中文摘要：

目的探讨丹酚酸B对异丙肾上腺素诱发的原代乳鼠心肌细胞肥大的保护作用及其机制。方法用异丙肾上腺素诱导制备原代乳鼠心肌细胞肥大模型。MTT法检测丹酚酸B对乳鼠心肌细胞活力的影响；RT-PCR技术检测心肌肥厚指标心钠肽（ANP）、脑钠肽（BNP）基因表达；分光光度法检测心肌细胞中超氧化物歧化酶（SOD）的活性和丙二醛（MDA）的量；Western blotting法测定心肌肥厚信号转导通路JAK、STAT蛋白的表达。结果不同浓度的丹酚酸B对乳鼠心肌细胞的活力无明显影响。与模型组比较，丹酚酸B浓度为10、20μmol／L时明显下调ANP、BNP基因表达（P〈0．05、0．01）：显著增强SOD活性和降低MDA的量（P〈0．05、0．01）；显著下调JAK1与STAT3蛋白的表达（P〈0．05、0．01）。结论丹酚酸B能有效抑制异丙肾上腺素诱发的原代乳鼠心肌细胞肥大，其机制可能与抗氧化应激以及抑制JAK1／STAT3信号通路有关。

英文摘要：

Objective To observe the effects of salvianolic acid B （Sal B） on isoproterenol （ISO）-induced cardiomyocyte hypertrophy of neonatal rats and clarify the underlying mechanisms. Methods Hypertrophy in neonatal rat ventricular myocytes was induced by ISO. The effect of Sal B on the myocardial viability of neonatal rats was measured by MTT. The mRNA expression levels of ANP and BNP were detected by RT-PCR. Colorimetric method was employed to measure SOD activity and MDA content. The expression levels of JAK1 and STAT3 were assessed by Western blotting. Results Sal B at different concentration had no effect on the myocardial viability of neonatal rats. Compared with the model group, Sal B at 10 and 20 μmol/L could obviously down-regulate the gene expression levels of ANP and BNP （P 〈 0.01, 0.05）, significantly increase SOD activity, and decrease MDA content. The protein expression levels of JAK1/STAT3 were down-regulated （P 〈 0.01, 0.05）. Conclusion Sal B could effectively inhibit ISO-induced cardiomyocyte hypertrophy of neonatal rats and the mechanism may be related with the anti-oxidative stress and the inhibition of JAK1/STAT3 signaling pathway.