Geraniol alleviates benzo[a]pyrene-induced neurotoxicity by regulating the NLRP3/Caspase-1 pathway and gut microbiome in mice
摘要
Benzo[a]pyrene (BaP) exposure has been associated with an increased risk of neurotoxicity, including learning and memory impairment. As an antioxidant and a potential prebiotic, geraniol is speculated the potential preventive agent against neurotoxicity. This study aims to reveal the neuroprotection of geraniol on BaP-induced neurotoxicity. The results indicate geraniol increases immunofluorescence intensity of PSD-95, and decreases the immunofluorescence intensity of Iba-1 and GFAP, as well as the level of inflammatory cytokines, and pyroptosis biomarkers. Geraniol also up-regulates the expression of tight junction proteins markedly. In addition, lipopolysaccharide (LPS), might originate from intestinal flora and closely correlated with inflammation and pyroptosis, varies in brain and serum between each group. It is summarized that the underlying mechanism of neuroprotection effect of geraniol might be located on improving intestinal physical barrier function, decreasing LPS releasing, down-regulating pyroptosis and inflammatory response, thereby alleviating neurotoxicity induced by BaP in mice model.