Effects of different selenium sources on duodenum and jejunum tight junction network and growth performance of broilers in a model of fluorine-induced chronic oxidative stress

Abstract

The protective effects and underlying molecular mechanisms of sodium selenite (SS) and selenomethionine (SM) against chronic oxidative stress-induced duodenum and jejunum tight junction (TJ) network disturbance and growth inhibition of broilers were investigated in the current experiment. At the age of 1 d, 720 Lingnan Yellow broiler chicks were allocated to 4 experimental diets (with 6 replicates per diet and 30 birds per replicate) and offered either a control diet (fluorine [F] 23 mg/kg, control [CoN] group) or test diets (800 mg/kg F, high F [HF] group; 800 mg/kg F+0.15 mg selenium [Se]/kg as SS [SS group] or SM [SM group]) for 56 d. The results showed that HF group could induce chronic oxidative stress and subsequently increased (P < 0.05) proinflammatory cytokines levels of duodenum and jejunum in comparison with the CoN group. Increased proinflammatory cytokines levels of HF group promoted myosin light chain kinase (MLCK) transcription, thus leading to a decrease (P < 0.05) in TJ proteins expression of duodenum and jejunum when compared with the CoN group. A reduction of TJ proteins expression destroyed the TJ structures in the HF group, which in turn increased intestinal mucosal permeability of duodenum and jejunum and ultimately induced growth inhibition of broilers. Dietary Se supplementation could ameliorate HF-induced duodenum and jejunum TJ network impairment and growth retardation of broilers, potentially by increasing (P < 0.05) the glutathione peroxidase and thioredoxin reductase activities, reducing (P < 0.05) the reactive oxygen species and malondialdehyde levels, regulating the secretion of proinflammatory cytokines, and mediating the transcription level of MLCK in the duodenum and jejunum. Additionally, our data also suggested that the protective effects of SM were superior to those of SS. This study will provide a theoretical basis for developing SM into an efficient protective agent for intestinal mucosal barrier in poultry.