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Updated: May 6, 2026

A Method to Study the Impact of Chemically-induced Ovarian Failure on Exercise Capacity and Cardiac Adaptation in Mice
Published on: April 7, 2014
Potential protective role of chlorogenic acid against cyclophosphamide-induced reproductive damage in male mice
Hong-Xing Zheng1, You-Mei Xu1, Shu-Cong Fan1
1Shaanxi Province Key Laboratory of Bio-resources/QinLing-Bashan Mountains Bioresources Comprehensive Development C. I. C./Qinba State Key Laboratory of biological resources and ecological environment, Shaanxi University of Technology, East on the 1st Ring Road, Hanzhong, Shaanxi 723000, China.
Background:
Cyclophosphamide (CP) is an anticancer drug; however, clinical utilization of CP is limited, resulting from its considerable toxicities. This research was performed to explore the protective effects of Chlorogenic acid (CGA) on reproductive damage induced by CP in mice.
Methods:
Blood samples were collected for analysis of hormone content subsequently; semen samples were evaluated for quality, and testis samples were used for histopathological evaluation and analysis of oxidative stress biomarkers, protein and gene expression levels of steroid regulatory factors, and steroid synthase.
Results:
The results noted that CGA increased serum testosterone (T), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) activity; increased SOD, GPx, and GSH oxidative stress levels in testis tissue; and decreased MDA content in testis tissue. Testicular cells in the CGA treatment group gradually returned to normal morphology, and CYP11A1 and CYP17A1 levels increased after CGA treatment. The mRNA levels of CYP11A1, CYP17A1, StAR, 3β-HSD, and 17β-HSD were significantly raised in the CGA dose group. In the test dose range, CGA can improve sperm quality, quantitative abnormality, and serum T synthesis disorder caused by CP. This mechanism may be correlated with the inhibition of oxidative stress and antioxidation levels.
Conclusions:
Therefore, CGA has a protective impact on testicular injuries arising from CP in mice.

