ArticleToxicology research2024
Potential protective role of chlorogenic acid against cyclophosphamide-induced reproductive damage in male mice.
Article in Toxicology research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Saroglitazar Mitigated Cyclophosphamide-Induced Testicular Injury: Crosstalk Between Oxidative Stress, Inflammation and Apoptosis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Multiomics analysis reveals that chlorogenic acid alleviates heat stress-induced oxidative damage in prepubertal boar testes via the BLVRA-GPX3 pathway: in vivo and in vitro evidence.Journal of animal science and biotechnology · 2026Article
- Addition of Chlorogenic Acid to Human Semen: Effects on Sperm Motility, DNA Integrity, Oxidative Stress, andAntioxidants (Basel, Switzerland) · 2025Article
- The role of plant-based dietary compounds in gut microbiota modulation in inflammatory bowel disease.Frontiers in nutrition · 2025Review
- Propolis extract nanoparticles alleviate diabetes-induced reproductive dysfunction in male rats: antidiabetic, antioxidant, and steroidogenesis modulatory role.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.