Hongjuan Cao, Lina Zhao, Yao Yuan, Chunyan Liao, Weidan Zeng, Aiyue Li, Quanfeng Huang, Yueyao Zhao, Yubing Fan, Liu Jiang, Dandan Song, Sha Li, Bei Zhang
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引用次数: 0
Abstract
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.
高血压患者心肌肥厚的过程会导致氧化应激过度激活。脂酰胺(ALM)具有显著的抗氧化和抗炎作用。本研究旨在研究 ALM 对高血压诱导的心肌肥厚的影响,并探索其潜在机制。我们评估了 ALM 对自发性高血压大鼠和 Ang II 处理的大鼠心肌细胞的影响。我们发现,ALM 并不能有效降低 SHR 的血压,但能减轻高血压介导的大鼠心脏纤维化、氧化应激、炎症和肥厚。之后,在用 Ang II 刺激培养的 H9C2 细胞中,ALM 增加了抗氧化蛋白的表达,而 Ang II 组的抗氧化蛋白表达则有所减少。ALM 还减轻了细胞肥大和 ROS 的积累,而 LY294002 则部分减弱了这些作用。总之,这些结果表明,ALM 可通过激活 PI3K/Akt 介导的 Nrf2 信号通路,减轻心脏肥大中的氧化应激。