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目的探讨糖尿病皮肤细胞外基质(ECM)糖基化改变与细胞增殖凋亡平衡的相关性。方法 DM或非DM患者的皮肤组织和溃疡创面标本组织学观察,同时免疫组化法检测皮肤组织增殖细胞核抗原(PCNA)、凋亡细胞、糖基化终末产物(AGE)和糖基化终末产物受体(RAGE)表达;体外建立糖基化基质,RAGE抗体干预后,检测细胞存活率、细胞周期和凋亡。结果与对照组相比,DM皮肤胶原萎缩,凋亡细胞比例增高;创面肉芽形成不良,细胞增殖能力减弱,凋亡细胞增加,AGE和RAGE表达增多;体外糖基化基质上接种成纤维细胞存活率明显减少,细胞周期运行障碍,凋亡增加,阻断AGE-RAGE间相互作用可基本缓解糖基化基质对细胞增殖凋亡过程的影响。结论 DM皮肤组织中糖基化ECM蓄积是细胞功能改变的重要环境介质,经RAGE介导影响细胞增殖凋亡平衡,致糖尿病皮肤创伤起点异常,创面难愈。
Objective To investigate the relationship between glycosylation of extracellular matrix (ECM) in diabetic skin and the balance of cell proliferation and apoptosis. Methods The histological changes of skin and ulcerated wounds in DM and non-DM patients were observed. The expressions of proliferating cell nuclear antigen (PCNA), apoptotic cells, advanced glycation end products (AGE) and glycosylation end products End product receptor (RAGE) expression; establishment of glycosylation matrix in vitro, after RAGE antibody intervention, cell viability, cell cycle and apoptosis were detected. Results Compared with the control group, the atrophy of collagen in DM skin increased and the percentage of apoptotic cells increased. The formation of wound granulation on the wound surface was weakened, the proliferation of cells was weakened, the number of apoptotic cells increased, the expression of AGE and RAGE increased, and the in vitro fibroblast-derived fibroblasts survived Significantly reduce the rate of cell cycle arrest, increased apoptosis, blocking the AGE-RAGE interaction can be basically alleviated glycosylation matrix on cell proliferation and apoptosis process. Conclusion Accumulation of glycosylated ECM in DM skin tissue is an important environmental mediator of cell function change. Mediated by RAGE, cell proliferation and apoptosis are balanced, resulting in an abnormal starting point of diabetic skin wound and difficult wound healing.