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机构地区:[1]宁夏医学院基础学院病理学教研室,银川750004 [2]宁夏医学院附属医院病理科,银川750004
出 处:《宁夏医学院学报》2008年第2期143-145,149,F0002,共5页Journal of Ningxia Medical College
基 金:宁夏回族自治区普通高等学校研究基金(200540)
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,P=0.000);血管平滑肌细胞中磷酸化ERK1/2与磷酸化ELK-1表达显示正相关(r=0.386,P=0.000)。结论在糖尿病病人胃肠微小血管中存在ERK1/2信号转导通路的异常激活。Objective To explore the mechanism 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 with non-diabetic patients were observed with immunohistochemistry. Results phospho-P44/P42MAPK positive expression in microvascular endothelial cells, the positive rate of Gastrointestinal organizations layers in diabetic group were significantly higher than that in non-diabetic group( P 〈 0.05) ;Phosphorylation-ELK- 1 positive expression in microvascular endothelial cells, the positive rate of gastrointestinal mucosa, submucosa, muscularis and serosal layer microvascular endothelial cells in diabetic group were 91.0%, 91.7%, 93.6% and 65.3%, and in non-diabetic group (respectively 92.7%, 91.3%, 91.3% and 0). in addition to serosal layer, the remainiy layers were no significant differenles( P 〉 0.05). In diabetic group, phospho-P44/P42MAPK positive expression rate of gastrointestinal mucosa, submucosa, muscularis, serosal layer microvascular smooth muscle cells had no significant difference compared with the non-diabetic group (P 〉0.05);In the diabetic group, Phosphorylation-ELK- 1 positive expression rate of gastrointestinal mucosa, submucosa, muscularis, serosal layer microvascular smooth muscle cells had significant difference compared with the non-diabetic group (P 〈0.05). In microvascular endothelial cells , phospho-P44/P42MAPK and Phosphorylation- ELK- 1 expression showed a positive correlation ( r =0.510, P = 0.000);In microvascular smooth muscle cells, phospho-P44/P42MAPK and Phosphorylation-ELk-1 expression showed a positive correlation ( r = 0.386, P = 0.000). Conclusion Abnormal activation by phosphorelation of ERK1/2 signal Wansduction pathway was probably involved in the changes of gastrointestinal microvessels in diabetic patients.
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