缬沙坦对自发性高血压模型鼠脑氧化应激的影响

Influence of brain oxidative stress in the brain tissue of the spontaneously hypertensive rat interference with Valsartan

目的探讨缬沙坦对自发性高血压模型鼠脑氧化应激的影响。方法以自发性高血压模型鼠为研究对象,通过缬沙坦干预,观察高血压鼠脑组织丙二醛(MDA)水平,超氧化物歧化酶(SOD)活性及P22PHOX基因表达状况。结果自发性高血压组SOD较正常对照组显著降低(P<0.01),MDA水平及P22PHOX mRNA表达显著高于正常对照组(P<0.01);缬沙坦治疗组血清SOD高于高血压组(P<0.05),MDA及P22PHOX mRNA表达显著低于高血压组(P<0.01,P<0.05)。结论 (1)自发性高血压鼠活性氧升高;(2)活性氧升高的机制可能与P22PHOX表达增强有关;(3)缬沙坦可能通过抑制P22PHOX mRNA的表达,发挥其抗氧化作用。

Objective To investigate the relationship between Valsartan and brain oxidative stress of the spontaneously hypertensive model rats.Methods The spontaneously hypertensive model rats were studied by using Valsartan treatment.The level of malondialdehyde （MDA） in hypertensive rat brain tissue,as well as superoxide dismutase （SOD） activity and P22PHOX gene expression were observed in this study.Results SOD activity in spontaneously hypertensive group compared with normal control group was significantly lower （P〈0.01）,but the MDA level and P22PHOX mRNA expression were significantly higher than the normal control group （P〈0.01）.The level of serum SOD in Valsartan treatment group was higher than that in hypertension group （P〈0.05）,but the MDA level and P22PHOX mRNA expression were significantly lower than the hypertension group （P〈0.01,P〈0.05）.Conclusion The reactive oxygen species （ROS） were increased in spontaneously hypertensive model rats.The mechanism of increased reactive oxygen species may be related to increased expression of P22PHOX.Valsartan may play their antioxidant activity through inhibiting P22PHOX mRNA expression.