Zeng Wenxiang, He Shiqiao, Zhao Ying, Jiang Minjian, Wang Wenla, Yang Limeng, Du Weibin, Zhuang Wei
The Third Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou 310053, China.
Hangzhou Xiaoshan Hospital of Traditional Chinese Medicine, Hangzhou 311200, China.
Toxics. 2024 Nov 22;12(12):840. doi: 10.3390/toxics12120840.
Microplastics (MPs) represent an emerging pollutant capable of entering the human body through the respiratory and digestive systems, thereby posing significant health risks. Systemic lupus erythematosus (SLE) is a complex autoimmune disease that affects multiple organ systems, often presenting with polyarticular joint manifestations. Despite its relevance, there is currently limited research on the impact of MPs on lupus arthritis. This study aims to investigate the effects of MPs on joint inflammation in SLE. / mice exhibit SLE similar to that of humans. We administered either 0.5 mg/kg or 5 mg/kg of MPs to 8-week-old female / mice via oral ingestion. Our findings indicate that exposure to MPs can lead to synovial damage, adversely affecting the morphology and function of the knee joint, along with increased oxidative stress, apoptosis, synovial fibrosis, and the secretion of inflammatory cytokines. Notably, MPs significantly enhanced synovial cell pyroptosis by upregulating the expression of NLRP3, CASPASE-1, GSDMD, IL-1β, and IL-18. Mechanistic analyses further demonstrated that MPs exposure activates the NF-κB and NRF2/KEAP1 signaling pathways. Overall, our in vivo findings suggest that MPs exposure promotes synovial cell pyroptosis through increased oxidative stress and NF-κB signaling, thereby disrupting the structure and function of synovial tissue. This research provides new insights into the synovial damage associated with MPs exposure.
微塑料（MPs）是一种新兴污染物，能够通过呼吸系统和消化系统进入人体，从而带来重大健康风险。系统性红斑狼疮（SLE）是一种复杂的自身免疫性疾病，会影响多个器官系统，常表现为多关节的关节症状。尽管其具有相关性，但目前关于微塑料对狼疮性关节炎影响的研究有限。本研究旨在调查微塑料对系统性红斑狼疮关节炎症的影响。/小鼠表现出与人类相似的系统性红斑狼疮。我们通过口服给8周龄雌性/小鼠施用0.5毫克/千克或5毫克/千克的微塑料。我们的研究结果表明，接触微塑料会导致滑膜损伤，对膝关节的形态和功能产生不利影响，同时增加氧化应激、细胞凋亡、滑膜纤维化以及炎性细胞因子的分泌。值得注意的是，微塑料通过上调NLRP3、CASPASE-1、GSDMD、IL-1β和IL-18的表达，显著增强了滑膜细胞焦亡。机制分析进一步表明，接触微塑料会激活NF-κB和NRF2/KEAP1信号通路。总体而言，我们的体内研究结果表明，接触微塑料会通过增加氧化应激和NF-κB信号传导促进滑膜细胞焦亡，从而破坏滑膜组织的结构和功能。这项研究为与接触微塑料相关的滑膜损伤提供了新的见解。
