胰岛素样生长因子Ⅰ对高糖条件下成骨细胞骨形成的影响

Effects of insulin-like growth factor Ⅰ on alveolar bone remodeling in diabetic rats

目的:研究胰岛素样生长因子I对高糖条件下成骨细胞骨形成的影响,探讨胰岛素样生长因子I对糖尿病性骨病的作用机制。方法:离体实验通过对细胞增殖和矿化的检测,从细胞分子水平评价胰岛素样生长因子I对高糖环境下成骨细胞的作用。体内实验诱导1型糖尿病大鼠动物模型,分别给予胰岛素(6～8U/d)和胰岛素样生长因子I(30μg/kg.d)治疗,通过X线、组织切片HE染色和四环素双标记的方法观察牙槽骨改建情况。结果:离体实验的结果显示胰岛素样生长因子I可减少高浓度葡萄糖引起的成骨细胞的异常增殖,促进钙沉积和矿化结节的形成。体内实验研究显示与正常组相比,糖尿病大鼠拔牙创骨愈合减慢,骨形成减少,牙槽骨高度和牙槽骨骨形成率显著降低。胰岛素样生长因子I的治疗不仅能控制糖尿病大鼠的血糖保持在正常范围内,还可以增加牙槽骨高度和提高骨形成率。结论:高浓度葡萄糖导致糖尿病大鼠拔牙后骨形成减少、牙槽骨高度降低等病理改变;胰岛素样生长因子I可以促进糖尿病状态下成骨细胞骨形成和矿化,有利于糖尿病大鼠拔牙后骨创愈合和新骨形成。

Objective：To investigate the effects and mechanism of hyperglycemia and insulin-like growth factor I（IGF-I）on osteogenesis ability of osteoblasts.Methods：The proliferation and mineralization of osteoblasts were observed to evaluate the effects of IGF-I on the development of osteoblasts in hyperglycemia.Diabetic rat model was established and IGF-I（30 μg/kg·d）was used to treat diabetic rats.Investigated the influences of diabetes and IGF-I on the remolding of alveolar bone after tooth extraction by the assay of X ray,tissue section and bone formation rate.Results：The results showed that IGF-I treatment was able to regulate abnormal proliferation,promote calcium deposition and increase bone nodule formation in hyperglycemic osteoblasts.Animal study showed that compared with the control group,the alveolar bone formation decreased in diabetic rats.The height of alveolar bone and the bone formation rate in the untreated diabetic group was significantly lower.IGF-I treatment was not only able to regulate abnormal blood glucose but also to increased the height of alveolar bone and the bone formation rate relative to results in diabetic animals.Conclusion：The results of the present study suggest that hyperglycemia stimulates cellular proliferation while concurrently inhibits calcium deposition in the matrix which may result in repressed bone formation.Similar to insulin,IGF-I treatment increases matrix mineralization and bone formation,thereby contributing to both wound healing and new bone formation in diabetic rats.