Sun Dongqi, Zhou Xiaoling, Wu Teng, Li Zepeng, Huang Shigao, Peng Zheng
Department of Gastroenterology, Liuzhou Traditional Chinese Medical Hospital, 545001, Liuzhou, Guangxi, China.
Graduate School of Guangxi University of Traditional Chinese Medicine, 530001, Nanning, Guangxi, China.
Recent Pat Anticancer Drug Discov. 2024 Oct 2. doi: 10.2174/0115748928318948240920044716.
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).
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.
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.
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.
探讨槲皮素（Que）调节巨噬细胞极化的潜在机制及其对肝纤维化（肝细胞癌（HCC）的重要病理前提）的后续治疗作用。
对RAW264.7小鼠巨噬细胞系进行体外实验。在用脂多糖诱导M1型巨噬细胞后，分析Que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大鼠作为四氯化碳诱导的肝纤维化模型，分析Que对血清转氨酶水平、肝组织病理结构以及肝组织中巨噬细胞相关蛋白表达的影响。
体外实验表明，Que可抑制JAK2/STAT3信号通路的激活，导致M1巨噬细胞表面标志物和细胞因子表达降低。此外，发现Que可增加M2巨噬细胞表面标志物和细胞因子的表达。在体内，实验证明Que可显著改善大鼠肝纤维化模型中的炎症和纤维化发展。
Que可通过促进M1向M2巨噬细胞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。
