黄芪甲苷对过氧化氢损伤模型人脐静脉内皮细胞的改善作用

Improvement Effect of Astragaloside Ⅳ on the Human Umbilical Vein Cell Injured by Hydrogen Peroxide

目的探讨黄芪甲苷对过氧化氢(H2O2)损伤模型人脐静脉内皮细胞(HUVEC)的改善作用。方法将对数生长期的HUVEC分为正常对照组(A组,常规培养基),H2O2组(B组,300μmol/L H2O2),阳性对照组(C组,300μmol/L H2O2+50μg/mL维生素E),以及黄芪甲苷高、中、低剂量组(D1组、D2组、D3组,300μmol/L H2O2+50.0,25.0,12.5μg/mL黄芪甲苷)。采用四氮唑盐(MTT)法测定细胞活力,测定乳酸脱氢酶(LDH)及超氧化物歧化酶(SOD)活性,采用实时荧光定量聚合酶链式反应(RT-PCR)法测定单核细胞趋化蛋白1(MCP-1)mRNA及细胞间黏附分子1(ICAM-1)mRNA表达情况。结果与A组比较,B组细胞活力及SOD活性显著减弱,LDH活性及MCP-1 mRNA,ICAM-1 mRNA表达显著增强(P<0.01);与B组比较,C组及D1组、D2组、D3组细胞活力及SOD活性显著增强,LDH活性及MCP-1 mRNA和ICAM-1 mRNA表达显著减弱(P<0.01)。结论黄芪甲苷对H2O2损伤HUVEC有一定改善作用,其机制可能与减弱MCP-1 mRNA和ICAM-1 mRNA表达有关。

Objective To investigate the improvement effect of astragalosideⅣon the human umbilical vein endothelial cell(HUVEC)injured by hydrogen peroxide(H2O2).Methods The HUVEC in logarithmic growth phase were divided into the normal control group(group A,conventional medium),H2O2 group(group B,300μmol/L H2O2),positive control group(group C,300μmol/L H2O2+50μg/mL vitamin E)and astragalosideⅣhigh,medium and low dosage groups(group D1,group D2,group D3,300μmol/L H2O2+50.0,25.0,12.5μg/mL astragaloside).The cell viability was measured by methyl thiazolyl tetrazolium(MTT)assay,the LDH and SOD activities were measured by biochemical detection,the monocyte chemoattractant protein-1(MCP-1)mRNA and intercellular adhesion molecule-1(ICAM-1)mRNA were measured by real-time fluorescence quantitative polymerase chain reaction(RT-PCR).Results Compared with those in group A,the cell viability and SOD activity were significantly decreased,while the LDH activity,MCP-1 mRNA and ICAM-1 mRNA expression were significantly increased in group B(P<0.01).Compared with those in group B,the cell viability and SOD activity were significantly increased,while the LDH activity,MCP-1 mRNA and ICAM-1 mRNA expression were significantly decreased in group C,group D1,group D2 and group D3(P<0.01).Conclusion AstragalosideⅣcan improve H2O2-induced HUVEC damage,and its mechanism may be related to the decrease of MCP-1 and ICAM-1 expression.