ArticleScientific reports2025
The protective effects of dapagliflozin on cisplatin-induced ovarian toxicity via NRF2-HO-1 pathway and TNF-α/Cas3 signaling.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Mitochondrial Function and Dysfunction in Female Fertility: Biological Mechanisms, Genetic Determinants, and Therapeutic Opportunities - A Review.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
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Authors and funding
3 authors.
Funding
Abstract
This study aimed to investigate the immunohistochemical expression patterns of proliferating cell nuclear antigen (PCNA), heat shock protein-70 (HSP-70), and kisspeptin-1 (KISS-1), as well as the gene expression levels of nuclear factor erythroid 2-related factor 2 (NRF2), heme oxygenase-1 (HO-1), tumor necrosis factor-alpha (TNF-α), and caspase-3 (CAS-3) in cisplatin (CIS)-induced ovarian toxicity, and to evaluate the protective effects of dapagliflozin (DAPA). Thirty-two female Wistar albino rats (n = 8 per group) were divided into four groups: Control, CIS (7.5 mg/kg, intraperitoneal), CIS + DAPA (10 mg/kg DAPA, oral for 7 days + CIS), and DAPA alone. Ovarian tissues were harvested for immunohistochemical and genetic evaluations. PCNA, HSP-70, and KISS-1 immunoreactivities were semi-quantitatively scored, and the mRNA expression levels of NRF2, HO-1, TNF-α, and CAS-3 were assessed using real-time quantitative PCR. All results were statistically analyzed. CIS administration led to a marked increase in PCNA, HSP-70, and KISS-1 immunoexpression, along with downregulation of NRF2 and HO-1 and upregulation of TNF-α and CAS-3 gene expressions (p < 0.001 for all) compared to the control group, indicating enhanced cellular proliferation, oxidative stress, inflammation, and apoptosis. In the CIS + DAPA group, a significant attenuation in PCNA (p < 0.001), HSP-70 (p < 0.001), and KISS-1 (p < 0.001) expression levels, and a reversal of genetic alterations were observed compared to the CIS group, demonstrating that DAPA mitigated proliferative, stress-associated, inflammatory, and apoptotic changes induced by CIS expressions (p < 0.001 for all). Ovarian tissues in the DAPA-alone group maintained expression profiles similar to the control. DAPA exerts protective effects against CIS-induced ovarian damage by modulating proliferation, cellular stress, inflammation, and apoptotic pathways, as evidenced by the downregulation of PCNA, HSP-70, KISS-1, TNF-α, and CAS-3, and upregulation of NRF2 and HO-1. These findings suggest that DAPA may offer a novel therapeutic approach for preserving ovarian function in patients undergoing chemotherapy.
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