College of Animal Science and Technology, Jiangxi Agricultural University, No. 1101 Zhimin Avenue, Economic and Technological Development District, Nanchang 330045, China.
Int J Mol Sci. 2022 Jun 2;23(11):6252. doi: 10.3390/ijms23116252.
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 μM) and/or Se (0.4 μM) 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-κB (NF-κB) signaling pathway.
镉（Cd）是一种有毒重金属，可在动物的肝脏中积累，损害肝功能。炎症和氧化应激被认为是镉引起肝损伤的主要原因。硒（Se）是一种抗氧化剂，可以抵抗镉对肝脏的有害影响。为了阐明硒对镉对肝细胞损伤的拮抗作用及其机制，用 Cd（4 μM）和/或 Se（0.4 μM）处理鸭胚肝细胞 24 h。然后，评估肝细胞活力、氧化应激和炎症状态。结果表明，Cd 组活性氧（ROS）的积累和促炎因子的水平升高。同时，免疫荧光染色显示 NOD 样受体富含吡喃结构域 3（NLRP3）和凋亡相关斑点样蛋白（ASC）之间的相互作用增强，高迁移率族蛋白 B1（HMGB1）从核到细胞质的运动增加，炎症反应进一步放大。然而，添加 Se 缓解了上述作用，从而减轻了细胞氧化应激和炎症。综上所述，结果表明 Se 可以减轻 Cd 刺激的肝细胞氧化应激和炎症，这可能与 NLRP3 炎性小体和 HMGB1/核因子-κB（NF-κB）信号通路有关。
