ArticleScientific reports2025
Morin hydrate protects against cisplatin-induced testicular toxicity by modulating ferroptosis and steroidogenesis genes' expression and upregulating Nrf2/Heme oxygenase-1.
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 9 papers.
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Who cites it
9 citing papers in PubMed.
- Hesperetin-Loaded PLGA Nanoparticles Ameliorate Cisplatin-Induced Oxidative Stress and Testicular Dysfunction in Rats: Association with NRF2/HO-1, NF-κB, and ACSL4/GPX4/SLC7A11 Signaling Modulation.Antioxidants (Basel, Switzerland) · 2026Article
- Article
- Morin-mediated regulation of apoptosis-autophagy crosstalk in Cancer: molecular mechanisms, preclinical evidence, and translational challenges.Molecular biology reports · 2026Review
- Diacerein mitigates cisplatin-induced testicular toxicity in rats; Role of Nrf2/ HO-1, NF-κB/caspase-3 and NLRP3/ASC/Caspase-1 signaling pathways.Molecular biology reports · 2026Article
- Morin and Morin Semicarbazone Combined with Fucoxanthin Have Potential Anti-Inflammaging Effects Through Modulation of Nrf2/HO-1 System in UVB-Exposed HaCaT Keratinocytes.Antioxidants (Basel, Switzerland) · 2026Article
- Potential gonadal-beneficial effect of sitagliptin against paclitaxel-induced testicular dysfunction via mediating PERK/CHOP/NLRP3/Sestrin2 signaling pathway.Scientific reports · 2026Article
- Protection byPharmaceuticals (Basel, Switzerland) · 2026Article
- HMGB1/NF-κB Axis, IL-8, and Cuproptosis Contribute to Cisplatin-Induced Testicular Injury: Protective Potential Effect of Thymol.Biomolecules · 2025Article
- Article
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Funding
Abstract
Cisplatin is a widely used, effective chemotherapy drug. However, its application is often limited by severe side effects, including testicular toxicity. Cisplatin-induced testicular damage is primarily driven by oxidative stress and inflammation. Ferroptosis has recently been identified to contribute to cisplatin-testicular toxicity. Morin hydrate (MH) is a naturally occurring flavonoid known for its powerful antioxidant, anti-inflammatory, and anti-apoptotic properties. The study was designed to evaluate the protective effects of MH against cisplatin-induced testicular toxicity in Wistar albino rats. Rats were given MH 50 mg/kg, p.o. daily for fourteen days, seven days before the injection of cisplatin 8 mg/kg. Assessment of sperm quality, testosterone, luteinizing hormone levels, and oxidative stress markers were carried out. Also, steroidogenesis and ferroptosis-related gene expressions were assessed. Results: Our findings demonstrated that MH significantly corrected the antioxidant/oxidant balance, evidenced by increased superoxide dismutase, glutathione peroxidase, and Nrf2/heme oxygenase-1 (HO-1) expression and reduced malondialdehyde in testicular tissue. Also, MH ameliorated the negative changes in sperm quality, hormone levels, and testicular histology induced by cisplatin, and this was accompanied by upregulation of steroidogenesis gene expressions (17β-HSD, 3β-HSD, and star). Moreover, MH inhibited cisplatin-induced ferroptosis via the modulation of ferroptosis genes' expression (ACSL4, SLC7A11, and TFRC) and the reduction of iron accumulation in testicular tissue. Conclusion: MH effectively protected against cisplatin-induced testicular toxicity by reducing oxidative stress and inhibiting ferroptosis signalling. This study points out that MH might mitigate iron-mediated apoptosis through the downregulation of Nrf2/HO-1 signaling, providing a potential therapeutic strategy for preventing infertility in male patients undergoing cisplatin chemotherapy.
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