氧化鱼油对草鱼肠道黏膜抗氧化应激通路基因表达水平的影响

为了探讨氧化鱼油对草鱼肠道黏膜损伤后, 参与抗氧化应激的基因通路及其通路基因表达活性的变化,以草鱼为试验对象, 灌喂氧化鱼油7d后, 采集肠道黏膜组织并提取总RNA, 采用RNA-seq方法, 进行了氧化鱼油组和正常鱼油组草鱼肠道黏膜基因注释、IPA基因通路分析和基因表达活性差异分析。结果显示, 组织切片观察发现氧化鱼油导致草鱼肠道黏膜出现严重的损伤; 肠道黏膜中具有较为完整的Keap1-Nrf2-ARE基因调控通路。肠道黏膜在受到氧化鱼油的氧化损伤作用后, 激活了细胞的抗氧化损伤保护机制, 使NRF2介导的氧化应激反应通路基因差异表达显著性地上调, 并导致了下游的GSH/GSTs通路基因差异表达显著性上调, 促进了GSH的生物合成和GSTs的抗氧化作用; 导致Keap1-Nrf2-ARE信号通路下游的热休克蛋白和泛素-蛋白酶体通路基因差异表达显著性上调, 清除受损伤蛋白质, 保护细胞结构完整性。研究表明, 上述三类抗氧化应激通路构成了对肠道黏膜损伤细胞、损伤蛋白质的降解系统和清除系统, 显示其对肠道黏膜组织和黏膜细胞的保护、修复发挥了重要的作用。

EFFECTS OF OXIDIZED FISH OIL ON OXIDATIVE STRESS PATHWAYS OF INTESTINAL MUCOSA OF GRASS CARP (CTENOPHARYNGODON IDELLUS)

To evaluate effects of the oxidized fish oil on the antioxidative stress pathways of intestine, grass carp Cteno-pharyngodon idellus were fed oxidized fish oil and normal fish oil for 7d before collecting intestinal mucosa for histo-logy and RNA-seq. The gene differential expression, the gene annotation and IPA gene pathway were analyzed. Severe damage was observed in the intestine of grass carp by oxidized fish oil. The RAN-seq results indicated increased“Keap1-Nrf2-ARE”signal pathway and GSH/GSTs pathway by oxidized fish oil treatment. The heat shock proteins and ubiquitin-proteasome system genes were also significantly up-regulated. The activations of these three anti-oxida-tion pathway systems serve the main components to remove the damaged cells and decompose the harmful proteins, which play the essential roles to protect the intestinal mucosa tissue and its cells and to repair the intestinal mucosa re-sponse to the oxidation injury.