As a lipid mediator with important immune function, prostaglandin E₂ (PGE₂) has been widely studied in mammals, whereas its synthetic pathway and immune function in fish have yet to be fully studied. To investigate the regulation of PGE₂ synthetic pathway and inflammatory genes expression by dietary different oils and the underlying relationship, a 10-week feeding experiment and an immune challenge were carried out in marine fish Larimichthys crocea. Replacement of dietary fish oil (FO) with four vegetable oils (VO), including soybean oil, linseed oil, palm oil, and olive oil, all reduced PGE₂ levels, and the decrease of arachidonic acid (ARA, substrate for PGE₂) could account for this decline. Meanwhile, the expression of PGE₂ synthesis related genes was basically upregulated, which seemed to be a feedback regulation, but it cannot compensate the deficiency of ARA. In addition, mRNA expression of inflammatory genes, including interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)α and interferon (IFN)γ was all upregulated in four VO groups compared with FO group, which was the opposite of PGE₂ levels. To verify the inflammatory regulation of PGE₂, an immune challenge was conducted, and PGE₂ alleviated LPS-induced expression of inflammatory genes, including IL-6, TNFα and IFNγ, and the similar downregulation of toll-like receptor (TLR) genes expression revealed that TLR signaling pathway participated in the anti-inflammatory regulation of PGE₂. In conclusion, replacement of dietary FO with four VO (lack of ARA) reduced the levels of PGE₂ that could alleviate LPS-induced inflammatory genes expression via TLR signaling pathway, which could be one of the reasons that VO induced inflammation in marine fish.

作为具有重要免疫功能的脂质介体，前列腺素E ₂（PGE ₂）已在哺乳动物中得到广泛研究，而其合成途径和在鱼类中的免疫功能尚未得到充分研究。为了研究日粮中不同油脂对PGE ₂合成途径和炎症基因表达的调控及其潜在的关系，对海水鱼类大嘴鲷进行了为期10周的喂养实验和免疫攻击。用四种植物油（VO）代替饮食中的鱼油（FO），包括大豆油，亚麻子油，棕榈油和橄榄油，均降低了PGE _2的含量，并降低了花生四烯酸（ARA，PGE _2的底物））可以解释这种下降。同时，PGE ₂合成相关基因的表达基本上调，这似乎是一种反馈调控，但不能弥补ARA的不足。另外，与FO组相比，四个VO组中包括白介素（IL）-1β，IL-6，肿瘤坏死因子（TNF）α和干扰素（IFN）γ在内的炎症基因的mRNA表达均上调。 PGE ₂级。为了验证PGE ₂的炎症调节，进行了免疫攻击，然后PGE ₂减轻LPS诱导的炎性基因（包括IL-6，TNFα和IFNγ）的表达，以及类似的下调Toll样受体（TLR）基因的表达，表明TLR信号通路参与了PGE ₂的抗炎调节。总之，用四个VO（缺乏ARA）替代日粮FO可以降低PGE ₂的水平，该PGE ₂可以通过TLR信号通路减轻LPS诱导的炎症基因表达，这可能是VO引起海水鱼类炎症的原因之一。