本文探索了三七皂苷R1对异丙肾上腺素诱导的H9c2心肌细胞肥大的保护作用，并验证了其对于心肌肥厚的治疗效果。实验以H9c2心肌细胞为模型，应用ISO 20 μg/mL诱导心肌细胞肥大，观察三七皂苷R1对心肌肥厚的影响。用MTT法检测心肌细胞活力；应用实时定量RT-PCR 法检测胚胎型基因ANP、β-MHC及炎症因子TNF-α、IL-6和IL-1β的mRNA表达水平；应用Western blot法检测p65、p-p65、I-κBα蛋白含量；荧光分光光度法检测Caspase-3活性。结果表明，三七皂苷R1能够有效地抑制ISO诱导的心肌细胞肥大，并增强心肌细胞活力；降低了ANP、β-MHC mRNA的表达水平；同时抑制了炎症因子TNF-α、IL-6和IL-1β mRNA表达，以及p65磷酸化的活化，并促进了I-κBα的激活；也抑制了Caspase-3的活性。可见，三七皂苷R1对ISO诱导的H9c2心肌细胞肥大有一定的保护作用，而且能够有效地抑制心肌肥厚，其机制可能与抑制NF-κB相关的的炎症信号通路有关。

The protection of notoginsenoside R1 against isoproterenol-induced hypertrophy in rats H9c2 cardiomyocyte was investigated, and its therapeutic effect on cardiac hypertrophy was also verified. The H9c2 cardiomyocytes was induced by ISO 20 μg/mL to observe the effect of notoginsenoside R1 on cardiac hypertrophy. The viability of cardiomyocytes was detected by MTT assay, and the mRNA levels of ANP, β-MHC, TNF-α, IL-6 and IL-1β were detected by real-time RT-PCR. Western blot was used to detect the protein levels of p65, p-p65, I-κBα; Fluorometric assay kit was used to detect caspase-3 activity. The results showed that, notoginsenoside R1 is effective in inhibiting ISO-induced cardiomyocyte hypertrophy, which manifects increased cardiomyocyte viability, decreased ANP, β-MHC, TNF-α, IL-6 and IL-1β mRNA levels, actived I-κBα protein level, inhibited p65 phosphorylation and decreased Caspase-3 activity. Therefore, notoginsenoside R1 exhibits a protection against ISO-induced H9c2 cardiomyocyte hypertrophy and can effectively inhibit cardiac hypertrophy, and its underlying mechanism may be associated with attenuation of the NF-κB signaling pathway.

国家自然科学基金青年基金项目（81302769；81202526）；北京市自然科学基金资助项目（47144226）