The Role of The Xihuang Pill in Inhibiting Triple-Negative Breast Cancer Through Immunogenic Cell Death.

Modern Western medicine uses surgeries, chemotherapy, targeted therapy, and radiotherapy to inhibit breast cancer cells through pathways such as apoptosis, necrosis, and autophagy. However, for triple-negative breast cancer (TNBC), a highly aggressive subtype lacking targeted therapies, conventional chemotherapy often leads to severe side effects and drug resistance, thereby limiting its clinical efficacy. Immunogenic cell death (ICD) can prompt dying tumor cells to release antigens and activate anti-tumor immune responses, converting "cold tumors" into "hot tumors". This opens up a new direction for overcoming tumor drug resistance and enhancing the efficacy of traditional therapies. Additionally, Xihuang Pill (XHP) has the potential for immunomodulation and chemotherapy sensitization. Studies have found that as an ICD inducer, XHP can trigger the production of three key damage-associated molecular patterns (DAMPs): HSP membrane translocation, massive ATP release, and HMGB1 secretion. The main active components of XHP include bilirubin, volatile oil, pentacyclic triterpenoids (such as boswellic acid), and steroids (such as hyodeoxycholic acid). These components possess anti-tumor effects, as well as functions in immunomodulation, efficacy enhancement, and toxicity reduction. This article elaborates on the role and mechanism of XHP in treating TNBC from aspects such as formula analysis, the mechanism of immunogenic cell death, the anti-tumor immune effects of XHP, and its relationship with immunogenic cell death. The aim is to provide a theoretical basis for the clinical application of XHP in treating TNBC through the immunogenic cell death pathway and to promote the secondary development of this medicine.