Cervical cancer (CC) is one of the most common malignant tumors of the female reproductive tract, with persistently high global incidence and mortality rates, posing a significant threat to women's health (Mayadev et al., 2022). Studies have confirmed that persistent infection with high-risk human papillomavirus (HR-HPV) is a well-established risk factor for the development of cervical intraepithelial neoplasia (CIN) and the progression to cervical cancer, especially HR-HPV 16 (Johnson et al., 2019). As a double-stranded DNA virus, HR-HPV exhibits strong host and tissue specificity. Upon infection, the virus integrates into the DNA of cervical epithelial cells, which, under viral stimulation, release a substantial amount of inflammatory cytokines, thereby creating an inflammatory microenvironment. This, in turn, activates signaling pathways involved in tumor initiation and progression (Revathidevi et al., 2021). Over time, chronic inflammation in the cervical epithelium gradually evolves into CIN, and eventually progresses to cervical cancer (Revathidevi et al., 2021). Cervical cancer is a well-defined inflammation-related tumor, with its precursor lesions developing slowly and progressively, exhibiting characteristics of reversibility (Revathidevi et al., 2021, Buskwofie et al., 2020). In terms of pathogenesis, blocking the transmission of HR-HPV is a highly effective preventive strategy against the onset of cervical cancer (Revathidevi et al., 2021). The World Health Organization (WHO) has declared that CC is the only cancer that can be eradicated (Lin et al., 2023). Therefore, early diagnosis and prevention are paramount in addressing CC, particularly through the elimination of HR-HPV infections and the reversal of CIN lesions, to effectively interrupt the early stages of cervical cancer development.

Traditional Chinese medicine (TCM) has long been recognized for its advanced approach of "treating diseases before they manifest," which encompasses strategies such as: preventing the onset of disease, halting disease progression, preemptively preventing disease before rehabilitation, and adjusting disease conditions after rehabilitation (Wu et al., 2024). Notably, recent studies have highlighted the significant advantages of TCM in modulating the immune system and mitigating inflammation, coupled with its non-toxic properties and low incidence of side effects. These characteristics have made TCM a growing area of interest for reversing CIN lesions (Wu et al., 2024, Wang et al., 2024). Research has demonstrated that Tanshinone IIA suppresses the expression of HR-HPV E6 and E7 genes, resulting in S-phase cell cycle arrest and effectively inhibiting further progression of CC (Munagala et al., 2015). The focus of this study is on Xiaoyou decoction (XYD), an herbal formulation made from Fructus cnidii, Tuckahoe, Sophora flavescens, Radix Sophorae Subprostratae, Phellodendron amurense, Lithospermum, Radix Stemonae, Crane lice, and Brucea Javanica (Qi et al., 2025). Previous studies have shown that XYD promotes CIN cell apoptosis by inhibiting the activation of the PI3K/AKT/NF-κB signaling pathway (Qi et al., 2025). However, the molecular mechanisms by which XYD inhibits HR-HPV infection and prevents CIN lesions remain underexplored, and further research in this area is essential.

Autophagy is a highly conserved cellular process in which cells degrade misfolded proteins and damaged organelles through lysosomes, recycling the degradation products and harmful intracellular substances to maintain cellular homeostasis (Debnath et al., 2023, Liu et al., 2023). Under normal, healthy conditions, autophagy is maintained at baseline levels. However, during the progression of CIN, the expression of autophagy-related proteins, such as Beclin1 and LC3, is downregulated, and the reduction in autophagic flux further facilitates tumor progression (Pathak and Manohar, 2023). p53 is a crucial gene that encodes a tumor suppressor protein. Studies have shown that in cervical cancer, HR-HPV, through its E6 protein, binds to p53, causing mutations that disrupt the cell cycle and promote uncontrolled growth (Conrady et al., 2020). In this study, we applied a network pharmacology approach based on the "disease phenotype-gene-target-drug" framework, combined with experimental research, to investigate the potential biological mechanisms by which XYD alleviates CIN lesions. These findings may provide new insights and perspectives for the early molecular-level prevention and treatment of CIN.