Lipoamide Attenuates Hypertensive Myocardial Hypertrophy Through PI3K/Akt-Mediated Nrf2 Signaling Pathway.
Hongjuan CaoLina ZhaoYao YuanChunyan LiaoWeidan ZengAiyue LiQuanfeng HuangYueyao ZhaoYubing FanLiu JiangDandan SongSha LiBei ZhangPublished in: Journal of cardiovascular translational research (2024)
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.
Keyphrases
- oxidative stress
- blood pressure
- induced apoptosis
- pi k akt
- signaling pathway
- diabetic rats
- cell cycle arrest
- dna damage
- ischemia reperfusion injury
- hypertensive patients
- angiotensin ii
- left ventricular
- heart rate
- cell proliferation
- epithelial mesenchymal transition
- cell death
- single cell
- type diabetes
- high glucose
- stem cells
- heat shock
- heart failure
- newly diagnosed
- stress induced
- physical activity