Antagonistic effect of selenium on lead-induced inflammatory injury through inhibiting the nuclear factor-κB signaling pathway and stimulating selenoproteins in chicken hearts

Abstract

Lead (Pb) is a toxic metal and can damage chicken organs. Selenium (Se) is an essential micronutrient and has antagonistic effect on heavy metal toxicity. However, the toxic effect of Pb on inflammatory factors and selenoproteins, and antagonistic effect of Se on Pb toxicity in chicken hearts remain unclear. In the present study, a chicken model to study Pb and Se was established. Seven-day-old male chickens were randomly divided into the control, the +Se group, the +Pb group, and the Se + Pb group. The feeding program of Pb and Se was as follows: lead acetate was added to drinking water and sodium selenite was added to the standard diet. Relative mRNA levels of four inflammatory factors (nuclear factor-κB (NF-κB), tumor necrosis factor-α, cyclooxygenase-2, and prostaglandin E synthases) and 25 selenoproteins (including glutathione peroxidase 1 (Gpx1), Gpx2, Gpx3, and Gpx4, thioredoxin reductase 1 (Txnrd1), Txnrd2, Txnrd3, iodothyronine deiodinase 1 (Dio1), Dio2, Dio3, selenoprotein n1 (Sepn1), selenoprotein K (Selk), Sels, Sepw1, Selt, Selh, Selm, 15 kDa selenoprotein, Seli, Selu, Selpb, Sepp1, Selo, Sepx1, selenophosphate synthetase 2 (SPS2)) were detected on the 30^th, 60^th, and 90^th days in chicken hearts. The results indicated that Pb poisoning increased mRNA levels of inflammatory factors, decreased mRNA levels of selenoproteins, and caused histological changes in the chicken hearts. Se alleviated Pb-caused all the above changes in the chicken hearts. Our results suggested that Se supplementation alleviated Pb-induced inflammatory injury through inhibiting the NF-κB signaling pathway and stimulating selenoproteins in the chicken hearts.