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目的 研究水杉总黄酮对实验性心肌肥厚的作用及其机制。方法 采用腹腔动 静脉造瘘建立大鼠容量超负荷心肌肥厚模型 ,水杉总黄酮灌胃给药 ,持续 5wk后 ,测定心室肌细胞内Ca2 +浓度、血浆和心肌AngⅡ、心肌MDA及SOD。结果 水杉总黄酮剂量依赖性地减轻大鼠心脏重量 ,抑制心室RNA和蛋白质合成 ,降低心室肌细胞内Ca2 +浓度和心室AngⅡ、MDA含量 ,增加SOD活性。 结论 水杉总黄酮可预防容量超负荷大鼠心肌肥厚的形成 ,其机制可能与拮抗心脏局部RAS ,减轻Ca2 +超负荷以及抗氧化作用有关
Objective To study the effect and mechanism of total flavonoids of Metasequoia on experimental myocardial hypertrophy. Methods Rat model of volume overload cardiac hypertrophy was established by intraperitoneal arteriovenous fistula. The total flavonoids of Metasequoia were administered intragastrically for 5 weeks. The concentration of Ca2 + in plasma, myocardial AngII, myocardial MDA and SOD were measured. Results The total flavonoids of Metasequoia glyptostroboides reduced the rat heart weight in a dose-dependent manner, inhibited the synthesis of ventricular RNA and protein, decreased the intracellular Ca2 + concentration, ventricular AngII, MDA content and increased SOD activity. Conclusion The total flavonoids of Metasequoia glyptostroboides can prevent the formation of cardiac hypertrophy in rats with volume overload. Its mechanism may be related to the antagonism of local RAS, the reduction of Ca2+ overload and antioxidation.