期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 23, 期 11, 页码 -出版社
MDPI
DOI: 10.3390/ijms23116252
关键词
cadmium; selenium; HMGB1; inflammation; oxidative stress; hepatocytes
资金
- National Natural Science Foundation of China [32060819]
- Jiangxi Provincial Department of Education Science and Technology Research Project [GJJ170299]
Cadmium is a toxic heavy metal that can accumulate in the liver, causing damage to liver function. Selenium, an antioxidant, can alleviate the detrimental effects of cadmium on the liver. This study found that selenium can mitigate cadmium-induced oxidative stress and inflammation in hepatocytes, possibly through the NLRP3 inflammasome and HMGB1/NF-kappa B signaling pathway.
Cadmium (Cd) is a toxic heavy metal that can accumulate in the liver of animals, damaging liver function. Inflammation and oxidative stress are considered primary causes of Cd-induced liver damage. Selenium (Se) is an antioxidant and can resist the detrimental impacts of Cd on the liver. To elucidate the antagonism of Se on Cd against hepatocyte injury and its mechanism, duck embryo hepatocytes were treated with Cd (4 mu M) and/or Se (0.4 mu M) for 24 h. Then, the hepatocyte viability, oxidative stress and inflammatory status were assessed. The findings manifested that the accumulation of reactive oxygen species (ROS) and the levels of pro-inflammatory factors were elevated in the Cd group. Simultaneously, immunofluorescence staining revealed that the interaction between NOD-like receptor pyran domain containing 3 (NLRP3) and apoptosis-associated speck-like protein (ASC) was enhanced, the movement of high-mobility group box 1 (HMGB1) from nucleus to cytoplasm was increased and the inflammatory response was further amplified. Nevertheless, the addition of Se relieved the above-mentioned effects, thereby alleviating cellular oxidative stress and inflammation. Collectively, the results suggested that Se could mitigate Cd-stimulated oxidative stress and inflammation in hepatocytes, which might be correlated with the NLRP3 inflammasome and HMGB1/nuclear factor-kappa B (NF-kappa B) signaling pathway.
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