Quercetin Promotes the M1-to-M2 Macrophage Phenotypic Switch During Liver Fibrosis Treatment by Modulating the JAK2/STAT3 Signaling Pathway.

Dongqi Sun, Xiaoling Zhou, Teng Wu, Zepeng Li, Shigao Huang, Zheng Peng
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Abstract

Objective: To investigate the underlying mechanism by which quercetin (Que) regulates macrophage polarization and its subsequent therapeutic effect on liver fibrosis, an important pathological precondition for hepatocellular carcinoma (HCC).

Methods: In vitro experiments were performed on the RAW264.7 mouse macrophage line. After the induction of M1-type macrophages with LPS, the effects of Que on cell morphology, M1/M2 surface marker expression, cytokine expression, and JAK2/STAT3 expression were analyzed. In vivo, male SD rats were used as a model of CCL4-induced hepatic fibrosis, and the effects of Que on serum aminotransferase levels, the histopathological structure of liver tissues, and macrophage-associated protein expression in liver tissues were analyzed.

Results: In vitro experiments revealed that Que can suppress the activation of the JAK2/STAT3 signaling pathway, leading to decreases in the expression of M1 macrophage surface markers and cytokines. Additionally, Que was found to increase the expression of M2 macrophage surface markers and cytokines. In vivo, assays demonstrated that Que significantly ameliorated the development of inflammation and fibrosis in a rat liver fibrosis model.

Conclusion: Que can inhibit hepatic fibrosis by promoting M1 to M2 macrophage polarization, which could be associated with its ability to suppress the JAK2/STAT3 signaling pathway in macrophages.

槲皮素通过调节 JAK2/STAT3 信号通路促进肝纤维化治疗过程中 M1-M2 巨噬细胞的表型转换
目的研究槲皮素(Que)调节巨噬细胞极化的内在机制及其对肝纤维化(肝细胞癌(HCC)的重要病理前提)的治疗作用:方法:在 RAW264.7 小鼠巨噬细胞系上进行体外实验。用 LPS 诱导 M1 型巨噬细胞后,分析阙对细胞形态、M1/M2 表面标志物表达、细胞因子表达和 JAK2/STAT3 表达的影响。在体内,以雄性 SD 大鼠作为 CCL4 诱导肝纤维化的模型,分析了 Que 对血清转氨酶水平、肝组织的组织病理学结构以及肝组织中巨噬细胞相关蛋白表达的影响:体外实验显示,阙能抑制 JAK2/STAT3 信号通路的激活,导致 M1 型巨噬细胞表面标志物和细胞因子的表达减少。此外,阙还能增加 M2 巨噬细胞表面标志物和细胞因子的表达。体内试验表明,在大鼠肝纤维化模型中,阙能显著改善炎症和纤维化的发展:结论:阙能通过促进巨噬细胞从 M1 到 M2 的极化来抑制肝纤维化,这可能与其抑制巨噬细胞中 JAK2/STAT3 信号通路的能力有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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