摘要
目的 研究心力衰竭（心衰）大鼠心肌β3,肾上腺素能受体（β3-AR）变化,观察选择性β3-AR抑制剂（SR59230A）对β3-AR、氧化应激状态的影响.方法 将异丙肾上腺素（ISO）诱导的心衰大鼠随机分成ISO组（18只）与ISO＋SR59230A组（21只）,同时以正常大鼠为对照组（7只）.ISO＋SR59230A组给予SR59230A,每日2次腹腔注射;ISO组给予相应生理盐水1 ml;对照组不予处置.6周后测定心功能、心肌β3-AR、内皮型一氧化氮合酶（eNOS）、小三磷酸鸟苷结合蛋白（Racl）mRNA、蛋白表达及脂质过氧化物（LPO）、总超氧化物歧化酶（T-SOD）指标.结果 心衰大鼠心功能恶化,心肌β3-AR mRNA表达增加,SR59230A可改善心功能,降低β3-AR mRNA表达（均为P〈0.05）.心衰时,eNOS、Racl mRNA及蛋白上调,LPO产生增加、T-SOD水平降低.SR59230A降低eNOS、Racl表达,增加心肌组织T-SOD水平,使LPO减少（均为P〈0.05）.结论 心衰时,β3-AR表达增加,加重心肌氧化应激反应,恶化心功能.β3-AR抑制剂改善心功能可能通过抑制氧化应激、延缓心衰进展来实现.
Objective To investigate the association between β3-adrenergic receptor （β3-AR） and oxidative stress in isoproterenol （ISO）-induced chronic heart failure （HF） rats. Methods Seven weight-matched normal adult rats （control）, 18 ISO induced heart failure rats and 21 ISO induced heart failure rats treated with specific （β3-AR inhibitor, SR59230A for 6 weeks were included in this study. Echocardiography was performed at the end of the study and the myocardial levels of total superoxide dismutase （T-SOD） and lipid peroxidation （LPO） were measured by colorimetry, myocardial expression of （β3-AR was detected by reverse transcription-polymerase chain reaction （ RT-PCR）. Result Compared with control group, the cardiac function was significantly reduced and myocardial β3-AR mRNA expression was significantly increased, LPO level was also significantly enhanced while T-SOD level was significantly reduced in ISO group and these changes could be significantly attenuated by treatment with SR59230A Conclusion Our results showed that myocardial upregulation of β3-AR is associated with increased oxidative stress in this model and β3-AR inhibitor may be a new therapeutic agent for heart failure treatment
出处
《中华心血管病杂志》
CAS
CSCD
北大核心
2010年第5期435-439,共5页
Chinese Journal of Cardiology
基金
基金项目：黑龙江省科技厅国际合作项目（WB07C01）
黑龙江省教育厅资助项目（11531108）
黑龙江省博士后启动基金（LRB04.242）
哈尔滨医科大学附属第一医院基金资助项目（2007106）
关键词
心力衰竭
充血性
受体
上腺素能β3
氧化应激
Heart failure, congestive
Receptors, adrenergic, beta-3
Oxidate stress
