糖尿病大鼠皮肤损害及其机制研究  

Mechanism of the skin lesions in diabeitic rats

作　　者：林炜栋[1] 陈向芳[2] 刘志民[2] 陆树良[4] 石勇铨[2] 邹俊杰[2] 廖万清[3] 

机构地区：[1]上海市公安消防总队医院灼伤科,200443 [2]第二军医大学附属长征医院内分泌科 [3]第二军医大学附属长征医院皮肤科 [4]上海交通大学医学院附属瑞金医院 上海市烧伤研究所

出　　处：《中华内分泌代谢杂志》2010年第1期62-65,共4页Chinese Journal of Endocrinology and Metabolism

基　　金：基金项目：上海市基础研究重点项目（08JC1407200）;国家重点基础研究发展规划项目资助（2005CB523304）

摘　　要：链脲佐菌素诱导的SD糖尿病大鼠4周时皮肤已开始变薄，8周时表皮厚度已明显低于正常大鼠[（0．016±0．006对0．041±0．007）mm，P〈0．01]，各时间点G2／M期的表皮细胞比例显著减少。12周时在真皮层中微血管病变常见。与同时间点正常大鼠相比，血浆晚期糖基化终末产物（AGEs）和丙二醛含量明显升高，谷胱甘肽下降（均P〈0．01），皮肤糖含量、AGEs水平均显著升高（P〈0．01）。提示局部高糖和AGEs的蓄积，可能是糖尿病皮肤损害的重要机制。Four weeks after SD diabetic rats were induced by streptozotocin, skin thickness was obviously reduced with obscure multilayer epithelium features. Moreover, the thickness of epidermic layers in diabetic rat skin was significantly thinner than that of normal rat skin at the eighth week [ （0.016±0.006 vs 0.041 ±0.007 ）ram, P〈 0.01 ]. The percentage of G2/M phase cells in epidermic layers of diabetic group was significantly lower than that in the normal group. At the twelfth week, skin microangiopathy was easily detected in the diabetic group. The blood levels of advanced glycation end products（AGEs）and malonialdehyde were significantly increased and glutathione decreased in diabetic rats compared with control rats（ all P〈0. 01 ）, along with the increased contents of local glucose and AGEs in the skin of diabetic rats. These results suggest that the local accumulation of glucose and AGEs seems to be one of the important mechanisms in the pathogenesis of diabetic skin lesions.

关 键 词：糖尿病 皮肤 病理生理 糖基化终产物 高级 

分 类 号：R587.2[医药卫生—内分泌]