Suppr超能文献

丁酸乙酯通过破坏细胞外基质重塑抑制成年斑马鱼的尾鳍再生。

Ethyl butyrate inhibits caudal fin regeneration in adult zebrafish by disrupting extracellular matrix remodeling.

机构信息

Jiangxi Province Key Laboratory of Synthetic Pharmaceutical Chemistry, School of Geography and Environmental Engineering, Gannan Normal University, Shiyuan South Rd, Ganzhou, Jiangxi 341000, China.

School of Medicine, Tongji University, Shanghai 200000, China.

出版信息

Aquat Toxicol. 2024 Nov;276:107111. doi: 10.1016/j.aquatox.2024.107111. Epub 2024 Sep 30.

Abstract

Wound healing and tissue regeneration are influenced by a variety of factors. Adverse lifestyle habits, such as excessive alcohol consumption, delay wound healing and increase the risk of secondary infections. Ethyl butyrate is a common food additive widely used to enhance the aroma of alcoholic beverages. This additive is generally considered harmless to human health in both industrial and domestic settings. However, the ecotoxicity and its effects on wound healing have not been elucidated. In this study, we used zebrafish as the experimental animal, and the caudal fins were amputated to explore the effects of ethyl butyrate on wound healing and tissue regeneration. The effect of ethyl butyrate on blastema and bone regeneration and its impact on the transcriptional levels of regeneration-related genes and inflammation-related genes were evaluated. RNA-seq was conducted to determine the differentially expressed genes (DEGs) between the treatment and the control groups. KEGG and GO analysis was conducted to explore the functions of DEGs. Significantly enriched GO terms and KEGG pathways were identified to explore the molecular mechanism underlying the inhibition of zebrafish caudal fin regeneration by ethyl butyrate. The results demonstrated that ethyl butyrate significantly inhibited the regeneration of zebrafish caudal fins, including blastema and bone regeneration. Ethyl butyrate exposure significantly downregulated the expression of genes associated with bone and blastema regeneration and inflammation response. KEGG and GO functional analyses revealed that the DEGs were associated with significant enrichment of extracellular matrix-receptor interactions. Ethyl butyrate treatment downregulated the expression of most extracellular matrix-related genes. These findings indicate that ethyl butyrate potentially modulates pathways associated with the structure, adhesion, modification, and degradation of the extracellular matrix, thereby disrupting extracellular matrix remodeling, inhibiting wound inflammation, impairing blastema and bone regeneration and ultimately hindering caudal fin regeneration. In summary, the findings demonstrate that ethyl butyrate disrupts extracellular matrix remodeling and inhibits the regeneration of zebrafish caudal fins. These results provide valuable insights into the rational use of ethyl butyrate and further investigation of wound healing mechanisms.

摘要

创伤愈合和组织再生受多种因素影响。不良的生活习惯,如过度饮酒,会延迟伤口愈合并增加二次感染的风险。丁酸乙酯是一种常见的食品添加剂,广泛用于增强酒精饮料的香气。在工业和家庭环境中,通常认为这种添加剂对人体健康无害。然而,其生态毒性及其对创伤愈合的影响尚未阐明。在本研究中,我们使用斑马鱼作为实验动物,通过切除尾鳍来探索丁酸乙酯对创伤愈合和组织再生的影响。评估了丁酸乙酯对芽基和骨再生的影响及其对再生相关基因和炎症相关基因转录水平的影响。进行 RNA-seq 以确定处理组和对照组之间的差异表达基因 (DEGs)。进行 KEGG 和 GO 分析以探索 DEGs 的功能。鉴定出显著富集的 GO 术语和 KEGG 途径,以探讨丁酸乙酯抑制斑马鱼尾鳍再生的分子机制。结果表明,丁酸乙酯显著抑制了斑马鱼尾鳍的再生,包括芽基和骨再生。丁酸乙酯暴露显著下调了与骨和芽基再生以及炎症反应相关的基因表达。KEGG 和 GO 功能分析表明,DEGs 与细胞外基质-受体相互作用显著富集有关。丁酸乙酯处理显著下调了大多数细胞外基质相关基因的表达。这些发现表明,丁酸乙酯可能调节与细胞外基质的结构、粘附、修饰和降解相关的途径,从而破坏细胞外基质重塑,抑制伤口炎症,损害芽基和骨再生,最终阻碍尾鳍再生。总之,这些结果表明丁酸乙酯破坏了细胞外基质重塑并抑制了斑马鱼尾鳍的再生。这些结果为合理使用丁酸乙酯提供了有价值的见解,并进一步探讨了伤口愈合机制。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验