PDF(Pubmed)
Abstract：
UNASSIGNED: Advanced glycation end products (AGEs) are featured metabolites associated with diabetic cardiomyopathy which is characterized by heart failure caused by myocyte apoptosis. Selenium was proved cardioprotective. This study was aimed at investigating the therapeutic effects and underlying mechanisms of selenium supplementation on AGE-induced heart failure.
UNASSIGNED: Rats and primary myocytes were exposed to AGEs. Selenium supplementation was administrated. Cardiac functions and myocyte apoptosis were evaluated. Oxidative stress was assessed by total antioxidant capacity (TAC), reactive oxygen species (ROS) generation, and GPX activity. Expression levels of DNA methyltransferases (DNMTs) and glutathione peroxidase 1 (GPX1) were evaluated. DNA methylation of the GPX1 promoter was analyzed.
UNASSIGNED: AGE exposure elevated intracellular ROS generation, induced myocyte apoptosis, and impaired cardiac functions. AGE exposure increased DNMT1 and DNMT2 expression, leading to the reduction of GPX1 expression and activity in the heart. Selenium supplementation decreased DNMT2 expression, recovered GPX1 expression and activity, and alleviated intracellular ROS generation and myocyte apoptosis, resulting in cardiac function recovery. DNA methylation analysis in primary myocytes indicated that selenium supplementation or DNMT inhibitor AZA treatment reduced DNA methylation of the GPX1 gene promoter. Selenium supplementation and AZA administration showed synergic inhibitory effect on GPX1 gene promoter methylation.
UNASSIGNED: Selenium supplementation showed cardioprotective effects on AGE-induced heart failure by suppressing ROS-mediated myocyte apoptosis. Selenium supplementation suppressed ROS generation by increasing GPX1 expression via inhibiting DNMT2-induced GPX1 gene promoter DNA methylation in myocytes exposed to AGEs.
UNASSIGNED: Rats and primary myocytes were exposed to AGEs. Selenium supplementation was administrated. Cardiac functions and myocyte apoptosis were evaluated. Oxidative stress was assessed by total antioxidant capacity (TAC), reactive oxygen species (ROS) generation, and GPX activity. Expression levels of DNA methyltransferases (DNMTs) and glutathione peroxidase 1 (GPX1) were evaluated. DNA methylation of the GPX1 promoter was analyzed.
UNASSIGNED: AGE exposure elevated intracellular ROS generation, induced myocyte apoptosis, and impaired cardiac functions. AGE exposure increased DNMT1 and DNMT2 expression, leading to the reduction of GPX1 expression and activity in the heart. Selenium supplementation decreased DNMT2 expression, recovered GPX1 expression and activity, and alleviated intracellular ROS generation and myocyte apoptosis, resulting in cardiac function recovery. DNA methylation analysis in primary myocytes indicated that selenium supplementation or DNMT inhibitor AZA treatment reduced DNA methylation of the GPX1 gene promoter. Selenium supplementation and AZA administration showed synergic inhibitory effect on GPX1 gene promoter methylation.
UNASSIGNED: Selenium supplementation showed cardioprotective effects on AGE-induced heart failure by suppressing ROS-mediated myocyte apoptosis. Selenium supplementation suppressed ROS generation by increasing GPX1 expression via inhibiting DNMT2-induced GPX1 gene promoter DNA methylation in myocytes exposed to AGEs.
摘要：
未经证实：晚期糖基化终产物（AGEs）是与糖尿病性心肌病相关的代谢产物，其特征是由心肌细胞凋亡引起的心力衰竭。硒被证明具有心脏保护作用。这项研究旨在研究补充硒对AGE诱导的心力衰竭的治疗效果和潜在机制。
未经授权：将大鼠和原代心肌细胞暴露于AGEs。给予硒补充剂。评价心功能和心肌细胞凋亡。氧化应激通过总抗氧化能力(TAC)来评估，活性氧（ROS）的产生，和GPX活性。评估DNA甲基转移酶（DNMT）和谷胱甘肽过氧化物酶1（GPX1）的表达水平。分析GPX1启动子的DNA甲基化。
未经批准：AGE暴露会增加细胞内ROS的产生，诱导心肌细胞凋亡，心脏功能受损.AGE暴露会增加DNMT1和DNMT2的表达，导致心脏中GPX1表达和活性降低。补硒降低DNMT2表达，恢复GPX1的表达和活性，并减轻细胞内ROS的产生和心肌细胞凋亡，导致心脏功能恢复。原代肌细胞中的DNA甲基化分析表明，硒补充或DNMT抑制剂AZA处理降低了GPX1基因启动子的DNA甲基化。硒补充和AZA给药对GPX1基因启动子甲基化具有协同抑制作用。
UNASSIGNED：补充硒通过抑制ROS介导的心肌细胞凋亡对AGE诱导的心力衰竭具有心脏保护作用。硒补充通过抑制暴露于AGEs的肌细胞中DNMT2诱导的GPX1基因启动子DNA甲基化增加GPX1表达来抑制ROS的产生。
未经授权：将大鼠和原代心肌细胞暴露于AGEs。给予硒补充剂。评价心功能和心肌细胞凋亡。氧化应激通过总抗氧化能力(TAC)来评估，活性氧（ROS）的产生，和GPX活性。评估DNA甲基转移酶（DNMT）和谷胱甘肽过氧化物酶1（GPX1）的表达水平。分析GPX1启动子的DNA甲基化。
未经批准：AGE暴露会增加细胞内ROS的产生，诱导心肌细胞凋亡，心脏功能受损.AGE暴露会增加DNMT1和DNMT2的表达，导致心脏中GPX1表达和活性降低。补硒降低DNMT2表达，恢复GPX1的表达和活性，并减轻细胞内ROS的产生和心肌细胞凋亡，导致心脏功能恢复。原代肌细胞中的DNA甲基化分析表明，硒补充或DNMT抑制剂AZA处理降低了GPX1基因启动子的DNA甲基化。硒补充和AZA给药对GPX1基因启动子甲基化具有协同抑制作用。
UNASSIGNED：补充硒通过抑制ROS介导的心肌细胞凋亡对AGE诱导的心力衰竭具有心脏保护作用。硒补充通过抑制暴露于AGEs的肌细胞中DNMT2诱导的GPX1基因启动子DNA甲基化增加GPX1表达来抑制ROS的产生。
