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二氧化硫减轻盲肠结扎穿刺诱导的脓毒症大鼠的器官损伤和炎症反应。

Sulfur Dioxide Alleviates Organ Damage and Inflammatory Response in Cecal Ligation and Puncture-Induced Sepsis Rat.

作者信息

Li Bin, Jiao Keping, Wang Binsheng, Gou Hongzhong, Chai Chen, Lu Yan, Liu Jian

机构信息

Department of General Surgery, The First Hospital of Lanzhou University, Lanzhou, 73000, Gansu, China.

The First Clinical Medical College of Lanzhou University, Lanzhou, 73000, Gansu, China.

出版信息

Mol Biotechnol. 2025 May;67(5):1908-1923. doi: 10.1007/s12033-024-01168-9. Epub 2024 Jun 3.

Abstract

The study aimed to elucidate the mechanisms by which sulfur dioxide (SO) 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 SO 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 SO 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, SO 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 SO in managing sepsis-induced organ damage.

摘要

该研究旨在利用RNA测序技术阐明二氧化硫(SO)减轻脓毒症期间器官损伤的机制。在大鼠中建立了盲肠结扎穿孔(CLP)脓毒症模型,并通过组织病理学检查评估SO治疗对器官损伤的影响。进行RNA测序以分析差异表达基因(DEG),随后进行功能注释和富集分析。CLP模型成功诱导了大鼠的脓毒症症状。组织病理学评估显示,SO治疗显著减轻了心脏、肾脏、肝脏和肺组织的损伤。RNA测序在治疗组和未治疗组之间鉴定出950个DEG,这些基因在与核糖体和翻译活动、氨基酸代谢以及PI3K-Akt信号传导相关的基因中显著富集。此外,基因集富集分析(GSEA)显示在与转录调控、细胞迁移、增殖和钙离子结合相关的途径中存在富集。总之,SO可有效减轻CLP脓毒症诱导的多器官损伤,可能是通过调节与关键生物学过程和信号通路相关的基因表达模式。这些发现突出了SO在治疗脓毒症诱导的器官损伤方面的治疗前景。

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