Lycopene protects against pressure overload-induced cardiac hypertrophy by attenuating oxidative stress
Lycopene protects against pressure overload-induced cardiac hypertrophy by attenuating oxidative stress
复制标题
番茄红素通过减轻氧化应激来防止压力超负荷引起的心脏肥大
DOI：
10.1016/j.jnutbio.2019.01.002
复制
发表时间：
2019-04-01
影响因子：
5.6
通讯作者：
Liu, Chen
中科院分区：
文献类型：
--
作者：
Zeng, Junyi;Zhao, Jingjing;Liu, Chen
氧化应激被认为是心肌肥大的重要致病过程。番茄红素是一种保护心血管系统的类胡萝卜素抗氧化剂，因此我们推测番茄红素可能通过减轻氧化应激来抑制心肌肥厚。分别用去甲肾上腺素和压力超负荷建立体外和体内肥大模型。我们的数据显示，在体外和体内研究中，番茄红素治疗可以显著阻止压力超负荷诱导的心肌肥厚。进一步的研究表明，番茄红素可以逆转肥厚过程中活性氧(ROS)生成的增加，并可以延缓ROS依赖的促肥厚MAPK和Akt信号通路的激活。此外，还观察了番茄红素对新生心肌细胞通透性转换孔开放的保护作用。此外，我们证明了番茄红素恢复了受损的抗氧化反应元件(ARE)活性，并激活了ARE驱动的抗氧化基因的表达。因此，我们的研究结果表明，番茄红素通过抑制ROS依赖机制来抑制心肌肥厚。(C)2019 Elsevier Inc.保留所有权利。
Oxidative stress is considered an important pathogenic process of cardiac hypertrophy. Lycopene is a kind of carotenoid antioxidant that protects the cardiovascular system, so we hypothesized that lycopene might inhibit cardiac hypertrophy by attenuating oxidative stress. Phenylephrine and pressure overload were used to set up the hypertrophic models in vitro and in vivo respectively. Our data revealed that treatment with lycopene can significantly block pressure overload-induced cardiac hypertrophy in in vitro and in vivo studies. Further studies demonstrated that lycopene can reverse the increase in reactive oxygen species (ROS) generation during the process of hypertrophy and can retard the activation of ROS-dependent pro-hypertrophic MAPK and Akt signaling pathways. In addition, protective effects of lycopene on the permeability transition pore opening in neonatal cardiomyocytes were observed. Moreover, we demonstrated that lycopene restored impaired antioxidant response element (ARE) activity and activated ARE-driven expression of antioxidant genes. Consequently, our findings indicated that lycopene inhibited cardiac hypertrophy by suppressing ROS-dependent mechanisms. (C) 2019 Elsevier Inc. All rights reserved.