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Protective Effects of Sesamin on Cytoxan-Induced Spermatogenesis Dysfunction by Regulating RNF8-ubH2A/ubH2B Pathways
Dong-Mei Hai1, Jia-Wei Ren1, Yan-Nan Chi1
1Department of Pharmacology, Ningxia Medical University, Yinchuan, China.
Abstract:
Most of the clinically infertile patients show spermatogenesis dysfunction. Cyclophosphamide, as an anticancer drug, can induce spermatogenesis dysfunction. Sesamin is the main bioactive component of natural lignans in sesame. It is abundant in sesame oil and has strong biological activities such as antioxidant, antibacterial, and hypoglycemic properties. By establishing the model of spermatogenic dysfunction induced by cyclophosphamide in male mice and then feeding sesamin (50, 100, and 200 mg/kg) for 2 weeks, we proved that sesamin can improve the reproductive organ damage induced by cyclophosphamide and increase the number and activity of sperms. Sesamin can resist cyclophosphamide-induced sperm nuclear maturity and DNA damage by increasing the expression levels of histones H2A and H2B in the testis. In addition, sesamin can improve the ubiquitination of histones regulated by RNF8 to protect the testis. In conclusion, these results suggest that sesamin can improve spermatogenic dysfunction induced by cyclophosphamide, which may be mediated by ubiquitination of histones.
Insights
Sesamin, a compound from sesame, combats chemotherapy-induced male infertility by improving sperm health and protecting testicular DNA. This natural lignan offers a potential therapeutic strategy for reproductive organ damage.
Area of Science:
- Reproductive Biology
- Toxicology
- Natural Product Chemistry
Background:
- Spermatogenesis dysfunction is a primary cause of clinical infertility.
- Cyclophosphamide, an anticancer drug, is known to induce spermatogenesis dysfunction.
- Sesamin, a lignan from sesame, possesses antioxidant and other beneficial biological activities.
Purpose of the Study:
- To investigate the protective effects of sesamin against cyclophosphamide-induced spermatogenesis dysfunction in male mice.
- To elucidate the molecular mechanisms underlying sesamin's protective action on testicular damage and sperm quality.
Main Methods:
- A mouse model of spermatogenic dysfunction was induced using cyclophosphamide.
- Mice were treated with varying doses of sesamin (50, 100, 200 mg/kg) for two weeks.
- Evaluated reproductive organ damage, sperm count, motility, sperm nuclear maturity, DNA integrity, and histone expression (H2A, H2B) and ubiquitination (RNF8).
Main Results:
- Sesamin treatment significantly improved reproductive organ damage and increased sperm number and activity in cyclophosphamide-treated mice.
- Sesamin mitigated cyclophosphamide-induced damage to sperm nuclear maturity and DNA integrity.
- Sesamin increased the expression of histones H2A and H2B and improved RNF8-regulated histone ubiquitination in the testis.
Conclusions:
- Sesamin effectively ameliorates cyclophosphamide-induced spermatogenic dysfunction and associated testicular damage.
- The protective effects of sesamin may be mediated through the regulation of histone modifications, specifically ubiquitination, enhancing sperm DNA and nuclear maturity.
- Sesamin represents a potential therapeutic agent for managing chemotherapy-induced male reproductive toxicity.
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