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首页> 外文期刊>The international journal of lower extremity wounds >Reduced dermis thickness and AGE accumulation in diabetic abdominal skin
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Reduced dermis thickness and AGE accumulation in diabetic abdominal skin

机译:减少糖尿病性腹部皮肤的真皮厚度和AGE积累

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摘要

Dermatological problems in diabetes might play an important role in the spontaneous ulcers and impaired wound healing that are seen in diabetic patients. Investigation of the cause of diabetic skin disorders is critical for identifying effective treatment. The abdominal full-thickness skin tissues of 33 patients (14 nondiabetic and 19 diabetic) were analyzed. The cell viability and malondialdehyde (MDA) production of fibroblasts were measured after advanced glycosylation end product (AGE)-bovine serum albumin (BSA) exposure. Cutaneous histological observation showed reduced thickness of the diabetic abdominal dermis with morphological characteristics of obscured multilayer epithelium and shortened, thinned, and disorganized collagen fibrils with focal chronic inflammatory cell infiltration when compared with controls of the same age. Accumulation of AGEs in diabetic skin was prominent. Less hydroxyproline, higher myeloperoxidase activity, and increased MDA content were detected in diabetic skin. In vitro, the time- and dose-dependent inhibitory effects of AGE-BSA on fibroblast viability as well as the fact that AGE-BSA could promote MDA production of fibroblasts were shown. It is shown that the accumulation of AGEs in diabetic skin tissue induces an oxidative damage of fibroblasts and acts as an important contributor to the thinner diabetic abdominal dermis. The authors believe that diabetic cutaneous properties at baseline may increase the susceptibility to injury, and diabetic wounds possess atypical origin in the repair process.
机译:糖尿病患者中的皮肤病问题可能在自发性溃疡和伤口愈合受损中起重要作用。调查糖尿病皮肤疾病的原因对于确定有效的治疗至关重要。分析了33例患者的腹部全层皮肤组织(14例非糖尿病患者和19例糖尿病患者)。在晚期糖基化终产物(AGE)-牛血清白蛋白(BSA)暴露后,测量成纤维细胞的细胞活力和丙二醛(MDA)产生。皮肤组织学观察显示,与相同年龄的对照组相比,糖尿病性腹部真皮的厚度减少,多层上皮的形态特征变暗,胶原纤维缩短,变薄和杂乱无章,并伴有局灶性慢性炎性细胞浸润。糖尿病皮肤中AGEs的积累是突出的。在糖尿病皮肤中检测到较少的羟脯氨酸,较高的髓过氧化物酶活性和增加的MDA含量。在体外,显示了AGE-BSA对成纤维细胞活力的时间和剂量依赖性抑制作用,以及AGE-BSA可以促进成纤维细胞MDA产生的事实。结果表明,AGEs在糖尿病皮肤组织中的积累会诱导成纤维细胞的氧化损伤,并成为糖尿病性腹部真皮变薄的重要因素。作者认为,糖尿病患者在基线时的皮肤特性可能会增加对损伤的敏感性,并且糖尿病伤口在修复过程中具有非典型起源。

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