论文部分内容阅读
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 perindopril in prevention and treatment of diabetic vascular complications. METHODS: Perindopril at concentrations of 0.1, 1.0 and 10.0 μmol / L were used to culture AGEs in vitro by reverse transcription-polymerase chain reaction (RT-PCR) and Northern blotting (TβRⅡ) and Ⅰα (Ⅳ) procollagen mRNA expression in human umbilical vein endothelial cells (HUVECs). Results: The expressions of TβRⅡ and Ⅰα (Ⅳ) procollagen mRNA in AGEs group were significantly higher than those in normal control group (P <0.01). Compared with AGEs group, the expression of procollagen mRNA of TβRⅡ and Ⅰa (Ⅳ) μmol / L, respectively. There was no significant difference between the two groups (1.0μmol / L, 16% and 10%, respectively) ). CONCLUSION: Perindopril may be one of the mechanisms of prevention and treatment of diabetic vascular complications by inhibiting the expression of TβRII induced by high glucose, thereby inhibiting the formation of extracellular matrix and preventing vascular remodeling.