期刊
出版社
MDPI
DOI: 10.3390/ijerph17010138
关键词
Cadmium; acute liver injury; Nrf2; NLRP3; NF-kappa B; MAPKs
资金
- National Natural Science Foundation of China [31802242]
- Young Talents Visiting and Training Program for Foreign Country of Anhui Education Department [gxgwfx2019047]
- Natural Science Key Foundation of Anhui Education Department [KJ2017A503, KJ2017A504]
- Talent Project of Anhui Science and Technology University [ZRC2014447]
- Leading Academic Discipline Project of Anhui Science and Technology University [AKZDXK2015A04]
- College Students' Innovative Training Program of Anhui Province [2018S10879013]
Acute Cadmium (Cd) exposure usually induces hepatotoxicity. It is well known that oxidative stress and inflammation causes Cd-induced liver injury. However, the effect of nuclear factor erythroid 2-related factor 2 (Nrf2) in Cd-induced liver injury is not completely understood. In this study, we observed Cd-induced liver damage and the potential contribution of Nrf2, nuclear factor-kappa B (NF-kappa B), Nod-like receptor 3 (NLRP3), and mitogen-activated protein kinases (MAPKs) signaling pathways. Changes in serum transaminases and proinflammatory cytokines expression showed that Cd could induce acute hepatotoxicity. Moreover, Nrf2 and its downstream heme oxygenase 1 (HO-1) were inhibited by Cd exposure, and Kelch-like ECH-associated protein 1 (Keap1), the inhibitory protein of Nrf2, was increased. Furthermore, NF-kappa B, NLRP3, and MAPKs signaling pathways were all activated by Cd intoxication. In conclusion, the inhibition of Nrf2, HO-1, and the activation of NF-kappa B, NLRP3, and MAPKs all contribute to Cd-induced liver injury.
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