摘要
目的探讨病程对糖尿病皮肤和真皮成纤维细胞(FB)生物学行为的影响。方法通过制备不同病程糖尿病模型,对皮肤中的组织生化和真皮FB的生物学行为进行检测。结果短程糖尿病皮肤厚度变薄,糖含量升高,且病程至8周有晚期糖基化终末产物(AGEs)蓄积,真皮S期细胞比例升高和单位面积皮肤羟脯氨酸含量减少。高糖和AGEHSA导致真皮FB生长抑制和凋亡,呈剂量依赖性。结论糖尿病皮肤随着病程延长,病理生理异常会不断加重;糖尿病真皮FB的生物学改变与皮肤高糖和AGEs蓄积存在直接关系。
Objective To study the effects of different courses of disease on biological behavior of dermal fibroblasts in diabetic rats. Methods Diabetic animal models with different courses of disease (short/long-term group) were prepared to study the changes of histology, biochemistry and the biological behavior of dermal fibroblasts in diabetic intact skin. Results The thickness of skin layer and the contents of glucose were reduced in short-term group. In long-term group, the contents of advanced glycation end products (AGEs) in diabetic skin and the percentage of S stag in the dermal cells were higher than those of controls. The contents of hydroxyproline in the same area were reduced obviously in long-term group with the morphological characteristic changes including the degenerated collagen fibers with focal chronic inflammatory cells infiltration. Proliferation of dermal fibroblasts derived from each group was significantly lower than control group when exposed to the high concentrations of AGE-HSA. The apoptotic rates of fibroblasts received from three groups were significantly higher than control group when cultured with AGE-HSA. The proliferation and apoptotic rate of fibroblasts showed a dose dependent effect with AGE-HSA. Conclusion It is found that there is a set of abnormal pathological changes in the diabetic skin. When the course of diabetes is prolonged, abnormality in the diabetic skin will aggravate continuously. The high contents of dermal glucose and AGEs in the diabetic rat skin show the inhibiting effects on the biological behaviors of dermal fibroblasts, this might be one of the most important mechanisms in the pathogenesis of impaired-wound healing.
出处
《上海第二医科大学学报》
CSCD
北大核心
2005年第5期459-462,466,共5页
Acta Universitatis Medicinalis Secondae Shanghai
基金
国家重点基础研究发展计划(973计划)(G1999054205)资助项目.
