Ameliorative effects of supranutritional selenium on TLR‐4‐NF‐kB‐TNF‐α‐mediated hepatic oxidative injury and inflammation in goats fed high concentrate diet

We examined whether surplus dietary selenium (Se) supply could alleviate high concentrate (HC) diet‐induced hepatic oxidative stress (OS) and inflammation. Eighteen young goats were distributed into three groups; were fed low (LC, concentrate: forage; 35: 65), high concentrate (HC, 65: 35), or Se‐supplemented HC (HCSe, 65: 35 + 0.5 mg Se kg(−1) diet) diets for 10 weeks. Short chain fatty acids, OS markers and immunoinflammatory genes expressions were assessed through gas chromatograph, kits, and RT‐qPCR, respectively. Compared with LC, HC diet increased (p < .05) colonic and serum lipopolysaccharide (LPS) levels and induced hepatic oxidative injury by increasing (p < .05) malondialdehyde (MDA) levels and decreasing (p < .05) activities of glutathione peroxidase, superoxide dismutase, and catalase. HC diet altered hepatic mRNA expressions of toll‐like receptor‐4 (TLR‐4), cluster of differentiation‐14 (CD‐14), tumor necrosis factor‐α (TNF‐α), TNF receptor‐associated factor‐6 (TRAF‐6), nuclear factor kappa B (NF‐κB), interleukin‐1β (IL‐1β), IL‐10, IL‐13, LPS‐binding protein (LBP), serum amyloid A (SAA), α‐acid glycoprotein (AGP), and albumin (ALB). Conversely, extra‐Se supply lowered LPS and attenuated antioxidant status and inflammation in liver. In conclusion, HC diet induced oxidative lesions and TLR‐4 pathway‐mediated inflammation, whereas supranutritional Se alleviated oxidative and inflammatory lesions through TLR‐4 pathway regulation in goat liver.