Lipoamide Attenuates Hypertensive Myocardial Hypertrophy Through PI3K/Akt-Mediated Nrf2 Signaling Pathway

被引:0
|
作者
Cao, Hongjuan [1 ]
Zhao, Lina [1 ,2 ]
Yuan, Yao [1 ]
Liao, Chunyan [1 ,2 ]
Zeng, Weidan [1 ]
Li, Aiyue [1 ]
Huang, Quanfeng [1 ]
Zhao, Yueyao [1 ]
Fan, Yubing [1 ]
Jiang, Liu [1 ]
Song, Dandan [1 ]
Li, Sha [1 ,2 ]
Zhang, Bei [1 ,2 ]
机构
[1] Guizhou Med Univ, Guiyang, Guizhou, Peoples R China
[2] Guizhou Med Univ, Dept Ultrasound Ctr, Affiliated Hosp, Guiyang, Guizhou, Peoples R China
基金
中国国家自然科学基金;
关键词
Lipoamide; Cardiac hypertrophy; PI3K/Akt; Oxidative stress; ALPHA-LIPOIC ACID; LEFT-VENTRICULAR HYPERTROPHY; OXIDATIVE STRESS; CARDIAC-HYPERTROPHY; ACTIVATION; PROTECTS;
D O I
10.1007/s12265-024-10488-9
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:910 / 922
页数:13
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