School of Basic Medical Sciences, Shanxi Medical University, Jinzhong 030619, China; Key Laboratory of Cellular Physiology (Shanxi Medical University), Ministry of Education, and Shanxi Key Laboratory of Cellular Physiology, Taiyuan 030001, China.
School of Basic Medical Sciences, Shanxi Medical University, Jinzhong 030619, China.
Int Immunopharmacol. 2024 Dec 5;142(Pt A):113103. doi: 10.1016/j.intimp.2024.113103. Epub 2024 Sep 6.
No approved effective therapy for non-alcoholic steatohepatitis (NASH) is currently available. Trichinella spiralis (T. spiralis) infection and their products have positive impact on several metabolic diseases. Considering, we firstly investigated the effects of the T. spiralis-derived Excretory-Secretory antigens (ESA) on high fat diet (HFD)-induced NASH mouse models. To further elucidate the mechanism of action, HepG2 cells were incubated with palmitic acid (PA) to construct NASH-like cell model, and then the culture medium supernatant collected from ESA-treated macrophages was applied to intervene the cell model in vitro. In NASH mouse models, ESA significantly alleviated hepatic steatosis and hepatic inflammation, as reflected by reducing pro-inflammatory cytokines and inactivating TLR4/MYD88/NF-κB pathway and NLRP3 inflammasome. Meanwhile, the HFD-induced oxidative stress was restored by ESA through lessening the level of MDA, increasing the activity of T-SOD and enhancing Nrf2 signaling-related proteins, including p-Nrf2, NQO1, HO-1, GPX4, and p-AMPK. Notably, ESA preferentially promoted macrophages polarization toward M2 anti-inflammatory phenotype in vivo and vitro. Moreover, in vitro, intervention of PA-treated HepG2 cells with medium supernatant of ESA-treated macrophages attenuated lipid accumulation, inflammation, as well as oxidative stress. In conclusion, T. spiralis-derived ESA may serve as a novel promising candidate for the treatment of NASH via its properties of driving macrophage anti-inflammatory activity.
目前尚无针对非酒精性脂肪性肝炎(NASH)的有效治疗方法。旋毛虫(T. spiralis)感染及其产物对多种代谢性疾病有积极影响。考虑到这一点,我们首先研究了旋毛虫衍生的排泄分泌抗原(ESA)对高脂肪饮食(HFD)诱导的 NASH 小鼠模型的影响。为了进一步阐明其作用机制,我们将 HepG2 细胞与棕榈酸(PA)孵育以构建 NASH 样细胞模型,然后将来自 ESA 处理的巨噬细胞的培养上清液应用于体外干预细胞模型。在 NASH 小鼠模型中,ESA 通过减少促炎细胞因子并激活 TLR4/MYD88/NF-κB 途径和 NLRP3 炎性体,显著减轻肝脂肪变性和肝炎症,从而发挥作用。同时,ESA 通过降低 MDA 水平、增加 T-SOD 活性以及增强 Nrf2 信号相关蛋白(包括 p-Nrf2、NQO1、HO-1、GPX4 和 p-AMPK)来恢复 HFD 诱导的氧化应激。值得注意的是,ESA 优先促进体内和体外巨噬细胞向抗炎表型 M2 极化。此外,在体外,用 ESA 处理的巨噬细胞培养上清液干预 PA 处理的 HepG2 细胞可减轻脂质积累、炎症和氧化应激。总之,旋毛虫衍生的 ESA 可能通过其驱动巨噬细胞抗炎活性的特性成为治疗 NASH 的一种有前途的新型候选药物。
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