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作 者:郑丽丽[1] 张治国[1] 李成光[2] 叶启发[1] 赵国强[2]
机构地区:[1]中南大学湘雅三院湘雅移植医学研究院,长沙410013 [2]郑州大学医学院
出 处:《临床心血管病杂志》2006年第12期735-737,共3页Journal of Clinical Cardiology
摘 要:目的:探讨培哚普利防治糖尿病血管并发症的作用机制。方法:用反转录-聚合酶链反应(RT-PCR)和Northern印迹杂交方法测定0.1,1.0,10.0μmol/L浓度的培哚普利对经体外制备的糖基化终产物(AGEs)培养的人脐静脉内皮细胞(HUVECs)转化生长因子βⅡ受体(TβRⅡ)和Ⅰα(Ⅳ)前胶原mRNA表达的影响。结果:AGEs组TβRⅡ及Ⅰα(Ⅳ)前胶原mRNA表达较正常对照组明显增高(P<0.01);与AGEs组相比,TβRⅡ和Ⅰa(Ⅳ)前胶原mRNA的表达在培哚普利组0.1μmol/L时无明显降低,1.0μmol/L时分别降低了16%和10%,差异无统计学意义;10.0μmol/L时分别降低46%和50%,差异有统计学意义(P<0.05)。结论:培哚普利通过抑制高糖所致的TβRⅡ的表达,从而抑制细胞外基质的生成,防止血管重构,可能是其防治糖尿病血管并发病的机制之一。Objective:To investigate the mechanism of preventive and therapeutic actions of Perindopril on diabetic angiopathy. Method: Reverse transcription-polymerase chain reaction(RT-PCR) and Northern blot were applied to determine the effect of Perindopril over the concentration range from 0. 1 to 10.0μmol/L on inhibiting both gene expression of transformation growth factor——β type receptor Ⅱ (TβRⅡ) and Ⅰα( Ⅳ ) procollage that were stimulated by advanced Glycation end products (AGEs) incultured human umbilical vein endothelial cells (HUVECs). Result:The expression of TβRⅡ and Ⅰα (Ⅳ) procollage mRNA was higher in the HUVECs stimulated by AGEs than in the cells of control groups. Administration of Perindopril suppressed the expression of TβRⅡ and Ⅰα (Ⅳ) procollage mRNA by 16% and 10% at 1.0μmol/L, 46% and 50% at 10.0μmol/L. Conclusion : Perindopril can reduce the forming of extracellular matrix by decreasing the expression of TβRⅡ mRNA, which may be one of the possible mechanisms of Perindopril in prevening diabetic angiopathy.
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