丹参
肝星状细胞
血小板源性生长因子受体
癌症研究
纤维化
血小板衍生生长因子
肝纤维化
肝硬化
化学
生物
生长因子
受体
医学
病理
内科学
内分泌学
生物化学
中医药
替代医学
作者
Fangbin Liu,Shengnan Li,Panpan Chen,Yanqiu Gu,Shaozhan Wang,Lei Wang,Chun Chen,Rong Wang,Yongfang Yuan
标识
DOI:10.1016/j.intimp.2023.110550
摘要
Liver fibrosis is a reversible pathological process and a wound healing response to liver injury. As an early stage of various liver diseases, liver fibrosis can develop into cirrhosis, liver failure, and even liver cancer if not controlled in time. Salvia miltiorrhiza is a medicinal plant with hepatoprotective effects. Salvianolic acid B (Sal B) is the representative component of S. miltiorrhiza. Many studies have reported the anti-liver fibrosis effects and mechanisms of Sal B. However, the direct anti-fibrotic targets of Sal B have not yet been reported. Platelet-derived growth factor receptor β (PDGFRβ) is one of the most classical targets in liver fibrosis, which is closely related to hepatic stellate cells (HSCs) activated. Previously, we established and applied a PDGFRβ affinity chromatography model, and found that Sal B binds well to PDGFRβ. Therefore, this study aimed to investigate the direct targets of Sal B against liver fibrosis. We confirmed the binding ability of Sal B to PDGFRβ by molecular docking and a surface plasmon resonance biosensor. Our findings indicated that Sal B targeted PDGFRβ to inhibit the activation, migration and proliferation of HSCs and suppressed the PDGF-BB-induced PDGFRβ signaling pathway. Annexin V-FITC/PI assay showed that Sal B reversed the PDGF-BB-induced decrease in HSC apoptosis rate. In the mouse liver fibrosis model, Sal B inhibited the PDGFRβ signaling pathway, HSC activation and reduced inflammatory response, ultimately improved CCl4-induced liver fibrosis. In summary, the direct anti-fibrotic targets of Sal B may be PDGFRβ, and this study clarified the anti-liver fibrosis effects and mechanism of Sal B.
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