ArticleJournal of ovarian research2025
Mechanisms of cell senescence and apoptosis in cyclophosphamide-induced premature ovarian failure in rats.
Article in Journal of ovarian research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Efficacy of low-dose versus high-dose intravenous cyclophosphamide in Lupus Nephritis: A systematic review and Meta-analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Pooled it
- Therapeutic effects of mesenchymal stem cell-derived extracellular vesicles from different tissue sources on diminished ovarian reserve and the related mechanisms.Journal of nanobiotechnology · 2026Article
- Relationship between different modes of death and premature ovarian insufficiency: a literature review.Apoptosis : an international journal on programmed cell death · 2026Review
- Association of lower serum and follicular fluid vitamin D levels with reduced fertilization rates in IVF patients with diminished ovarian reserve.Frontiers in endocrinology · 2026Article
- Systems-level actions of luteolin in female reproductive disorders: from molecular mechanisms to clinical translation.Frontiers in pharmacology · 2026Review
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Authors and funding
7 authors.
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Abstract
backgroundPremature ovarian failure (POF) is a clinical condition characterized by a diminished ovarian reserve occurring before the age of 40, significantly affecting female reproductive health. However, its exact pathogenesis remains unclear. This research aimed to examine the mechanisms of cyclophosphamide (CTX)-induced senescence and apoptosis in the ovarian and cerebral cortex tissues of rats to provide insights into delaying aging and protecting female reproductive health.
methodsA rat model of POF was established by intraperitoneal injection of CTX. Model efficacy was evaluated by measuring ovarian volume, weight, estrogen, and anti-Müllerian hormone levels. Serum marker changes were detected via enzyme-linked immunosorbent assay (ELISA). Senescence and apoptosis in cerebral cortical and ovarian tissues were observed using β-galactosidase (SA-β-gal) staining and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay. Western Blot and quantitative polymerase chain reaction (RT-qPCR) were employed to detect the expression levels of cell senescence- and apoptosis-related proteins and genes, verifying the correlation between POF and cellular senescence/apoptosis.
resultsHigh-dose CTX induced POF. In rats with POF, the levels of anti-Müllerian hormone (AMH), estradiol (E2), and vitamin D (VD) significantly decreased (P < 0.0001), whereas the levels of testosterone (T) and insulin (INS) significantly increased (P < 0.0001). The number of senescent and apoptotic-positive cells in the ovarian and cerebral cortex tissues of rats with POF was substantially augmented (P < 0.05; P < 0.01). Additionally, the expression of senescence-related proteins cyclin-dependent kinase inhibitor 1 A (CDKN1A), cyclin-dependent kinase inhibitor 2 A (CDKN2A), tumor protein p53 (P53), apoptosis-related protein BCL2-Associated X Protein (Bax), and cysteine-aspartic acid protease 3 (caspase 3) was upregulated. In contrast, the expression of the anti-apoptotic protein BCL-2 was downregulated. The changes ranged from 1.7- to 7.1-fold. These findings demonstrated that high-dose CTX injection leads to cellular senescence and apoptosis, resulting in ovarian pathology.
conclusionHigh-dose CTX induced POF in rats, resulting in aging and apoptosis in the cerebral cortex and ovarian tissues. Therefore, inhibiting cellular senescence and apoptosis may be a potential approach for restoring ovarian reserve function in POF.
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