Role of quercetin on sterigmatocystin-induced oxidative stress-mediated toxicity

Oxidative stress appears to be a common trigger for many of the effects associated with the exposure to various mycotoxins, including sterigmatocystin (STE). However, studies to alleviate STE toxicity through the use of natural antioxidants are sparsely reported in literature. In the present study, the cytoprotective effect of quercetin (QUE) was tested in SH-SY5Y cells against STE-induced oxidative stress and cytotoxicity. The MTT assay revealed that STE decreased cell viability, whereas pre-treatment of cells with QUE restored it. The QUE was also found to counteract STE-induced ROS generation and decrease STE-induced up-regulation of the expression of the stressinducible enzymes HO-1 and NOS-2. Pre-treatment with QUE also prevented STE-induced nuclear translocation of NF-kappa B, as measured by immunofluorescence. Finally, considering the key role played by NF-kappa B in the regulation of inflammation, the effect of STE on the pro-inflammatory cytokines TNF-alpha and IL-6 expression was evaluated. Our results showed the down-regulation of TNF-alpha and IL-6 following STE exposure, suggesting a negative immunomodulatory effect of STE. In QUE pre-treated samples, TNF-alpha and IL-6 were significantly further reduced, indicating the anti-inflammatory role of QUE. The results of the present study demonstrate for the first time that QUE exerts a cytoprotective role in STE-induced toxicity.

Automated summary

The present study demonstrated for the first time that quercetin exerts a cytoprotective role in sterigmatocystin-induced toxicity, potentially through antioxidative and anti-inflammatory mechanisms, offering promising applications in alleviating mycotoxin-related effects.