Ginkgolide B (GB) is an active ingredient extracted from Ginkgo biloba leaves. However, the effects of GB on cardiac hypertrophy remain unclear. The study is aimed at determining whether GB could alleviate cardiac hypertrophy and exploring its underlying molecular mechanism. Rat cardiomyocyte cell line H9c2 cells were pretreated with GB and incubated with angiotensin II (Ang II) to simulate an in vitro cardiac hypertrophy model. Cell viability, cell size, hypertrophy markers, and autophagy were determined in H9c2 cells after Ang II treatment. Proteins involved in autophagy and the SIRT1 pathway were determined by western blot. Our data demonstrated that GB attenuated Ang II-induced cardiac hypertrophy and reduced the mRNA expressions of hypertrophy marker, atrial natriuretic peptide (ANP), and β-myosin heavy chain (β-MHC). GB further increased Ang II-induced autophagy in H9c2 cells and modulated expressions of autophagy-related proteins Beclin1 and P62. Modulation of autophagy using autophagy inhibitor 3-methyladenine (3-MA) could abrogate GB-downregulated transcription of NPPA. We then showed that GB attenuated Ang II-induced oxidative stress and reduction in SIRT1 and FoxO1 protein expression. Finally, the effect of GB on autophagy and cardiac hypertrophy could be reversed by SIRT1 inhibitor EX-527. GB inhibits Ang II-induced cardiac hypertrophy by enhancing autophagy via the SIRT1-FoxO1 signaling pathway and might be a potential agent in treating pathological cardiac hypertrophy.

中文翻译：

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银杏内酯 B 通过 SIRT1-FoxO1 调节自噬保护心肌细胞免受血管紧张素 II 诱导的肥大

Ginkgolide B (GB) 是从银杏叶中提取的活性成分。然而，GB 对心脏肥大的影响仍不清楚。该研究旨在确定 GB 是否可以缓解心脏肥大并探索其潜在的分子机制。大鼠心肌细胞系 H9c2 细胞用 GB 预处理并与血管紧张素 II (Ang II) 一起孵育以模拟体外心脏肥大模型。在 Ang II 处理后，在 H9c2 细胞中测定细胞活力、细胞大小、肥大标志物和自噬。通过蛋白质印迹确定参与自噬和 SIRT1 途径的蛋白质。我们的数据表明 GB 减弱了 Ang II 诱导的心脏肥大并降低了肥大标志物、心房钠尿肽 (ANP) 和β的 mRNA 表达-肌球蛋白重链 ( β - MHC )。GB 进一步增加了 H9c2 细胞中 Ang II 诱导的自噬，并调节了自噬相关蛋白 Beclin1 和 P62 的表达。使用自噬抑制剂 3-甲基腺嘌呤 (3-MA) 调节自噬可以消除 GB 下调的 NPPA 转录。然后我们发现 GB 减弱了 Ang II 诱导的氧化应激和 SIRT1 和 FoxO1 蛋白表达的降低。最后，SIRT1 抑制剂 EX-527 可以逆转 GB 对自噬和心脏肥大的影响。GB 通过 SIRT1-FoxO1 信号通路增强自噬来抑制 Ang II 诱导的心脏肥大，并且可能是治疗病理性心脏肥大的潜在药物。