The process of myocardial hypertrophy in hypertension can lead to excessive activation of oxidative stress. Lipoamide (ALM) has significant antioxidant and anti-inflammatory effects. This study aimed to investigate the effects of ALM on hypertension-induced cardiac hypertrophy, as well as explore its underlying mechanisms. We evaluated the effects of ALM on spontaneously hypertensive rats and rat cardiomyocytes treated with Ang II. We found that ALM was not effective in lowering blood pressure in SHR, but it attenuated hypertension-mediated cardiac fibrosis, oxidative stress, inflammation, and hypertrophy in rats. After that, in cultured H9C2 cells stimulated with Ang II, ALM increased the expression of antioxidant proteins that were decreased in the Ang II group. ALM also alleviated cell hypertrophy and the accumulation of ROS, while LY294002 partially abrogated these effects. Collectively, these results demonstrate that ALM could alleviate oxidative stress in cardiac hypertrophy, potentially through the activation of the PI3K/Akt-mediated Nrf2 signaling pathway.

Graphical Abstract

中文翻译：

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硫辛酰胺通过 PI3K/Akt 介导的 Nrf2 信号通路减轻高血压心肌肥厚

高血压心肌肥厚过程可导致氧化应激过度激活。硫辛酰胺（ALM）具有显着的抗氧化和抗炎作用。本研究旨在探讨ALM对高血压引起的心脏肥大的影响，并探讨其潜在机制。我们评估了 ALM 对自发性高血压大鼠和接受 Ang II 治疗的大鼠心肌细胞的影响。我们发现 ALM 不能有效降低 SHR 中的血压，但它可以减轻高血压介导的大鼠心脏纤维化、氧化应激、炎症和肥大。之后，在用 Ang II 刺激的培养的 H9C2 细胞中，ALM 增加了抗氧化蛋白的表达，而在 Ang II 组中抗氧化蛋白的表达则减少。 ALM 还减轻了细胞肥大和 ROS 积累，而 LY294002 部分消除了这些作用。总的来说，这些结果表明 ALM 可能通过激活 PI3K/Akt 介导的 Nrf2 信号通路来减轻心脏肥大中的氧化应激。

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