Environmental pollutant cadmium (Cd) can cause macrophage dysfunction, and the imbalance of M1/M2 is involved in the process of tissue fibrosis. In order to explore the effect of subacute CdCl₂ exposure on pig lung tissue fibers and its mechanism, based on the establishment of this model, ICP-MS, H&E staining, Masson staining, Immunofluorescence, RT-PCR, and Western Blot methods were used to detect related indicators. The results found that lung tissue fibrosis, Cd content significantly increased, lung tissue ion disturbance, miR-20a-3p down-regulation, M1/M2 imbalance, LXA4/FPR2 content decreased, MDA content increased, NF-κB/NLRP3, TGFβ pathway, PPARγ/Wnt pathway activated, and the expression of fibrosis-related factors increased. The above results indicate that subacute CdCl₂ exposure increase Cd content in the pig lungs, which leads to M1/M2 imbalance and down-regulates the content of LXA4/FPR2, further activates the oxidative stress/NF-κB/NLRP3 pathway, thereby activating the TGFβ and PPARγ/Wnt pathways to induce fibrosis. This study aims to reveal the toxic effects of CdCl₂ and will provide new insights into the toxicology of Cd.

环境污染物镉（Cd）可引起巨噬细胞功能障碍，M1/M2失衡参与组织纤维化过程。为探讨亚急性CdCl ₂暴露对猪肺组织纤维的影响及其作用机制，在建立该模型的基础上，采用ICP-MS、H&E染色、Masson染色、免疫荧光、RT-PCR、Western Blot等方法检测相关指标。结果发现肺组织纤维化、Cd含量显着升高、肺组织离子紊乱、miR-20a-3p下调、M1/M2失衡、LXA4/FPR2含量降低、MDA含量升高、NF-κB/NLRP3、TGFβ通路，PPARγ/Wnt通路激活，纤维化相关因子表达增加。以上结果表明亚急性 CdCl ₂暴露增加猪肺中Cd含量，导致M1/M2失衡，下调LXA4/FPR2含量，进一步激活氧化应激/NF-κB/NLRP3通路，从而激活TGFβ和PPARγ/Wnt通路，诱发纤维化。本研究旨在揭示 CdCl ₂的毒性作用，并将为 Cd 的毒理学提供新的见解。