糖尿病胃肠组织微血管中细胞外信号调节激酶磷酸化的探讨论文.docVIP

　　糖尿病胃肠组织微血管中细胞外信号调节激酶磷酸化的探讨论文 【摘要】 目的 探讨糖尿病微小血管病变的发生机制。方法 采用免疫组织化学方法，观察糖尿病和非糖尿病病人胃肠微小血管内皮细胞及平滑肌细胞中细胞外信号调节激酶(ERK1/2)和ets样基因-1(ELK-1)的磷酸化情况。结果 糖尿病组胃肠道组织各层中微小血管内皮细胞磷酸化ERK1/2阳性率明显高于非糖尿病组(P＜0.05)。糖尿病组胃肠道组织黏膜层、黏膜下层、肌层及浆膜层微小血管内皮细胞中，磷酸化ELK-1阳性率分别为91.0%、91.7%、93.6%和65.3%，与非糖尿病组比较(分别为92.7%、91.3%、91.3%和0)，除了浆膜层以外，其余各层差异无统计学意义(P＞0.05)。在糖尿病组，胃肠道组织黏膜层、黏膜下层、肌层、浆膜层微小血管中平滑肌细胞磷酸化ERK1/2阳性率与非糖尿病组差异无统计学意义(P＞0.05)；糖尿病组胃肠道组织各层微小血管平滑肌细胞中磷酸化ELK-1阳性率与非糖尿病组比较，差异有统计学意义(P＜0.05)。糖尿病组内皮细胞中磷酸化ERK1/2与磷酸化ELK-1阳性率正相关(r=0.510.freelechanism of diabetic microangiopathy. Methods The phosphorylation of extracellular signal-regulated kinase(ERK1/2) and ets like gene-1 (ELK-1)in the gastrointestinal microvascular endothelial cells and smooth muscle cells in diabetic munohistochemistry. Results phospho-P44/P42MAPK positive expression in microvascular endothelial cells, the positive rate of Gastrointestinal organizations layers in diabetic group icrovascular endothelial cells, the positive rate of gastrointestinal mucosa, submucosa, muscularis and serosal layer microvascular endothelial cells in diabetic group ainiy layers ucosa, submucosa,.freeluscularis, serosal layer microvascular smooth muscle cells had no significant difference pared ucosa, submucosa, muscularis, serosal layer microvascular smooth muscle cells had significant difference pared icrovascular endothelial cells , phospho-P44/P42MAPK and Phosphorylation-ELK-1 expression shoicrovascular smooth muscle cells, phospho-P44/P42MAPK and Phosphorylation-Elk-1 expression shoal activation by phosphorelation of ERK1/2 signal transduction pathicrovessels in diabetic patients. Key ellitus；gastrointestine；Microvessel；extracellular signal -regulated kinase1/2；ets-like gene-1 糖尿病微血管病变是多种器官损害的病理生理基础，是糖尿病致死致残的主要原因之一。在糖尿病时，可能有多种因素参与微血管病变的形成［1］。近来的研究提示，某些细胞外信号转导通路的异常变化可能介导了糖尿病微血管病变，丝裂原激活蛋白激酶(mitogen-activated protein kinases，MAPK)，尤其是细胞外调节蛋白激酶(extracellular regulated protein kinases，ERK)可能参于了糖尿病血管并发症的发生发展［2］。本研究采用免疫组织化学技术，对比研究了糖尿病人胃肠组织微血管中磷酸化ERK1/2及其下游作用底物磷酸化e