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亓文隆, 贾志诚, 石梦雨, 杨鑫鑫, 孙昕玮, 郭颖.中药改善环磷酰胺所致卵巢衰老的机制研究进展[J].湖南中医药大学学报英文版,2026,46(1):208-216.[Click to copy
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| 中药改善环磷酰胺所致卵巢衰老的机制研究进展 |
| 亓文隆,贾志诚,石梦雨,杨鑫鑫,孙昕玮,郭颖 |
| (山东中医药大学第一临床医学院, 山东 济南 250014;中国中医科学院广安门医院, 北京 100053;山东中医药大学附属医院生殖与遗传中心, 山东 济南 250011) |
| 摘要: |
| 环磷酰胺（CTX）是临床常用的烷化剂类化疗药物，其生殖毒性可损伤卵巢功能并加速卵巢衰老。本文从细胞凋亡、氧化应激及线粒体功能障碍等多个层面系统阐述CTX诱导卵巢衰老的现代分子机制；同时梳理近年研究，总结中药单体与复方多靶点、多途径干预上述环节并缓解卵巢损伤的实验证据。以期为中药在化疗患者生育力保护中的应用提供理论依据。 |
| 关键词: 中药 卵巢衰老 环磷酰胺 细胞凋亡 氧化应激 线粒体功能障碍 |
| DOI：10.3969/j.issn.1674-070X.2026.01.030 |
| Received:October 11, 2025 |
| 基金项目:国家自然科学基金面上项目（82374505）；山东省自然科学基金面上项目（ZR2023MH219）；泰山学者青年专家项目（202211353）。 |
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| Research progress on the mechanisms of Chinese Medicines in ameliorating cyclophosphamide-induced ovarian aging |
| QI Wenlong, JIA Zhicheng, SHI Mengyu, YANG Xinxin, SUN Xinwei, GUO Ying |
| (The First Clinical Medical College, Shandong University of Traditional Chinese Medicine, Jinan, Shandong 250014, China;Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China;Reproductive and Genetic Center, The Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong 250011, China) |
| Abstract: |
| Cyclophosphamide (CTX), a commonly used alkylating agent in clinical chemotherapy, can impair ovarian function and accelerate ovarian aging due to its reproductive toxicity. This paper systematically elucidates the modern molecular mechanisms of CTX-induced ovarian aging from multiple perspectives, including cellular apoptosis, oxidative stress, and mitochondrial dysfunction. Additionally, it reviews recent studies and summarizes experimental evidence demonstrating that monomers and compound formulas of Chinese medicines can intervene in the aforementioned processes through multiple targets and pathways, thereby alleviating ovarian damage. The aim is to provide a theoretical basis for the application of Chinese Medicines in protecting fertility in chemotherapy patients. |
| Key words: Chinese medicines ovarian aging cyclophosphamide cellular apoptosis oxidative stress mitochondrial dysfunction |
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