β-肾上腺素刺激前后小鼠心肌一氧化氮合酶对超氧化物水平的调节作用  

Regulation of nitric oxide synthase on the levels of superoxide in mice myocardium before and afterβ-adrenergic stimulation

作　　者：丁君 宋柏仪 郭镇熠 李敏 郑伟达 崔兰[1] DING Jun;SONG Baiyi;GUO Zhenyi;LI Min;ZHENG Weida;CUI Lan(Department of Cardiology,Affiliated Hospital of Yanbian University,Yanji 133000,Jilin,China)

机构地区：[1]延边大学附属医院心血管内科,吉林延吉133000

出　　处：《延边大学医学学报》2020年第1期1-5,共5页Journal of Medical Science Yanbian University

摘　　要：[目的]探讨β-肾上腺素刺激前后左心室神经型一氧化氮合酶(nNOS)和内皮型一氧化氮合酶(eNOS)对超氧化物水平的调节作用.[方法]取年龄匹配(2~5个月)的eNOS基因敲除(eNOS^-/-)和nNOS基因敲除(nNOS^-/-)小鼠与年龄相匹配的野生型同胞(eNOS^+/+或nNOS^+/+)心肌组织,利用单管发光计通过发光素增强化学发光法测量心脏组织中肾上腺素(ISO,10,100 nmol/L)刺激前后超氧化物的生成量.[结果]nNOS^-/-和nNOS^+/+或eNOS^-/-和eNOS^+/+小鼠左心室心肌组织中的超氧化物含量间差异无统计学意义(P>0.05).给予ISO 100 nmol/L处理可显著增加nNOS^-/-小鼠心肌组织超氧化物生成量(P=0.01),但nNOS^+/+,eNOS^-/-和eNOS^+/+小鼠心肌组织中的超氧化物含量未见有明显变化(P>0.05).用特异性nNOS抑制剂S-甲基^-L-硫代瓜氨酸(SMTC,200 nmol/L)抑制nNOS可增加eNOS^+/+小鼠心肌组织中的超氧化物含量,在SMTC处理的前提下ISO(100 nmol/L)并未增加nNOS^-/-小鼠心肌组织产生超氧化物.[结论]nNOS是调节心肌超氧化物水平的主要一氧化氮合成酶,nNOS的活性可抑制β-肾上腺素刺激下心肌组织生成超氧化物.OBJECTIVE To explore the regulation effects of left ventricular neuronal nitric oxide synthase(nNOS)and endothelial nitric oxide synthase(eNOS)on the levels of superoxide before and afterβ-adrenergic stimulation.METHODS Myocardial tissue was taken from age-matched(2-5 months)eNOS knockout(eNOS^-/-)and nNOS knockout(nNOS^-/-)mice and age-matched wild-type siblings(eNOS^+/+or nNOS^+/+).A single tube luminometer was used to measure the production of superoxide in cardiac tissue by luminescence-enhanced chemiluminescence before and after adrenaline(ISO,10,100 nmol/L)stimulation.RESULTS There was no significant difference in the content of superoxide in the left ventricular myocardium between nNOS^-/-and nNOS^+/+mice or eNOS^-/-and eNOS^+/+mice(P>0.05).The treatment of isoproterenol(ISO,100 nmol/L)significantly increased the production of superoxide in the myocardial tissue of nNOS^-/-mice(P=0.01),but no significant changes were observed in nNOS^+/+,eNOS^-/-or eNOS^+/+mice.Inhibition of nNOS with a specific nNOS inhibitor S-methyl^-L-thiocitrulline(SMTC,200 nmol/L)increased the content of superoxide in the myocardial tissue of eNOS^+/+mice.ISO(100 nmol/L)did not increase the production of superoxide in the myocardial tissue of nNOS^-/-mice treated with the SMTC.CONCLUSION NNOS is the main NOS that regulates the levels of myocardial superoxide.The activity of nNOS can inhibit the production of superoxide in myocardial tissue underβ-adrenergic stimulation.

关 键 词：神经型一氧化氮合酶 内皮型一氧化氮合酶 超氧化物 β-肾上腺素刺激 心肌 小鼠 

分 类 号：R54[医药卫生—心血管疾病]