SelW protects against H2O2-induced liver injury in chickens via inhibiting inflammation and apoptosis

Selenium (Se) is recognized as a necessary trace mineral in animal diets. Se deficiency induces a number of diseases and injuries in chickens including liver damage, which is related to oxidative stress. Selenoprotein W (SelW) plays a crucial role in antioxidant defense mechanisms in mammals; however, little is known about the role of SelW and cytokines in H2O2-mediated chicken liver damage since chicken SelW has no cysteine (Cys) at residue 37 (Cys37) that is required for its presumed antioxidant function in mammals. The aim of this study was to evaluate whether chicken SelW possessed the same function as mammal SelW and to investigate the protective role of SelW against H2O2 by influencing the expression of inflammation and apoptosis via building a model of overexpressed or/and knocked down SelW in cultured chicken hepatic cells. The results showed that after the cells were exposed to H2O2, the levels of P53, caspase-3, Bax, Bak, COX-2, PTGEs, TNF-α, iNOS and NF-κB were lower in the SelW overexpressed cells but higher in the SelW knockdown cells compared to the H2O2-only treatment group. However, the result for Bcl-2 was opposite to that of the other apoptosis-promoting genes. Moreover, chickens were fed with a Se-deficient diet containing 0.032 mg kg−1 Se for 15, 25, 35, 45, and 55 days, and their liver tissues were collected and examined for apoptosis and inflammation. The results showed that the levels of P53, Bax, Bak, COX-2, PTGEs, TNF-α, iNOS and NF-κB in the Se-deficient chicken livers were dramatically higher than the levels in the normal control group. In conclusion, our findings suggested that chicken SelW possess an antioxidant function similar to the mammalian homologs despite the lack of Cys37 in the peptide, and SelW regulated related-inflammation and apoptosis during H2O2-dependent chicken liver damage.