Abstract
This study was designed to study the protective effects and mechanisms of N-acetylcysteine (NAC) in concanavalin A-induced hepatitis in mice. In this study, pretreatment with NAC ameliorated the histopathological changes and suppressed inflammatory cytokines in ConA-induced hepatitis. The expression of IL-2, IL-6, TNF-α, and IFN-γ was significantly reduced in the NAC-treated groups. NAC activated PI3K/Akt pathway and inhibited the activation of NF-κB. Additionally, NAC reduced autophagosome formation, as assessed by detecting the expression of LC3 and Beclin 1. Our results demonstrate that NAC can alleviate ConA-induced hepatitis by regulating the PI3K/Akt pathway and reducing the late stages of autophagy. Our results described a new pharmaceutical to provide more effective therapies for immune hepatitis.
Highlights
Liver diseases, including viral hepatitis, toxic liver diseases, alcoholic liver diseases, and autoimmune hepatitis, represent a global health problem in humans
These results indicated that NAC-treatment ameliorated concanavalin A (ConA)-induced immune hepatitis in mice
We found that IL-2, IL-6, IFN-γ, and tumor necrosis factor- (TNF-)α were significantly increased in the ConAtreated group and were diminished in the NAC-treated groups for both mRNA and protein expression levels at all three time points
Summary
Liver diseases, including viral hepatitis, toxic liver diseases, alcoholic liver diseases, and autoimmune hepatitis, represent a global health problem in humans. The activation of T cells has been established to be the initial trigger of most cases of autoimmune and viral hepatitis [6, 7]. These conditions are characterized by increased levels of aspartate transaminase (AST) and alanine transaminase (ALT) enzyme activities, and accompanied with lymphocyte activation and the inflammatory cytokines accumulation [8, 9]. In mice injected with the T-cell mitogenic plant lectin concanavalin A (ConA), T lymphocytes become activated This process is consistent with a liver-specific inflammatory response that induces T-cell mediated hepatitis [9, 10]. We focus on the protective effects and probable mechanisms of NAC in concanavalin Ainduced hepatitis in mice
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