Chinese Herbal Medicine for the Treatment of Abnormal Uterine Bleeding: A Comprehensive Review of Molecular Mechanisms.

Abnormal uterine bleeding (AUB) is a highly prevalent clinical condition affecting women of reproductive age. Beyond causing severe secondary complications such as iron-deficiency anemia and infertility, AUB profoundly impairs women's emotional well-being, social functioning, and overall quality of life. Current mainstream guidelines typically recommend conventional treatments as first-line strategies; however, these approaches face significant challenges regarding long-term efficacy and patient tolerability. This unmet need has prompted both patients and clinicians to seek safer and more effective alternative therapies. Chinese Herbal Medicine (CHM) is widely utilized in the management of gynecological disorders, demonstrating remarkable clinical advantages in alleviating AUB symptoms, reducing recurrence rates, and improving patient tolerability. This review provides a comprehensive synthesis of the molecular mechanisms underlying CHM formulas and plant-derived bioactive monomers for the treatment of AUB, based on a three-tiered body of evidence encompassing clinical studies, animal models, and in vitro experiments. Current evidence indicates that classical CHM prescriptions and Chinese patent medicines primarily exert their therapeutic effects by rectifying endocrine imbalances, promoting structural repair of the endometrium, regulating systemic metabolism, and restoring coagulation homeostasis. Regarding CHM-derived bioactive monomers (eg alkaloids and flavonoids), their principal mechanisms are characterized by the inhibition of inflammatory cell infiltration, attenuation of oxidative stress, and suppression of pathological angiogenesis. Furthermore, they contribute to endometrial tissue remodeling through the regulation of abnormal cellular proliferation and the induction of apoptosis. It should be emphasized, however, that the mechanistic evidence summarized herein originates primarily from preclinical investigations. Robust clinical evidence targeting specific PALM-COEIN subtypes is still lacking and does not yet permit firm subtype-specific therapeutic recommendations. Moreover, available clinical evidence is unevenly distributed across AUB etiologies, and safety reporting remains inconsistent; these limitations should be considered when interpreting the clinical relevance of findings derived from animal, cellular, omics, or computational studies. Notwithstanding these limitations, the present review offers a coherent scientific framework for deciphering the "multi-component, multi-target" pharmacological paradigm of CHM against AUB and identifies critical avenues for subsequent research endeavors.