糖尿病大鼠皮肤损害及其机制研究

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.

Mechanism of the skin lesions in diabeitic rats

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 ofnornlal rat skin at the eighth week(0.016±0.006 vs 0.041±0.007)mm,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(aU 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.