Trans fatty acids (TFA) in food can cause liver inflammation. Activation of NOD-like receptor protein-3 (NLRP3) inflammasome is a key factor in the regulation of inflammation. Accumulating evidence suggests that ERS-induced NLRP3 inflammasome activation underlies the pathological basis of various inflammatory diseases, but the precise mechanism has not been fully elucidated. Therefore, this paper focused on TFA, represented by elaidic acid (EA), to investigate the mechanism of liver inflammation. Levels of mRNA and protein were detected by RT-qPCR and Western blotting, the release of proinflammatory cytokines was measured by ELISA, and intracellular Ca²⁺ levels were determined by flow cytometer using Fluo 4-AM fluorescent probes. Our research indicated that EA induced the endoplasmic reticulum stress (ERS) response in Kupffer cells (KCs), accompanied by the activation of the mitogen-activated protein kinase (MAPK) signaling pathway, which resulted in NLRP3 inflammasome formation, and eventually increased the release of inflammatory factors. NLRP3 inflammasome activation was inhibited when KCs were pretreated with ERS inhibitors (4-PBA) and MAPK selective inhibitors. Furthermore, when ERS was blocked, the MAPK pathway was inhibited.

食物中的反式脂肪酸 (TFA) 会引起肝脏炎症。NOD样受体蛋白3（NLRP3）炎症小体的激活是炎症调节的关键因素。越来越多的证据表明，ERS 诱导的 NLRP3 炎症小体激活是各种炎症性疾病的病理基础，但其确切机制尚未完全阐明。因此，本文以反油酸（EA）为代表的TFA，研究肝脏炎症的机制。RT-qPCR和Western blotting检测mRNA和蛋白水平，ELISA检测促炎细胞因子的释放，细胞内Ca ²⁺使用Fluo 4-AM 荧光探针通过流式细胞仪测定水平。我们的研究表明，EA 诱导库普弗细胞 (KCs) 内质网应激 (ERS) 反应，同时激活丝裂原活化蛋白激酶 (MAPK) 信号通路，导致 NLRP3 炎性体形成，并最终增加释放炎症因子。当 KCs 用 ERS ​​抑制剂 (4-PBA) 和 MAPK 选择性抑制剂预处理时，NLRP3 炎症小体的激活受到抑制。此外，当 ERS ​​被阻断时，MAPK 通路被抑制。