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Fabp4 contributes toward regulating inflammatory gene expression and oxidative stress in Ctenopharyngodon idella

文献类型： 外文期刊

作者： Lei, Cai-xia 1 ; Xie, Yu-jing 2 ; Li, Sheng-jie 1 ; Jiang, Peng 2 ; Du, Jin-xing 2 ; Tian, Jing-jing 2 ;

作者机构： 1.Chinese Acad Fishery Sci, Pearl River Fisheries Res Inst, Key Lab Aquat Anim Immune Technol Guangdong Prov, Guangzhou 510380, Peoples R China

2.Chinese Acad Fishery Sci, Pearl River Fisheries Res Inst, Minist Agr & Rural Affairs, Key Lab Trop & Subtrop Fishery Resource Applicat, Guangzhou 510380, Peoples R China

3.Shanghai Ocean Univ, Coll Fisheries & Life Sci, Shanghai 201306, Peoples R China

关键词： fabp4; Reactive oxygen species; Inflammation; Ctenopharyngodon idella

期刊名称：COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY B-BIOCHEMISTRY & MOLECULAR BIOLOGY （ 影响因子：2.495； 五年影响因子：2.567 ）

ISSN： 1096-4959

年卷期： 2022 年 259 卷

页码：

收录情况： SCI

摘要： Fatty acid-binding protein (Fabp)-4 is a member of the FABP family. Mammalian fabp4 has been demonstrated to involve in inflammation and immunity, whereas the related data of fish fabp4 remain limited. Therefore, we further investigated the effects of fabp4 on immunity in Ctenopharyngodon idella. The fabp4 sequence spanned 405 bp was cloned first, sharing high identity to fabp4 from other fish and mammals. Fabp4 expression was the highest in the adipose tissue, followed by the heart, muscle, and liver. In vivo, lipopolysaccharide (LPS) triggered the expression of fabp4, toll-like receptor (tlr)-22, interleukin (il)-1 beta, and tumor necrosis factor (tnf)-alpha in the kidney and spleen. In vitro, exposing C. idella CIK cells to LPS decreased their viability, and the expression of fabp4 was also increased by LPS. However, BMS309403, an inhibitor of FABP4, mitigated these effects. Furthermore, treating the cells with LPS or fabp4 overexpression plasmids resulted in reactive oxygen species (ROS) generation and upregulation of inflammatory genes expression, including tlr22, type-I interferon (ifn-1), interferon regulatory factor (irf)-7, tnf alpha, il-1 beta, and interferon-beta promoter stimulator 1. These effects were ameliorated by preincubation with BMS309403. Moreover, incubating the cells with glutathione reduced the production of ROS and the expression of inflammatory genes that were evoked by LPS and plasmid treatments. These results showed that fabp4 acts as a pro-inflammatory molecule via elevating ROS levels, providing a novel understanding of the molecular regulation of innate immunity in teleosts.

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