糖尿病大鼠深Ⅱ度烫伤后真皮成纤维细胞的生物学特征

The biological characteristics of dermal fibroblasts of the diabetic rats with deep-partial thickness scald

目的观察糖尿病(DM)大鼠深Ⅱ度烫伤后创画皮肤组织及真皮成纤维细胞(Fb)生物学特征。探讨其与DM创面愈合延迟的病理关系。方法将90只SD大鼠分为DM组(50只)和 NM组(NM,40只),DM组大鼠制成链脲菌素诱导的DM模型,之后将两组大鼠造成10％TBSA深Ⅱ度烫伤。各组大鼠均于伤前及伤后3、7、14、21 d(每组每时相点6只)留取创画皮肤组织标本,对其各项生物学特征进行检测。结果与NM组大鼠比较,DM组伤前真皮厚度明显变薄(P<0.01)、胶原排列紊乱、真皮内出现大量的慢性炎性细胞浸润,皮肤糖含量升高(DM组2．77 mg/g,NM组0．85 mg/g,P<0．01)和高级糖基化终产物(AGEs)蓄积。深Ⅱ度烫伤后,DM组大鼠Pb的S期细胞百分比和羟脯氨酸合成量明显低于NM组,而Fb的凋亡率却明显高于NM组(P<0．05或0．01)。结论 DM大鼠合并深Ⅱ度烫伤后真皮中Fb的生物学特征异常,可能与局部皮肤组织糖含量升高和 AGEs的蓄积有关,推测是DM患者容易并发慢性溃疡的病理基础之一。

Objective To investigate the biological characteristics of dermal fibroblasts of tire diabetic rats with deep partial thickness scald, and tn explore its relationship with delayed wound healing due tn diabetes. Methods Sprague-Dawley rats weighing 250 g were randomly divided into control （ NM, n = 40） and STZ-induced diabetic （ DM,n =50） groups, and then deep partial thickness scald involving 10% TBSA were reproduced in the two groups. Skin samples were harvested from the wounds on 0,3,7,14 and 21 post scald day （PSD） for the determination of certain histological characteristics. Results The thickness of dermis layer in DM group before injury was obviously thinner than that in NM group （ P 〈0.01 ）. There was an infiltration of a large amount of chronic inflammatory cells and increased content of cutaneous glucose in the dermal tissue in DM group （2.77 mg/g ） compared with 0.85 mg/g in NM group, （ P 〈 0.01 ）. An aecumulation of advanced glycation end products （AGEs） was found in the dermal tissue in DM group. After the scalding, the percentage of fibroblasts in S phase and hydroxyprotine synthesis in DM group was evidently lower than those in NM group. But the apoptosis rate of fibroblasts was much higher in DM group than that in NM group（ P 〈 0.05 or 0.01 ）. Conclusion It is found that the high contents of gtucose and AGEs in diabetic skin exert untoward effects on biological characteristics of dermal fibroblast, probably constituting one of the underlying mechanisms of delay wound healing of scald in diabetic rats.