Objective: to study and analyze the possible mechanism of Tingli Shengmai recipe in preventing and treating myocardi-al remodeling in rats with chronic heart failure (CHF) . Methods: Healthy male SD rats were subjected to abdominal aorta constriction operation to replicate rat heart failure models. Four weeks after operation, drug intervention therapy was begun. At the end of the 8th week, blood samples were taken from femoral artery and the heart was taken out by thoracotomy. Plasma endothelin-1 (ET-1), serum nitric oxide (NO) and NO levels in myocardium were measured. ET-1, endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase ( iNOS) levels in myocardium were measured by Western Blot technique. Results: Compared with sham operation group, ET-1 in plasma, NO in serum and myocardium of model group increased significantly, ET-1 and iNOS protein expression in my-ocardium increased, and eNOS protein expression decreased ( P <0.01); compared with model group, in other groups, ET-1 in plas-ma, NO in serum and myocardium decreased significantly, ET-1 in myocardium tissue and iNOS protein expression decreased signifi-cantly, and eNOS protein expression increased ( P <0.01). Conclusion: The mechanism of Tingli Shengmai recipe in inhibiting my-ocardial remodeling of CHF rats is related to the reduction of ET-1 production and the regulation of NO/NOS expressions.%目的: 研究分析葶苈生脉方防治慢性心力衰竭 ( CHF) 大鼠心肌重构的可能作用机制.方法: 采用健康雄性SD大鼠, 腹主动脉缩窄手术法复制大鼠心力衰竭模型.手术4周后开始给予药物干预治疗, 第8周末股动脉取血并开胸摘取心脏, 检测血浆内皮素 (ET-1)、血清一氧化氮 (NO) 及心肌组织NO含量, Western Blot 技术测定心肌组织ET-1、内皮型一氧化氮合酶 ( eNOS) 及诱导型一氧化氮合酶 ( iNOS) 蛋白的表达.结果: 与假手术组比较, 模型组大鼠血浆ET-1、血清及心肌组织NO含量显著升高, 心肌组织ET-1、 iNOS蛋白表达升高, eNOS蛋白表达降低 ( P <0.01); 与模型组比较, 各给药组大鼠血浆ET-1、血清及心肌组织NO含量明显降低, 心肌组织ET-1、 iNOS蛋白表达降低, eNOS蛋白表达升高 ( P <0.01).结论: 葶苈生脉方抑制CHF大鼠心肌重构的机制与其减少ET-1生成, 调节NO/NOS表达有关.
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