摘要
目的:探讨自发性高血压大鼠(SHR)主动脉活性氧(ROS)、AT1 受体和 p22phox mRNA表达的相关性及阿托伐他汀治疗对其影响。方法:以正常血压大鼠为对照,观察SHR给予阿托伐他汀50 mg·kg-1·d-1灌胃30 d后,血压、血浆血管紧张素Ⅱ(AngⅡ)、血清一氧化氮(NO)、主动脉 ROS含量、AT1 受体蛋白和 mRNA以及 p22phox mRNA表达的变化。结果:阿托伐他汀治疗 30 d后,SHR血压、血浆 AngⅡ、主动脉 ROS含量、AT1 受体蛋白和mRNA及 p22phox mRNA表达下降,血清NO水平上升。多元逐步回归分析显示 AT1 受体为血管ROS的主要影响因素。结论:血管AT1 受体mRNA表达增加引起 p22phox亚单位表达上调,导致 ROS合成增加是高血压血管 ROS增多的重要机制。阿托伐他汀可下调血管 AT1 受体和 p22phox亚单位表达,减少ROS,减轻血管内皮功能受损。
Objective: To investigate changes and association of reactive oxygen species(ROS),AT 1 receptor and p22phox mRNA expression in aorta of SHR and effects of atorvastatin. Method:WKY were used as control, SHR were treated with atorvastatin [50 mg/(kg·d)] for 30 d. Blood pressure,plasma AngⅡ,serum nitric oxide(NO),ROS,AT 1 receptor protein,AT 1 receptor and p22phox mRNA in aorta were measured. Result:After 30 d of treatment of atorvastatin, blood pressure, concentration of plasma AngⅡ, production of vascular ROS, protein and mRNA expression of AT 1 receptor and mRNA expression of p22phox in aorta of SHR significantly decreased. Levels of serum NO significantly increased. AT 1 receptor is an important factor of ROS. Conclusion:Increased production of vascular ROS in SHR is correlated with AT 1 receptor which can upregulate p22phox mRNA expression. Atorvastatin can reduce ROS by downregulating AT 1 receptor and p22phox expression.
出处
《临床心血管病杂志》
CAS
CSCD
北大核心
2005年第2期104-107,共4页
Journal of Clinical Cardiology
关键词
自发性高血压大鼠
活性氧
AT1受体
P22PHOX
阿托伐他汀
Spontaneously hypertensive rats
Reactive oxygen species
Angiotensin type 1 receptor
p22phox
Atorvastatin
