基于非靶向代谢组学的化疗致卵巢早衰代谢产物及潜在机制研究数据集

A dataset of metabolites and potential mechanisms of chemotherapy-induced premature ovarian failure based on non-targeted metabolomics

摘要:

卵巢早衰(premature ovarian failure, POF)严重影响女性生殖健康与生活质量，环磷酰胺(cyclophosphamide, CTX)是临床常见的导致卵巢功能损伤的化疗药物，但其诱导POF发生的潜在代谢调控机制尚不明确，亟需从代谢层面揭示其发病机理。本研究基于CTX诱导的POF小鼠模型，获得正常组与模型组小鼠血清代谢组数据，共筛选并鉴定出41个定性差异代谢物，其中脂质及脂质类似物占比54%，表明POF模型小鼠血清代谢谱出现了显著改变。本研究选取8只SPF级雌性C57BL/6小鼠，随机分为正常组与POF模型组，模型组腹腔注射CTX构建POF模型，经HE染色验证模型成功；采用超高效液相色谱-高分辨质谱(ultra-performance liquid chromatography-high resolution mass spectrometry, UPLC-HRMS)技术结合多元统计分析筛选血清差异代谢物，并进行KEGG通路富集分析。本研究揭示了胆碱代谢与甘油磷脂代谢异常是CTX致POF的核心调控环节，证实多条代谢通路协同紊乱参与POF进程，为POF的早期诊断标志物筛选、发病机制阐释及靶向干预策略提供了基础数据与科学依据。

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.