Cpt1a promoted ROS-induced oxidative stress and inflammation in liver injury via the Nrf2 HO-1 and NLRP3 inflammasome signaling pathway

被引:23
作者
Luo, Xigang [1 ]
Sun, Dapeng [2 ]
Wang, Yinxiang [3 ]
Zhang, Fengxiang [2 ]
Wang, Yi [4 ]
机构
[1] Jinzhou Med Univ, Affiliated Hosp 3, Dept Lab Med, Jinzhou 121000, Peoples R China
[2] Jinzhou Med Univ, Affiliated Hosp 1, Dept Clin Pharm, Jinzhou 121000, Peoples R China
[3] Jinzhou Med Univ, Dept Clin Med, Jinzhou 121001, Peoples R China
[4] Jinzhou Med Univ, Affiliated Hosp 3, Dept Blood Transfus, Jinzhou 121000, Peoples R China
关键词
Cpt1a; ROS; oxidative stress; liver injury; Nrf2/HO-1; inflammasome; HEPATIC-FIBROSIS; INHIBITION; DEFICIENCY;
D O I
10.1139/cjpp-2020-0165
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
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 palmitoyltransferase 1(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 in vitro model of liver injury. It was also shown that overexpression of Cpt1a suppressed the nuclear factor erythroid-2-related factor 2 (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 protein 3 (NLRP3) inflammasome signaling pathway.
引用
收藏
页码:468 / 477
页数:10
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