Abstract Context Xiayuxue decoction (XYXD), a traditional Chinese medicine, is used for treating liver disease. However, the potential active constituents and mechanisms are still unclear. Objective To explore the main active fraction extracts, active ingredients and possible mechanisms of XYXD for anti-hepatic fibrosis. Materials and methods Different fractions including ethyl acetate fraction (EF) were prepared from XYXD. These fractions, especially EF, were used to evaluate cell viability, proliferation, cell cycle, cytotoxicity and activation in hepatic stellate cells (HSCs). Liver fibrosis model was established by CCl4 in C57BL/6 mice, and allocated to CCl4 group, XYXD group and EF group with normal mice as control. Further, mitochondrial apoptosis-related proteins of HSCs, destruction and angiogenesis of liver sinusoidal endothelial cells (LSECs) and active ingredients of EF were evaluated. Results The inhibition of proliferation, increase of S or/and G2/M phase population and suppression of α-SMA and COL-1 expression were obeserved in EF treated-JS1 and -LX2. Liver fibrosis-related indicators were improved by EF similar to XYXD in vivo. EF induced the apoptosis of HSCs in CCl4-induced fibrosis, and inhibited the expression of HSCs apoptosis pathway-related proteins (JNK and p38-MAPKs), and LSECs destruction and angiogenesis. Multiple ingredients (emodin, rhein, aloe-emodin, prunasin) in EF have shown inhibited the activation of JS1. Discussion and Conclusion EF was the main active fraction extracts of XYXD, and the underlying mechanisms might relate to induction of HSCs apoptosis. Emodin, rhein, aloe-emodin and prunasin were main active ingredients of EF, which provides a potential drug for the treatment of liver fibrosis.

中文翻译：

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夏郁血汤乙酸乙酯组分通过诱导细胞凋亡和抑制肝星状细胞活化对四氯化碳诱导的小鼠肝纤维化的保肝作用

摘要 背景 夏郁血汤（XYXD）是一种治疗肝病的中药。然而，潜在的活性成分和机制仍不清楚。目的探讨XYXD抗肝纤维化的主要活性部位提取物、活性成分及可能的作用机制。材料和方法 包括乙酸乙酯级分 (EF) 在内的不同级分由 XYXD 制备。这些级分，尤其是 EF，用于评估肝星状细胞 (HSC) 的细胞活力、增殖、细胞周期、细胞毒性和活化。用CCl4在C57BL/6小鼠中建立肝纤维化模型，分为CCl4组、XYXD组和EF组，正常小鼠为对照。此外，HSC 的线粒体凋亡相关蛋白，评估了肝窦内皮细胞 (LSEC) 和 EF 活性成分的破坏和血管生成。结果在EF处理的-JS1和-LX2中观察到增殖抑制、S或/和G2/M期种群增加以及α-SMA和COL-1表达的抑制。EF 在体内改善了肝纤维化相关指标，类似于 XYXD。EF 在 CCl4 诱导的纤维化中诱导 HSCs 凋亡，并抑制 HSCs 凋亡途径相关蛋白（JNK 和 p38-MAPKs）的表达，以及 LSECs 的破坏和血管生成。EF 中的多种成分（大黄素、大黄酸、芦荟大黄素、prunasin）已显示抑制 JS1 的激活。讨论与结论 EF 是 XYXD 的主要活性组分提取物，其潜在机制可能与诱导 HSCs 凋亡有关。大黄素、大黄酸、