探析了含黄芩-白术药对方剂治疗妊娠期肝内胆汁淤积症（intrahepatic cholestasis of pregnancy, ICP）的应用规律及作用机制。检索维普，万方，中国知网数据库中含黄芩-白术药对方剂治疗ICP的文献，利用R语言对方剂进行分析并归纳其用药规律及核心方；再运用网络药理学预测核心方抗ICP的作用机制，并进行分子对接和实验验证。共纳入68首方剂，包含67味中药，多为寒性、苦味、归脾经的药物。综合中药数据分析获得“茵陈-大黄-栀子-黄芩-白术-茯苓”为核心方，其中槲皮素、芹菜素等关键活性成分可能作用于蛋白激酶B1（serine/threonine kinase B1, AKT1）、BCL-2相关X蛋白（BCL-2 associated X protein, BAX）等核心靶点，参与磷脂酰肌醇3-激酶／蛋白激酶B （phosphatidylinositol 3-kinase/protein kinase B, PI3K-AKT）、凋亡等多靶点、多通路发挥治疗ICP作用。在分子对接中，芹菜素与11个核心靶点间的结合效能显著优于槲皮素、β-谷甾醇。HTR-8/SVneo细胞实验表明，芹菜素对牛磺胆酸（taurocholic acid, TCA）诱导的细胞凋亡率、Bax/Bcl-2蛋白表达增加具有显著抑制作用（P < 0.01），并可促进p-PI3K/PI3K、p-AKT/AKT蛋白的表达（P < 0.01），而LY294002预处理可逆转芹菜素的抗凋亡作用和上述蛋白的表达水平。综上，含黄芩-白术药对的核心方可为ICP的临床遣方用药提供参考，其中关键活性成分芹菜素可抑制TCA诱导HTR-8/SVneo细胞凋亡而具有治疗ICP的潜力，其机制可能与调控PI3K-AKT信号通路相关。

To explore the application regularity and mechanism of formulas containing Huang Qin (Scutellariae radix)-Bai Zhu (Atractylodis macrocephalae Rhizoma) (HQ-BZ) herb pair in the treatment of ICP (intrahepatic cholestasis of pregnancy). All literature on prescriptions containing HQ-BZ herb pairs against ICP was screened from the VIP, Wanfang, and CNKI databases. Subsequently, the R language was employed to analyze and summarize its medication rules and core prescriptions. Network pharmacology was used to predict the mechanism of core prescriptions against ICP, followed by molecular docking and experimental verification to confirm the potential mechanism. A total of 68 prescriptions were included, involving 67 herbs characterized mainly by cold, bitter, and spleen meridian. The core prescription "Artemisiae scopariae Herba-Rhei radix et Rhizoma-Gardeniae fructus-Scutellariae radix-Atractylodis macrocephalae Rhizoma-Poriacocos" was obtained based on the comprehensive analysis of traditional Chinese medicine data, among which quercetin, apigenin, and other key active components may act on core targets such as AKT1 (serine/threonine kinase B1), BAX(BCL2-associated X protein), and participate in PI3K-AKT (phosphatidylinositol 3-kinase/protein kinase B), apoptosis, and other multiple targets and pathways to play the role of ICP therapy. The molecular docking results showed that apigenin demonstrated superior binding affinity with the top 11 core targets compared to quercetin and beta-sitosterol. HTR-8/SVneo cell experiments proved that apigenin significantly reduced the apoptosis rate induced by TCA (taurocholic acid) and elevated the protein expression levels of Bax/Bcl-2 (P < 0.01), as well as p-PI3K/PI3K, and p-AKT/AKT (P < 0.01). Pre-treatment with LY294002 could reverse the anti-apoptosis effects and the expression levels of the aforementioned proteins induced by apigenin. In summary, the core prescription that includes the HQ-BZ can provide references for the clinical prescription of ICP. Apigenin, a key component of core prescription, can inhibit the apoptosis in HTR-8/SVneo cells induced by TCA and has the potential to treat ICP, and its mechanism may be related to the regulation of the PI3K-AKT signaling pathway.