毛萼乙素通过NF-κB/NLRP3信号通路抑制巨噬细胞的M1极化来减轻自身免疫性心肌炎。
Erianin alleviates autoimmune myocarditis by suppressing the M1 polarization of macrophages via the NF-κB/NLRP3 signaling pathway.
作者信息
Liu Wenhu, Mao Yuyuan, Li Han, Hu Jing, Gan Ting, Wang Yan, Wang Ya, Wang Zhaohui
机构信息
Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Hubei Key Laboratory of Biological Targeted Therapy, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Hubei Provincial Engineering Research Center of Immunological Diagnosis and Therapy for Cardiovascular Diseases, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Department of Infectious Diseases, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
出版信息
Eur J Pharmacol. 2025 Mar 5;990:177292. doi: 10.1016/j.ejphar.2025.177292. Epub 2025 Jan 23.
BACKGROUND
Myocarditis tends to lead to a poor prognosis, but there are no satisfactory preventive or therapeutic strategies. Erianin, a natural benzene compound, has been found to have antioxidant and anti-inflammatory effects. However, the effects of erianin on myocarditis remain unclear. This study aimed to investigate the effects of erianin on myocarditis and the involved mechanisms.
METHODS
We developed a mouse model of experimental autoimmune myocarditis (EAM) and assessed the effects of erianin using echocardiography and pathological staining. In vitro experiments, flow cytometry, immunofluorescence and western blotting were performed to determine whether erianin inhibits macrophage activation.
RESULTS
Erianin ameliorated cardiac fibrosis and cardiac dysfunction and reduced the percentage of M1-type macrophages and the secretion of inflammatory factors. Mechanistically, erianin inhibits the activation of the NLRP3 inflammasome by inhibiting the NF-κB pathway.
CONCLUSION
Erianin could be a natural therapeutic drug for EAM by inhibiting NLRP3 activation and M1 macrophage-mediated inflammation through the IκBα/NF-κB pathway.
背景
心肌炎往往导致预后不良，但尚无令人满意的预防或治疗策略。毛兰素是一种天然苯化合物，已被发现具有抗氧化和抗炎作用。然而，毛兰素对心肌炎的影响尚不清楚。本研究旨在探讨毛兰素对心肌炎的影响及其相关机制。
方法
我们建立了实验性自身免疫性心肌炎（EAM）小鼠模型，并使用超声心动图和病理染色评估毛兰素的作用。在体外实验中，进行了流式细胞术、免疫荧光和蛋白质印迹分析，以确定毛兰素是否抑制巨噬细胞活化。
结果
毛兰素改善了心脏纤维化和心脏功能障碍，降低了M1型巨噬细胞的百分比和炎症因子的分泌。机制上，毛兰素通过抑制NF-κB途径抑制NLRP3炎性小体的活化。
结论
毛兰素可能是一种治疗EAM的天然药物，它通过IκBα/NF-κB途径抑制NLRP3活化和M1巨噬细胞介导的炎症。
Zotero 插件