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目的研究异钩藤碱(Iso)对血管紧张素Ⅱ(AngⅡ)引起的大鼠心肌肥大的抑制作用,并探讨其机制。方法采用初生大鼠原代心肌细胞培养法,BCA法检测细胞总蛋白含量,测定细胞表面积和心房利钠因子mRNA的表达以观察Iso对AngⅡ诱发心肌细胞肥大的抑制作用。通过测定细胞培养上清液中一氧化氮(NO)含量和一氧化氮合酶(NOS)活性、Real time RT-PCR检测内皮型一氧化氮合酶(eNOS)mRNA的表达,探讨Iso可能的作用机制。结果 AngⅡ0.1μmol·L-1明显促进了心肌细胞肥大,增加心肌细胞表面积、蛋白含量,降低细胞上清液中NO含量及NOS活性,降低eNOS mRNA表达。Iso 1、10μmol·L-1明显抑制AngⅡ诱发心肌细胞肥大的作用,增加细胞中NO的合成、释放和增加NOS活性,上调eNOS mRNA的表达。结论Iso可抑制AngⅡ诱导的心肌细胞肥大,其作用机制可能与促进NOS的活性、增加NO合成和释放有关。
Objective To investigate the inhibitory effect of Isoine on cardiac hypertrophy induced by angiotensin Ⅱ (Ang Ⅱ) in rats and its mechanism. Methods Primary rat primary cardiomyocyte culture was used. BCA was used to detect total cellular protein. Cell surface area and atrial natriuretic factor mRNA expression were measured to observe the inhibitory effect of Iso on Ang Ⅱ-induced cardiomyocyte hypertrophy. The expression of nitric oxide (NO) and nitric oxide synthase (NOS) in cell culture supernatants were determined by real time RT-PCR and the expression of eNOS mRNA was detected by real time RT-PCR. Mechanism. Results AngⅡ0.1μmol·L-1 significantly increased cardiomyocyte hypertrophy, increased myocardial cell surface area and protein content, decreased NO content and NOS activity in cell supernatant and decreased eNOS mRNA expression. Iso 1,10μmol·L-1 significantly inhibited Ang Ⅱ-induced cardiomyocyte hypertrophy, increased cell NO synthesis, release and increase NOS activity, eNOS mRNA expression increased. Conclusion Iso can inhibit Ang Ⅱ-induced hypertrophy of cardiomyocytes, and its mechanism may be related to the promotion of NOS activity, increase of NO synthesis and release.