Background. Cardiac hypertrophy is one of the initial disorders of the cardiovascular system and can induce heart failure. Oxidative stress is an important pathophysiological mechanism of cardiac hypertrophy. Wogonin (Wog), an important flavonoid derived from the root of Scutellaria baicalensis Georgi, is known to possess antioxidant properties. Methods. An in vitro model of cardiac hypertrophy was established by stimulating H9C2 cells and neonatal rat cardiomyocytes (NRCMs) with angiotensin II (AngII). The indices related to myocardial hypertrophy and oxidative stress were detected. An in vivo model of cardiac hypertrophy was induced by transverse aortic constriction (TAC) in C57BL/6 mice. Cardiac function was monitored by chest echocardiography, and the hypertrophy index was measured. The mice were then sacrificed for histological assays, with mRNA and protein detection. To further explore the role of nuclear factor- (erythroid-derived 2-) like 2 (Nrf-2) in regulating the antioxidant effects of Wog in cardiac hypertrophy, siRNA analysis was conducted. Results. Our results showed that Wog significantly ameliorated AngII-induced cardiomyocyte hypertrophy by inhibiting oxidative stress in H9C2 cells and NRCMs. In addition, Wog treatment prevented oxidative stress and improved cardiac hypertrophy in mice that underwent TAC. Using gene-specific siRNA for Nrf-2, we discovered that these antioxidative effects of Wog are mediated through Nrf-2 induction. Conclusions. Our results provide further evidence for the potential use of Wog as an antioxidative agent for treatment of cardiac hypertrophy, and Nrf-2 might serve as a therapeutic target in the treatment of cardiac hypertrophy.

中文翻译：

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汉黄芩素通过激活 Nrf-2 介导的抗氧化反应抑制心脏肥大

背景。心脏肥大是心血管系统的初始疾病之一，可诱发心力衰竭。氧化应激是心肌肥厚的重要病理生理机制。汉黄芩(Wog) 是一种从黄芩根中提取的重要类黄酮，已知具有抗氧化特性。方法。通过用血管紧张素 II (AngII) 刺激 H9C2 细胞和新生大鼠心肌细胞 (NRCMs) 建立了心脏肥大的体外模型。检测与心肌肥大和氧化应激相关的指标。体内_在 C57BL/6 小鼠中通过横向主动脉缩窄 (TAC) 诱导心脏肥大模型。胸部超声心动图监测心功能，测定肥大指数。然后处死小鼠进行组织学分析，检测mRNA和蛋白质。为了进一步探索核因子-（红细胞衍生2-）样2（Nrf-2）在调节Wog在心脏肥大中的抗氧化作用中的作用，进行了siRNA分析。结果。我们的研究结果表明，Wog 通过抑制 H9C2 细胞和 NRCM 中的氧化应激显着改善 AngII 诱导的心肌细胞肥大。此外，Wog 治疗可预防接受 TAC 的小鼠的氧化应激并改善心脏肥大。对Nrf-2使用基因特异性 siRNA，我们发现 Wog 的这些抗氧化作用是通过 Nrf-2 诱导介导的。结论。我们的研究结果为 Wog 作为抗氧化剂治疗心脏肥大的潜在用途提供了进一步的证据，并且 Nrf-2 可能作为治疗心脏肥大的治疗靶点。