Abstract：
The study aimed to elucidate the mechanisms by which sulfur dioxide (SO2) alleviates organ damage during sepsis using RNA-Seq technology. A cecal ligation and puncture (CLP) sepsis model was established in rats, and the effects of SO2 treatment on organ damage were assessed through histopathological examinations. RNA-Seq was performed to analyze differentially expressed genes (DEGs), and subsequent functional annotations and enrichment analyses were conducted. The CLP model successfully induced sepsis symptoms in rats. Histopathological evaluation revealed that SO2 treatment considerably reduced tissue damage across the heart, kidney, liver, and lungs. RNA-Seq identified 950 DEGs between treated and untreated groups, with significant enrichment in genes associated with ribosomal and translational activities, amino acid metabolism, and PI3K-Akt signaling. Furthermore, gene set enrichment analysis (GSEA) showcased enrichments in pathways related to transcriptional regulation, cellular migration, proliferation, and calcium-ion binding. In conclusion, SO2 effectively mitigates multi-organ damage induced by CLP sepsis, potentially through modulating gene expression patterns related to critical biological processes and signaling pathways. These findings highlight the therapeutic promise of SO2 in managing sepsis-induced organ damage.
摘要：
该研究旨在阐明使用RNA-Seq技术在脓毒症期间二氧化硫（SO2）减轻器官损伤的机制。建立大鼠盲肠结扎穿孔(CLP)脓毒症模型,并通过组织病理学检查评估SO2处理对器官损伤的影响。RNA-Seq用于分析差异表达基因（DEG），并进行了随后的功能注释和富集分析。CLP模型成功诱发大鼠脓毒症症状。组织病理学评估显示，SO2治疗大大减少了整个心脏的组织损伤，肾,肝脏,还有肺.RNA-Seq鉴定了处理组和未处理组之间的950个DEG，与核糖体和翻译活性相关的基因显著富集，氨基酸代谢，和PI3K-Akt信号。此外，基因集富集分析(GSEA)展示了与转录调控相关的途径的富集，细胞迁移，扩散,和钙离子结合。总之,SO2有效缓解CLP脓毒症引起的多器官损伤，可能通过调节与关键生物过程和信号通路相关的基因表达模式。这些发现强调了SO2在治疗败血症引起的器官损伤方面的治疗前景。
