RNA-seq of a high glucose induced oxidative stress and apoptosis model on primary rat cardiomyocytes

Diabetic hyperglycemia promotes reactive oxygen species (ROS) production to lead to oxidative stress and apoptosis responsible for progressive deterioration of the structure and function of organs. It has been indicated that factors and pathways regulating ROS production and the cellular redox state play a key role in the progression of diabetes and diabetes complications including cardiomyopathy. Recent studies had demonstrated that long non-coding RNAs (lncRNAs) played crucial roles on modulation of oxidative stress and apoptosis activity. In this study, we first established a high glucose induced oxidative stress and apoptosis model on primary rat cardiomyocytes. ROS formation and apoptosis activity were significantly increased at 24h/48h after high glucose stimulation. RNA sequencing analysis was applied to detect differentially expressed lncRNAs during cardiomyocytes oxidative stress and apoptosis.糖尿病性高血糖可促进活性氧（reactive oxygen species, ROS）生成，进而引发氧化应激与细胞凋亡，最终导致器官结构与功能发生进行性恶化。已有研究表明，调控ROS生成与细胞氧化还原状态的各类因子及信号通路，在糖尿病及其包括心肌病在内的并发症的发病进展中发挥关键作用。近期研究证实，长链非编码RNA（long non-coding RNAs, lncRNAs）在调控氧化应激与细胞凋亡活性过程中扮演至关重要的角色。本研究首先在原代大鼠心肌细胞中构建了高糖诱导的氧化应激与细胞凋亡模型；经高糖刺激24小时与48小时后，ROS生成量与细胞凋亡活性均显著升高。本研究通过RNA测序分析，检测了心肌细胞在氧化应激与细胞凋亡过程中差异表达的长链非编码RNA。