糖尿病对大鼠皮肤角质形成细胞功能损害的影响

Reseach on epidermal keratinocyte function impairing in rats with diabetes mellitus

目的 探讨糖尿病对大鼠皮肤角质形成细胞生物学行为的影响.方法 将SD大鼠随机分为糖尿病组和对照组,诱导糖尿病大鼠模型,并制作深Ⅱ度烫伤大鼠模型,测定伤后3、7、14 d和21 d的创面愈合率;观察两组表皮组织的组织学特征及厚度,测定两组角质形成细胞贴壁率、细胞周期、早期凋亡率、迁移能力,观察晚期糖基化终末产物（AGEs）蓄积情况.结果 糖尿病组与对照组比较,在伤后7、14 d和21 d创面愈合面积百分比显著减少（P〈0.05）.糖尿病组皮肤表皮细胞层次欠清晰,部分表皮细胞缺乏复层排列,细胞数量明显减少;糖尿病组角质形成细胞12、24 h贴壁率显著下降（P〈0.05）,进入G2/M期的细胞显著减少（P〈0.05）,早期凋亡细胞的比例显著增高（P〈0.05）,细胞迁移能力明显低于对照组.糖尿病大鼠表皮层中有大量的AGES蓄积.结论 糖尿病大鼠创面愈合过程中存在再上皮化受阻,这一现象与表皮角质形成细胞的生物学功能受抑有关.表皮层大量AGEs蓄积可能与糖尿病环境下角质形成细胞生物学功能受抑有关.

Objective To explore the effect of diabetes mellitus （DM） on biological behavior of epidermal keratinocyte in rats. Methods A total of 40 Sprague-Dawley rats were randomized into control group and streptozotocin （STZ） -induced diabetes group. Of each group, 10 rats were implemented with deep partial-thickness scalding. The re-epithelialization rate was observed at the 3rd, 7th, 14th and 21th post-burn day. Histological characteristics and thickness of epidermal tissue in both groups were observed. The adhesion rate, cell cycles, apoptosis rate and migration ability of keratinocyte were measured. The accumulation of advanced glycosylation end products （AGEs） of epidermal tissue was observed. Results The percentages of re-epithelialized area at the 7th, 14th and 21th post-burn day were much lower in DM group than in control group （P〈0.05）. In DM group, the epidermal thickness was reduced obviously with obscure multilayered epithelium and less amount of prickle cells; The adhesion rates of 12, 24 h after culturing keratinocyte and the percentage of G2/M phase cells were lower in DM group than in control group （P〈0.05）. However, apoptosis rate of keratinocyte was higher, the amount of migration cell was significantly less in DM group than in control group （both P〈0.05）. There were lots of AGEs accumulated in epidermal tissue in DM group, while there were hardly AGEs in control group. Conclusions Re-epithelization blocked exists on non-healing wound in DM rats, which is related with the impaired keratinocyte biological behavior. A large of AGEs accumulate in the epidermal tissue of DM rats, which may be a important reason to inhibit keratinocyte function in diabetic environment.