The inflammatory response is a self-defense process that fights the pathogen invasion by eliminating harmful stimuli. However, excessive inflammation may disrupt immune homeostasis, even causing chronic inflammation or autoimmune diseases. MicroRNAs (miRNAs) are a crucial regulator that can negatively regulate gene expression and participate in multiple biological processes of growth, development, and immune response in organisms. However, the miRNA-mediated modulation networks of inflammatory responses remain largely unclear in lower vertebrates. In this study, miR-128 was identified as a negative regulator to participate in the NF-κB signaling pathway by targeting TAB2 in miiuy croaker. First, we predicted target genes of miR-128 through the bioinformatics software programs and found that TAB2 is a direct target of miR-128. We also found that miR-128 can inhibit TAB2 expression at the mRNA and protein levels. Besides, upon LPS stimulation, miR-128 inhibits the expression of inflammatory cytokines by targeting TAB2 to avoid excessive inflammation. Particularly, we found that miR-128 can regulate TAB2-mediated NF-κB signaling pathways. In summary, our results indicate that miR-128 plays a critical role in suppressing inflammatory responses by regulating the TAB2-mediated NF-κB signaling pathway in miiuy croaker.

炎症反应是一种自我防御过程，通过消除有害刺激来对抗病原体的入侵。然而，过度的炎症可能会破坏免疫稳态，甚至导致慢性炎症或自身免疫性疾病。MicroRNAs (miRNAs) 是一种重要的调节因子，可以负向调节基因表达并参与生物体中生长、发育和免疫反应的多个生物学过程。然而，在低等脊椎动物中，miRNA 介导的炎症反应调节网络在很大程度上仍不清楚。在本研究中，miR-128 被鉴定为通过靶向 miiuy croaker 中的 TAB2 参与 NF-κB 信号通路的负调节因子。首先，我们通过生物信息学软件程序预测了miR-128的靶基因，发现TAB2是miR-128的直接靶基因。我们还发现 miR-128 可以在 mRNA 和蛋白质水平抑制 TAB2 的表达。此外，在 LPS 刺激下，miR-128 通过靶向 TAB2 来抑制炎症细胞因子的表达，以避免过度炎症。特别是，我们发现 miR-128 可以调节 TAB2 介导的 NF-κB 信号通路。总之，我们的研究结果表明，miR-128 通过调节 TAB2 介导的 NF-κB 信号通路在大黄鱼中发挥关键作用，从而抑制炎症反应。