糖尿病胃肠组织微血管中细胞外信号调节激酶磷酸化医药学论文.docVIP

糖尿病胃肠组织微血管中细胞外信号调节激酶磷酸化医药学论文 【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，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。 【关键词】糖尿病；胃；肠；微血管；细胞外调节蛋白激酶；ets样基因-1 Abstract:ObjectiveToexplorethemechanismofdiabeticmicroangiopathy.MethodsThephosphorylationofextracellularsignal-regulatedkinase(ERK1/2)andetslikegene-1(ELK-1)inthegastrointestinalmicrovascularendothelialcellsandsmoothmusclecellsindiabeticwithnon-diabeticpatientswereobservedwithimmunohistochemistry.Resultsphospho-P44/P42MAPKpositiveexpressioninmicrovascularendothelialcells,thepositiverateofGastrointestinalorganizationslayersindiabeticgroupweresignificantlyhigherthanthatinnon-diabeticgroup(P＜0.05)；Phosphorylation-ELK-1positiveexpressioninmicrovascularendothelialcells,thepositiverateofgastrointestinalmucosa,submucosa,muscularisandserosallayermicrovascularendothelialcellsindiabeticgroupwere91.0%,91.7%,93.6%and65.3%,andinnon-diabeticgroup(respectively92.7%,91.3%,91.3%and0).inadditiontoserosallayer,theremainiylayerswerenosignificantdifferenles(P＞0.05).Indiabeticgroup,phospho-P44/P42MAPKpositiveexpressionrateofgastrointestinalmucosa,submucosa,muscularis,serosallayermicrovascularsmoothmusclecellshadnosignificantdifferencecomparedwiththenon-diabeticgroup(P＞0.05)；Inthediabeticgroup,Phosphorylation-ELK-1positiveexpressionrateofgastrointestinalmucosa,submucosa,muscularis,serosallayermicrovascularsmoothmusclecellshadsignificantdifferencecomparedwiththenon-diabeticgroup(P＜0.05).Inmicrovascularendothelialcells,phospho-P44/P42MAPKandPhosphorylation-