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.