Dietary selenomethionine ameliorates lipopolysaccharide-induced renal inflammatory injury in broilers via regulating the PI3K/AKT pathway to inhibit necroptosis.

Selenomethionine (SeMet) has antioxidant and anti-inflammatory effects, as a widely used organic Se source in food supplements, and its inhibitory effect on the prevention and treatment of renal inflammatory injury is unclear. Here, in order to explore the protective effect of SeMet on kidney tissue of broilers and determine its potential molecular mechanism, we took broilers as the research object, lipopolysaccharide (LPS) was used as the source of stimulation, and the model was established by adding SeMet to the diet. The histopathological observation indicated that SeMet alleviated the LPS-induced characteristic changes of renal inflammatory injury. Besides, SeMet inhibited LPS-induced PI3K, AKT, caspase 8 and IκB-α downregulation, the necroptosis marker genes (FADD, RIP1, RIP3, MLKL and TNF-α), pro-inflammatory factors (NF-κB, PTGEs, COX-2, iNOS, IL-1β and IL-6) and HSP60, HSP70 and HSP90 overexpression. We concluded that SeMet ameliorates LPS-induced renal inflammatory injury in broilers by inhibiting necroptosis via the regulation of the PI3K/Akt pathway. Thus, we speculated that dietary SeMet may be a potential new strategy for the treatment of renal injury.