Procyanidine alleviates bisphenol A-induced apoptosis in TM3 cells via the Nrf2 signaling pathway
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View abstract on PubMed
Summary
This summary is machine-generated.Procyanidin (PC) protects against BPA-induced Leydig cell damage by reducing oxidative stress and apoptosis. PC activates the Nrf2 pathway, suggesting it can alleviate bisphenol A (BPA) toxicity.
Area Of Science
- Endocrinology
- Toxicology
- Cell Biology
Background
- Bisphenol A (BPA), found in food packaging, is linked to reproductive dysfunction.
- The protective mechanisms of natural antioxidants like Procyanidin (PC) against BPA-induced Leydig cell damage require elucidation.
Purpose Of The Study
- To investigate the protective effects of PC against BPA-induced damage in TM3 Leydig cells.
- To elucidate the underlying molecular mechanisms of PC's protective action.
Main Methods
- TM3 Leydig cells were exposed to BPA and treated with PC.
- Oxidative stress, apoptosis, and the Nrf2 signaling pathway were assessed.
- The NRF2 inhibitor ML385 was used to confirm pathway involvement.
Main Results
- PC treatment attenuated BPA-induced TM3 cell damage, suppressing oxidative stress and apoptosis.
- PC upregulated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and its antioxidant target genes.
- Inhibition of Nrf2 reversed the beneficial effects of PC on gene expression.
Conclusions
- PC mitigates BPA-induced TM3 cell damage by activating the Nrf2 signaling pathway.
- PC supplementation shows potential for alleviating bisphenol A (BPA) toxicity in Leydig cells.
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