化疗耐药是乳腺癌复发的根本原因，“扶正祛邪”是中医预防复发的核心理论。乳腺癌干细胞（CSCs）是化疗耐药的关键细胞亚群，Cav-1/Nrf2信号通路对CSCs的分化生长具有决定作用，可调控CSCs活性氧自由基（ROS）水平，低水平ROS对维持CSCs存活至关重要。课题组前期研究筛选并证明黄芪甲苷（AS-Ⅳ）联合紫杉醇对乳腺癌细胞、CSCs可协同增效，其协同增效机制是调控CSCs的Cav-1与Nrf2表达，提高ROS水平，触发CSCs凋亡。本研究拟采用乳腺癌CSCs进行体外、体内实验，并通过MOE计算机模拟分子对接，进一步探讨AS-Ⅳ是否通过靶向抑制Cav-1表达，进而下调Nrf2通路活性，升高ROS水平，以达协同增敏。为中医药预防乳腺癌化疗耐药寻找新的分子靶点，推动防治肿瘤中药现代化，并丰富“扶正祛邪”理论的科学内涵。

Chemotherapy resistance is the fundamental cause of recurrence of breast cancer. "Strengthening the body and dispel evil" is the core theory of preventing recurrence in TCM. Breast cancer stem cells (CSCs) are the key cell subsets for chemotherapy resistance. Cav-1/Nrf2 signaling pathway plays a decisive role in the differentiation and growth of CSCs, which regulates the level of reactive oxygen species (ROS) in CSCs and low level ROS is essential for maintaining CSCs alive. The previous study of the research group screened and proved that astragaloside IV (AS-IV) combined with paclitaxel could synergistically enhance breast cancer cells and CSCs, and its synergistic mechanism was to regulate the expression of CSCs caveolin (Cav-1) and Nrf2, raise the level of ROS, and trigger the apoptosis. In this study, breast cancer CSCs was used for in vitro and in vivo experiments, and MOE computer simulation of molecular docking was used to further explore whether AS IV could inhibit Cav-1 expression by targeting, down regulate the activity of Nrf2 pathway, and increase ROS level in order to achieve synergistic sensitization. In order to find new molecular targets for preventing breast cancer chemotherapy resistance by TCM, we should promote the modernization of Chinese medicine for prevention and treatment of cancer and enrich the scientific connotation of the theory of "strengthening the body and dispel evil".