.
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