Selenium (Se) deficiency is associated with the development of Keshan disease, a cardiomyopathy associated with massive cardiac immune cell infiltration that can lead to heart failure (HF). The purpose of this study was to determine whether high Se diet can attenuate systolic overload-induced cardiopulmonary inflammation and HF. Briefly, transverse aortic constriction (TAC)-induced cardiopulmonary oxidative stress, inflammation, left ventricular (LV) dysfunction, and pulmonary remodeling were determined in male mice fed with either high Se diet or normal Se diet. High Se diet had no detectable effect on LV structure and function in mice under control conditions, but high Se diet significantly protected mice from TAC-induced LV hypertrophy, dysfunction, increase of lung weight, and right ventricular hypertrophy. As compared with mice treated with normal Se diet, high Se diet also reduced TAC-induced LV cardiomyocyte hypertrophy, fibrosis, leukocyte infiltration, pulmonary inflammation, pulmonary fibrosis, and pulmonary micro-vessel muscularization. In addition, high Se diet significantly ameliorated TAC-induced accumulation and activation of pulmonary F4/80+ macrophages, and activation of dendritic cells. Interestingly, high Se diet also significantly attenuated TAC-induced activation of pulmonary CD4+ and CD8+ T cells. Moreover, we found that TAC caused a significant increase in cardiac and pulmonary ROS production, increases of 4-hydroxynonenal (4-HNE) and 3-nitrotyrosine (3-NT), as well as a compensatory increases of LV glutathione peroxidase 1 (GPX1) and 4 (GPX4) in mice fed with normal Se diet. Above changes were diminished in mice fed with high Se diet. Collectively, these data demonstrated that high Se diet significantly attenuated systolic pressure overload-induced cardiac oxidative stress, inflammation, HF development, and consequent pulmonary inflammation and remodeling.

中文翻译：

---

高硒饮食可减轻压力超负荷诱发的心肺氧化应激、炎症和心力衰竭


硒 （Se） 缺乏与克山病的发展有关，克山病是一种与大量心脏免疫细胞浸润相关的心肌病，可导致心力衰竭 （HF）。本研究的目的是确定高 Se 饮食是否可以减轻收缩期超负荷诱导的心肺炎症和 HF。简而言之，在饲喂高 Se 饮食或正常 Se 饮食的雄性小鼠中测定横主动脉收缩 （TAC） 诱导的心肺氧化应激、炎症、左心室 （LV） 功能障碍和肺重塑。在对照条件下，高 Se 饮食对小鼠 LV 结构和功能没有可检测的影响，但高 Se 饮食显着保护小鼠免受 TAC 诱导的 LV 肥大、功能障碍、肺重量增加和右心室肥大的影响。与正常 Se 饮食处理的小鼠相比，高 Se 饮食还减少了 TAC 诱导的 LV 心肌细胞肥大、纤维化、白细胞浸润、肺部炎症、肺纤维化和肺微血管肌肉化。此外，高 Se 饮食显著改善了 TAC 诱导的肺 F4/80+ 巨噬细胞的积累和活化，以及树突状细胞的活化。有趣的是，高 Se 饮食还显着减弱了 TAC 诱导的肺 CD4 + 和 CD8 + T 细胞的激活。此外，我们发现 TAC 导致心脏和肺 ROS 产生显着增加，4-羟基壬烯醛 （4-HNE） 和 3-硝基酪氨酸 （3-NT） 的增加，以及 LV 谷胱甘肽过氧化物酶 1 （GPX1） 和 4 （GPX4） 的代偿性增加在用正常 Se 饮食喂养的小鼠中。在喂食高 Se 饮食的小鼠中，上述变化减少。 总的来说，这些数据表明，高 Se 饮食显着减轻了收缩压超负荷诱导的心脏氧化应激、炎症、HF 发展以及随之而来的肺部炎症和重塑。