article · Life
This study investigated the neurotoxic effects of silver nanoparticles (AgNPs) and the protective role of quercetin in Wistar rats. Rats exposed to AgNPs showed increased oxidative stress, indicated by higher lipid peroxidation and reduced antioxidant enzyme activity in brain tissue. AgNPs also decreased neurotransmitter activity, upregulated inflammatory markers, and altered gene expression related to cell survival and brain function. Histopathological examination revealed neuronal degeneration and necrosis. However, oral administration of quercetin effectively counteracted these adverse effects. Quercetin modulated tight junction proteins, antioxidant pathways, inflammatory cytokines, and apoptotic processes, thereby mitigating the neurotoxicity induced by silver nanoparticles in the brain.
Understanding the neurotoxic effects of silver nanoparticles is crucial given their increasing use. This research identifies a potential natural compound, quercetin, that could offer protection against such toxicity, which is important for public health and safety in an increasingly nanotech-driven world.
This early-stage research, conducted in an animal model, suggests quercetin could be developed as a therapeutic or preventative agent. It might be useful for individuals at risk of silver nanoparticle exposure, or as a component in formulations aimed at mitigating neurotoxicity. Further research would be needed to assess its applicability in humans and develop specific products.
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This study aimed to investigate the oxidative neurotoxicity induced by silver nanoparticles (AgNPs) and assess the neuroprotective effects of quercetin against this toxicity. Forty adult male rats were divided into four equal groups: control, AgNPs (50 mg/kg intraperitoneally), quercetin (50 mg/kg orally), and quercetin + AgNPs. After 30 days, blood and brain tissue samples were collected for further studies. AgNP exposure increased lipid peroxidation and decreased glutathione peroxidase, catalase, and superoxide dismutase activities in brain tissue. AgNPs decreased serum acetylcholine esterase activity and γ-aminobutyric acid concentrations. AgNPs upregulated tumor necrosis factor-α, interleukin-1β, and <i>Bax</i> transcript levels. AgNPs reduced the transcripts of claudin-5, brain-derived neurotrophic factor, paraoxonase, nuclear factor-erythroid factor 2 (Nrf2), and <i>Bcl-2</i>. Histopathologically, AgNPs caused various degenerative changes and neuronal necrosis associated with glial cell reactions. AgNPs increased the immunohistochemical staining of glial fibrillary acidic protein (GFAP) in the cerebrum and cerebellum. Oral treatment with quercetin efficiently counteracted the opposing effects of AgNPs on brain tissue via modulation of tight junction proteins, Nrf2, and paraoxonase, and its positive mechanism in modulating pro-inflammatory cytokines and the downregulation of GFAP expression, and the apoptotic pathway. AgNPs also altered the severity of histopathological lesions and modulated GFAP immunostaining in the examined tissue.
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DOI: 10.3390/life12040578
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