Sheng Wu Gong Cheng Xue Bao. 2026 Jul 25;42(7):3006-3018. doi: 10.13345/j.cjb.260131.
ABSTRACT
Premature ovarian failure (POF) severely impairs women’s reproductive health and quality of life. Cyclophosphamide (CTX) is a common chemotherapeutic drug that clinically induces ovarian function damage. However, the potential metabolic regulatory mechanism underlying CTX-induced POF remains unclear, and it is urgent to reveal its pathogenesis from a metabolic perspective. Based on the CTX-induced POF mouse model, this study obtained serum metabolomic data from mice in the normal group and the model group, screened and identified 41 qualitatively differential metabolites, among which lipids and lipid-like molecules accounted for 54%, and clarified the significant alterations in the serum metabolic profile of POF model mice. Eight SPF-grade female C57BL/6 mice were randomly divided into the normal control group and the POF model group. The model group received an intraperitoneal injection of CTX to establish the POF model, and the successful establishment of the model was verified by hematoxylin-eosin (HE) staining. UPLC-HRMS technology combined with multivariate statistical analysis was used to screen differential serum metabolites, followed by KEGG pathway enrichment analysis. This study reveals that abnormal choline metabolism and glycerophospholipid metabolism are the core regulatory links of CTX-induced POF, and confirms that the coordinated disorder of multiple metabolic pathways is involved in POF progression. It provides foundational data and scientific evidence for the screening of early diagnostic biomarkers, the elucidation of pathogenesis, and the development of targeted intervention strategies for POF.
PMID:42522614 | DOI:10.13345/j.cjb.260131
