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作 者:张翠[1] 杨波[1] 万为国[1] 黄从新[1] 李海涛[1] 王瑾[1]
出 处:《疑难病杂志》2009年第9期513-516,F0003,共5页Chinese Journal of Difficult and Complicated Cases
摘 要:目的探讨诱生型一氧化氮合酶(iNOS)抑制剂氨基胍(AG)对大鼠心肌梗死后心肌保护作用。方法将SD雄性大鼠随机分为A组(假手术组)、B组(模型组)、C组(干预组)。A组仅开胸于冠状动脉前降支下穿线而不结扎。B、C组大鼠左冠状动脉前降支结扎造成大鼠心肌梗死模型。4周后,HE染色观察心肌结构的改变,采用逆转录—聚合酶链反应(RT-PCR)测定梗死区及非梗死区心肌AT_1、AT_2受体及Ⅰ型、Ⅲ型胶原mRNA表达水平的变化。结果与A组比较,B组、C组的AT_1、AT_2受体及Ⅰ、Ⅲ型胶原mRNA的表达水平明显增高,并且梗死区的表达高于非梗死区(P<0.05)。而iNOS抑制剂AG可以使梗死组大鼠心肌AT_1受体及Ⅰ、Ⅲ型胶原mRNA的表达水平下调,AT_2受体mRNA的表达水平继续升高,与B组比较,差异有统计学意义(P<0.05)。结论AG干预后,大鼠心肌内AT_1受体、Ⅰ型胶原和Ⅲ型胶原mRNA表达减少,AT_2受体mRNA的表达升高,这可能与AG抑制心肌重构有关。Objective To explore the myocardial preservation effect of inducible nitricoxide synthase inhibitors (aminoguanidine,AG) after myocardial infarction in rats. Methods The SD male rats were randomized divided into three groups, sham-group(A) , operation group(B) ,operation with AG group(C). Myocardial infarction was induced by ligation of the anterior descending coronary artery. After treatment for 4 weeks, the micro slices were stained with hematoxylineosin, and observed for histological changes, the AT1 , AT2 receptor and collagen type Ⅰ and type Ⅲ mRNA expression in infarction area and non infarction area were detected by RT-PCR. Results Compared with group A, the expression of AT1 , AT2 receptor and collagen type Ⅰ, type Ⅲ mRNA were significantly increased in both infarction zone and non infarction zone in group B find C, furthermore, the expression of them in infarction zone was higher than non infarction zone ( P 〈 0.05 ). The treatment of AG significantly reduced the mRNA expression of AT1 receptor and collagen type Ⅰ, type Ⅲ, and still up regulated the level of AT2 ( P 〈 0.05). Conclusion After the interventional of AG, the mRNA expression of AT1, AT2 receptor and collagen type Ⅰ, type Ⅲ were decreased after myocardial infarction, probably associated with the inhibiting cardiac ventricle remolding of AG.
分 类 号:R542.22[医药卫生—心血管疾病]
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