Isatin improves oligoasthenospermia caused by busulfan by regulating GSH/GPX4 axis to inhibit ferroptosis
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View abstract on PubMed
Summary
This summary is machine-generated.Isatin (ISA) effectively treats oligoasthenospermia in mice by reversing reproductive damage and ferroptosis. This natural compound offers a potential therapeutic strategy for male infertility by regulating oxidative stress and improving sperm health.
Area Of Science
- Reproductive Biology
- Oxidative Stress Research
- Pharmacology
Background
- Ferroptosis, driven by iron overload and redox imbalance, generates reactive oxygen species (ROS) and lipid peroxides, impacting spermatogenesis.
- Imbalances in lipid peroxidation can cause reproductive damage and oligoasthenospermia, a key factor in male infertility.
- Isatin (ISA), a natural compound with antioxidant and anti-aging properties, shows promise for treating oligoasthenospermia.
Purpose Of The Study
- To investigate the therapeutic effects of Isatin (ISA) on oligoasthenospermia.
- To elucidate the underlying molecular mechanisms of ISA's action in reversing reproductive damage and ferroptosis.
Main Methods
- A mouse model of oligoasthenospermia was induced using busulfan (BUS).
- Mice were treated with varying doses of ISA (25, 50, 100 mg/kg) via gavage for 28 days.
- Evaluations included testicular histomorphology, sperm parameters, serum sex hormones, oxidative stress markers, and ferroptosis indicators.
Main Results
- ISA treatment reversed busulfan-induced testicular damage, improving sperm concentration and motility.
- ISA normalized serum sex hormone levels and testicular oxidative stress indices.
- ISA mitigated testicular ferroptosis by inhibiting nuclear factor erythroid 2-related factor 2 (NRF2) translocation and modulating the glutathione (GSH)/glutathione peroxidase 4 (GPX4) pathway.
Conclusions
- Isatin (ISA) effectively ameliorates oligoasthenospermia in a mouse model.
- ISA demonstrates potential as a therapeutic agent for male infertility associated with oxidative stress and ferroptosis.
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