大鼠放射性肝损伤分子应答及机制研究.docxVIP

大鼠放射性肝损伤分子应答及机制研究 摘要： 本文旨在研究大鼠放射性肝损伤的分子应答及机制。通过建立大鼠放射性肝损伤模型，采用实时荧光定量PCR、Western blot、免疫组化、转录组测序等多种技术方法，对放射性肝损伤后大鼠肝脏组织中一些重要的分子（包括转录因子、细胞凋亡相关因子、细胞增殖相关因子等）的变化进行了全面分析和研究。结果表明，放射性损伤后大鼠肝脏组织中多种分子表达水平出现显著变化，其中NF-κB、JNK、p53、PPARα等转录因子显著上调，Bax、Caspase-3、Caspase-9等凋亡相关因子显著上调，同时p21、cyclin D1等增殖相关因子显著下调。通过分析转录组测序结果，发现放射性肝损伤后大鼠肝组织中多个信号通路（包括细胞凋亡、细胞周期调节、氧化应激反应、炎症反应等）被激活，同时多个代谢途径（包括脂质代谢、葡萄糖代谢及细胞信号传导等）也被受到严重影响。研究结果拓展了对放射性肝损伤的认知，为探索放射性肝损伤防治措施提供了重要的理论依据。 关键词：放射性肝损伤；肝组织；转录因子；细胞凋亡；细胞周期调节 Abstract： The purpose of this study is to investigate the molecular response and mechanism of radiation-induced liver injury in rats. By establishing a rat model of radiation-induced liver injury, various techniques including real-time fluorescent quantitative PCR, Western blot, immunohistochemistry, transcriptome sequencing, etc. were used to comprehensively analyze and study the changes of some important molecules (including transcription factors, apoptosis-related factors, cell proliferation-related factors, etc.) in the liver tissue of rats after radiation-induced liver injury. The results showed that the expression levels of multiple molecules in the liver tissues of rats after radiation injury were significantly changed, including upregulation of transcription factors such as NF-κB, JNK, p53, PPARα, upregulation of apoptosis-related factors such as Bax, Caspase-3, Caspase-9, and significant downregulation of proliferation-related factors such as p21, cyclin D1. By analyzing the sequencing results of the transcriptome, it was found that multiple signal pathways (including cell apoptosis, cell cycle regulation, oxidative stress response, inflammation response, etc.) were activated in the liver tissues of rats after radiation-induced liver injury, and multiple metabolic pathways (including lipid metabolism, glucose metabolism, and cell signaling) were also severely affected. The results of this study have expanded our understanding of radiation-induced liver injury and provided important theoretical b