Angelica dahurica (A. dahurica) has a wide range of pharmacological effects, including analgesic, anti-inflammatory and hepatoprotective effects. In this study, we investigated the effect of A. dahurica extract (AD) and its effective component bergapten (BG) on hepatic fibrosis and potential mechanisms. Hepatic fibrosis was induced by intraperitoneal injection with carbon tetrachloride (CCl₄) for 1 week, and mice were administrated with AD or BG by gavage for 1 week before CCl₄ injection. Hepatic stellate cells (HSCs) were stimulated by transforming growth factor-β (TGF-β) and cultured with AD, BG, GW4064 (FXR agonist) or Guggulsterone (FXR inhibitor). In CCl₄-induced mice, AD significantly decreased serum aminotransferase, reduced excess accumulation of extracellular matrix (ECM), inhibited caspase-1 and IL-1β, and increased FXR expressions. In activated HSCs, AD suppressed the expressions of α-SMA, collagen I, and TIMP-1/MMP-13 ratio and inflammatory factors, functioning as FXR agonist. In CCl₄-induced mice, BG significantly improved serum transaminase and histopathological changes, reduced ECM excessive deposition, inflammatory response, and activated FXR expression. BG increased FXR expression and inhibited α-SMA and IL-1β expressions in activated HSCs, functioning as GW4064. FXR deficiency significantly attenuated the decreasing effect of BG on α-SMA and IL-1β expressions in LX-2 cells. In conclusion, AD could regulate hepatic fibrosis by regulating ECM excessive deposition and inflammation. Activating FXR signaling by BG might be the potential mechanism of AD against hepatic fibrosis.

白当归（A. dahurica）具有广泛的药理作用，包括镇痛、抗炎和保肝作用。在本研究中，我们研究了白芷提取物（AD）及其有效成分香柠檬烯（BG）对肝纤维化的影响及其潜在机制。腹腔注射四氯化碳(CCl ₄ )诱导肝纤维化1周，注射CCl ₄前给小鼠灌胃AD或BG 1周。通过转化生长因子-β (TGF-β) 刺激肝星状细胞 (HSC)，并与 AD、BG、GW4064（FXR 激动剂）或 Guggulsterone（FXR 抑制剂）一起培养。在CCl ₄诱导的小鼠中，AD显着降低血清转氨酶，减少细胞外基质（ECM）的过量积累，抑制caspase-1和IL-1β，并增加FXR表达。在活化的HSC中，AD抑制α-SMA、I型胶原、TIMP-1/MMP-13比值和炎症因子的表达，起到FXR激动剂的作用。在CCl ₄诱导的小鼠中，BG显着改善血清转氨酶和组织病理学变化，减少ECM过度沉积、炎症反应并激活FXR表达。 BG 在活化的 HSC 中增加 FXR 表达并抑制 α-SMA 和 IL-1β 表达，起到 GW4064 的作用。 FXR 缺陷显着减弱了 BG 对 LX-2 细胞中 α-SMA 和 IL-1β 表达的降低作用。总之，AD可以通过调节ECM过度沉积和炎症来调节肝纤维化。 BG激活FXR信号可能是AD抗肝纤维化的潜在机制。