Abstract
Various liver diseases caused by liver damage seriously affect people's health. The purpose of this study was to clarify the effects and the mechanisms of carnitine palmitoyltransferase1 (Cpt1a) on oxidative stress and inflammation in liver injury. It was found that the expression of Cpt1a mRNA was upregulated in a model of liver injury in mice. Thus, overexpression of Cpt1a increased reactive oxygen species (ROS) production and malondialdehyde (MDA) levels and reduced superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GSH-px) levels in an invitro model of liver injury. It was also shown that overexpression of Cpt1a suppressed the nuclear factor erythroid-2-related factor2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. In summary, these data indicate that Cpt1a promotes ROS-induced oxidative stress in liver injury via the Nrf2/HO-1 and nucleotide-binding oligomerization domain-like receptor protein3 (NLRP3) inflammasome signaling pathway.
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