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目的探讨糖尿病对长骨发育的影响机制。方法建立速发型链脲佐菌素(STZ)糖尿病大鼠模型,分为糖尿病5周组(DM1)、10周组(DM2)及15周组(DM3),每组10只,另设正常5周组(CON1)、10周组(CON2)及15周组(CON3),每组10只,共60只。对各组大鼠股骨头生长板,光镜下作组织病理学分析及组织计量学测定;利用Van Gieson胶原纤维染色法观察胶原纤维沉积变化;墨汁灌注行边缘微血管密度测定;观察生长板血管内皮生长因子(VEGF)mRNA原位杂交表达强度并分析;采用RT-PCR技术,对蛋白聚糖的表达进行了观察。结果糖尿病15周组生长板厚度、生长板细胞柱密度均明显小于对照组(P<0.01);生长板钙化区胶原纤维明显增多;VEGFmRNA表达均高于正常组(P<0.01);边缘微血管密度增大,但渗透性大。15周蛋白聚糖的表达水平显著高于对照组。结论糖尿病大鼠股骨头生长板出现早闭。VEGF促进成骨矿化,糖尿病股骨头生长板边缘微血管密度的变化直接影响生长板软骨细胞的增殖分化与成骨矿化。
Objective To investigate the mechanism of diabetes on long bone development. Methods The model of STZ-induced diabetic rats was established. The rats were divided into diabetic DM5 group, DM2 group and DM3 group for 15 weeks. Each group consisted of 10 normal rats. (CON1), 10 weeks group (CON2) and 15 weeks group (CON3), 10 rats in each group, a total of 60 rats. The histopathology and histomorphometry of the femoral head growth plate in each group were observed under light microscope. The deposition of collagen fibers was observed by Van Gieson collagen fiber staining. The edge microvessel density was measured by ink perfusion. The expression of VEGF mRNA in situ hybridization was analyzed and analyzed. The expression of proteoglycan was observed by RT-PCR. Results The thickness of the growth plate and the density of the growth plate cells in the 15-week diabetic group were significantly lower than those in the control group (P <0.01). The collagen fibers in the calcification area of the plate were significantly increased and the VEGF mRNA expression was significantly higher than that in the normal group (P <0.01) Increase, but permeability. The expression of 15-week proteoglycan was significantly higher than that of the control group. Conclusion Diabetic rat femoral head growth plate appears early closure. VEGF promotes osteo-mineralization. The changes of microvascular density at the edge of diabetic femoral head have a direct impact on the proliferation, differentiation and osteogenesis of chondrocytes.