Erucin Alleviates Cardiac Hypertrophy by Improving Mitochondrial Function via Nrf2‐Sirt3 Pathway

SIRT3 肌肉肥大 压力过载 心功能曲线 线粒体 苯肾上腺素 心肌细胞 药理学 基因沉默 锡尔图因 心室重构 细胞生物学 化学 生物 内科学 内分泌学 医学 心肌肥大 NAD+激酶 生物化学 心力衰竭 血压 基因
作者
Siyu Jiang,Cheng Wang,Dong Yin,Long Chen,M. Shi,Fengxiao Zhang,Zhaohui Wang,Minglu Liang
出处
期刊:Phytotherapy Research [Wiley]
卷期号:39 (6): 2989-3001 被引量:1
标识
DOI:10.1002/ptr.8458
摘要

Numerous studies have documented erucin's anticancer and vasodilatory properties, yet its impact on pathological cardiac hypertrophy remains to be fully understood. This study aimed to explore the therapeutic potential of erucin in cardiac hypertrophy induced by pressure overload. Cardiac hypertrophy was induced in mice by transverse aortic constriction (TAC) surgery, and in neonatal rat cardiomyocytes via phenylephrine (PE) treatment. Cardiac function and remodeling were evaluated using echocardiography, histological assessment, and molecular analyses. Mitochondrial function was assessed by measuring mitochondrial respiration, ATP concentration, the NAD+/NADH ratio, and reactive oxygen species (ROS) levels. Molecular docking was performed to identify erucin's downstream effector. Nrf2 and Sirt3 were silenced using siRNAs, and their activities were inhibited with ML385 and 3-TYP, respectively. Here, we found that erucin improved cardiac function and remodeling in TAC-induced hypertrophic mice, mitigated PE-induced cell hypertrophy, and restored mitochondrial function. Molecular docking analysis identified Nrf2 as a target protein of erucin. Erucin increased Nrf2 protein levels and activated the Nrf2 signaling pathway, which in turn promoted Sirt3 transcription. This effect was blocked by silencing Nrf2 or using ML385. Additionally, silencing Nrf2 and Sirt3 or using ML385 and 3-TYP abolished erucin's protective effects. This study is the first to demonstrate that erucin protects against cardiac hypertrophy by improving mitochondrial function through the activation of the Nrf2-Sirt3 pathway. Erucin may emerge as a promising therapeutic candidate for treating cardiac hypertrophy.
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