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以链脲佐菌素建立糖尿病大鼠模型,缬沙坦干预治疗12周,光镜下观察大鼠胸主动脉组织结构,并用RT-PCR方法测定血管紧张素II(AngII)mRNA表达平,用Elisa方法测定血清血管假血友病因子(VWF)、内皮素-1(ET-1)、8脱氧鸟酐(8-OHdG)、超氧化物歧化酶(SOD)含量。结果缬沙坦干预治后,8OHdG含量降低,SOD活性增加;ET-1、VWF含量均降低;光镜下观察大鼠胸主动脉病理损伤得到改善。结论氧化应激和肾素血管紧张素(RAS)系统的紊乱参与了糖尿病大鼠的胸主动脉病变过程,缬沙坦通过阻断RAS系统活性,下调AngII基因表达,降低氧化应激反应,从而减轻血管内皮细胞损伤,可能是缬沙坦保护胸主动脉内皮功能的基本机制之一。
The model of diabetic rats was established by streptozotocin. After valsartan treatment for 12 weeks, the structure of thoracic aorta in rats was observed under light microscope. The expression of AngII mRNA was detected by RT-PCR. Elisa method was used to determine the contents of VWF, ET-1, 8-OHdG and SOD. Results After valsartan treatment, the content of 8OHdG decreased and the activity of SOD increased. The contents of ET-1 and VWF decreased. The pathological changes of thoracic aorta were observed under light microscope. Conclusions The disorder of oxidative stress and renin angiotensin system (RAS) is involved in the process of thoracic aorta in diabetic rats. Valsartan can reduce the activity of RAS and down regulate the expression of AngII and the oxidative stress Reducing the damage of vascular endothelial cells may be one of the basic mechanisms by which valsartan protects the endothelial function of the thoracic aorta.