医学文献中英文对照

医学文献中英文对照

动脉粥样硬化所导致的心脑血管疾病是目前发病率和死亡率较高的疾病之一。在动脉粥样硬化的形成过程中, 内皮细胞病变是其中极其重要的因素，最显著的变化是动脉内皮功能紊乱, 血管内皮细胞的损伤和功能改变是动脉粥样硬化发生的起始阶段。Cardiovascular and cerebrovascular disease caused by atherosclerosis is one of diseases with higher mortality and morbidity at present . In the formation of atherosclerosis, the endothelial cell lesion is one of the most important factors, in which, the most significant change is endothelial dysfunction. In addition, the injuries and the changes of vascular endothelial cells are the initial factors of atherosclerosis.

许多因素会导致血管内皮细胞受损, 主要包括脂多糖( Lipopolysaccharides，LPS)、炎症介质、氧自由基等。其中脂多糖因其广泛的生物学作用, 越来越引起研究者的关注。LPS 是一种炎症刺激物, 是革兰阴性杆菌细胞壁的主要组成成分，其通过刺激血管内皮细胞，引起其相关细胞因子和炎性因子的表达紊乱，尤其是Ca2+ 和活性氧簇（Reactive Oxygen Species，ROS）的合成和释放发生改变诱导细胞氧化应激内环境紊乱。大量研究表明, LPS直接参与动脉粥样硬化的形成过程, 特别是动脉粥样硬化血管炎症的初始阶段, LPS可通过直接作用或间接影响的方式激活并损伤内皮细胞,

从而引起血管内皮细胞形态与功能的改变。

Many factors induce vascular endothelial cell damage, including lipopolysaccharides (LPS), inflammatory mediators and oxygen free radical. Of which, LPS, due to its general biologic effects, is paid more and more attention from researchers. As a component of the outer membrane outer Gram-negative bacteria, LPS is an inflammatory stimulus, which induces disorder expression of apoptosis-related factors, by stimulating vascular endothelial cells, especially the releases of Ca2? And reactive oxygen species (ROS) induce oxidative stress in human umbilical vein endothelial cells (HUVECs) . Previous studies have indicated that LPS was directly involved in the process of atherosclerosis, especially in the initial stage of vascular inflammation, and damaged endothelial cells, causing the morphological and functional change of vascular endothelial cells.

线粒体是由内、外双层膜组成的重要细胞器，是细胞呼吸和氧化磷酸化的主要场所，不仅为细胞的生命活动提供所需能量；而且线粒体结构功能受损与心血管疾病的发生密切相关。线粒体在细胞中起着很多重要作用，它不仅通过氧化磷酸化为细胞提供能量，同时也是凋亡信号的调节器和放大器。线粒体途径在细胞凋亡中至关重要，是细胞不可逆的进入凋亡程序的前兆。

Mitochondria, composing of the inner membrane and outer membrane, is not only a crucial place for generating cellular energy by cellular respiration and oxidative phosphorylation (OXPHO), but also involved in the endothelial cells apoptotic progression of atherosclerosis. Mitochondrial pathway of apoptosis is an essential signaling, which is the precursor of irreversible apoptosis。

实验表明磷酸肌酸通过线粒体氧化磷酸化信号通路对抗LPS诱导的HUVECs细胞起到重要的作用。磷酸肌酸可以通过稳定细胞整体能量代谢、ATP合成酶和线粒体肌酸激酶（CKmt），尤其是对细胞线粒体呼吸链FAD途径的显著影响来对抗LPS诱导的HUVECs细胞凋亡，提示磷酸肌酸可能通过保护内皮细胞功能对动脉粥样硬化或其他验证相关的心血管疾病起到治疗作用。

Our present study strongly suggests that PCr plays a vital role in LPS-induced HUVECs through mitochondrial oxidative phosphorylation signaling pathway. PCr improves creatine shuttle of HUVECs through directly enhanced ATP synthase and mitochondrial creatine kinase, and reactived FADH2pathway in mitochondrial respiration chain. Our work provides new insight for the noval antiapoptotic effects of PCr in endothelial cells, which may give a pharmacological basis for the clinical application of PCr for treatment of