Our previous studies show that vitamin C (VC) plays promising hepatoprotection in mice. Intrahepatic exposure of perfluorooctane sulfonate (PFOS) can induce dose-dependent cytotoxicity. However, pharmacology-based assessment of VC on PFOS remains uninvestigated. This study aimed to evaluate the therapeutic benefits of VC on inhibiting PFOS-induced liver steatosis in mice, followed by representative biochemical analysis and immunoassay. As results, VC was beneficial for reduced PFOS-induced liver damages, as showed in reductions of serological levels of transaminases (ALT and AST), lipids (TG and TC), fasting glucose and insulin, inflammatory cytokines (TNF-α and IL6), while content of fibroblast growth factor 21 (FGF21) in serum was increased. In addition, VC reduced histiocytic changes of PFOS-lesioned livers, as revealed in reduced TNF-α-labeled cells and increased FGF21-labeled cells in immunofluorescence assay. Further, intrahepatic expressions of endoplasmic reticulum (ER) stress-based ATF6, eIF2α, GRP78, XBP1 proteins were down-regulated by treatments of VC. Taken together, our preliminary findings set forth that VC exerts pharmacological benefits against PFOS-induced liver steatosis in mice, and the underlying biological mechanism may be linked to suppressing hepatocellular inflammatory reaction and ER stress.
Keywords: Endoplasmic reticulum stress; Inflammation; Liver steatosis; Perfluorooctane sulfonate; Vitamin C.
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