title: Dietary L-arginine supplementation alleviates liver injury caused by Escherichia coli LPS in weaned pigs.
abstract: This study was conducted to evaluate whether dietary supplementation with L-arginine (Arg) could attenuate Escherichia coli LPS-induced liver injury through the TLR4 signaling pathway in weaned pigs. Eighteen weaned pigs were allotted to three treatments: non-challenged control, LPS challenged control and LPS + 0.5% Arg. On d 18, pigs were injected with LPS at 100 µg/kg of body weight (BW) or sterile saline. Blood samples were obtained at 4 h post-injection. Pigs were then sacrificed for the collection of liver samples. Arg supplementation (0.5%) alleviated liver morphological impairment, including hepatocyte caryolysis, karyopycnosis and fibroblast proliferation induced by LPS challenge; it mitigated the increase of serum aspartate aminotransferase and alkaline phosphatase activities induced by LPS (P < 0.05); it prevented the increase of hepatic TNF-α, malondialdehyde contents and mast cell number induced by LPS administration (P < 0.05); and it attenuated the elevation of hepatic NF-κB and TLR4-positive cell percentages (P < 0.05). These results indicate that Arg supplementation has beneficial effects in attenuating hepatic morphological and functional injury induced by LPS challenge in piglets. Additionally, it is possible that the protective effects of Arg on the liver are associated with a decreased release of liver pro-inflammatory cytokines and free radicals through inhibiting TLR4 signaling.
authors.affiliation: Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan, People's Republic of China.
authors.forename: Quan
authors.initials: Q
authors.lastname: Li
authors.forename: Yulan
authors.initials: Y
authors.lastname: Liu
authors.forename: Zhengquan
authors.initials: Z
authors.lastname: Che
authors.forename: Huiling
authors.initials: H
authors.lastname: Zhu
authors.forename: Guoquan
authors.initials: G
authors.lastname: Meng
authors.forename: Yongqing
authors.initials: Y
authors.lastname: Hou
authors.forename: Bingying
authors.initials: B
authors.lastname: Ding
authors.forename: Yulong
authors.initials: Y
authors.lastname: Yin
authors.forename: Feng
authors.initials: F
authors.lastname: Chen
mesh_terms: D000469:Alkaline Phosphatase / Q000378:metabolism; D000818:Animals; D001120:Arginine / Q000008:administration & dosage*; D001219:Aspartate Aminotransferases / Q000378:metabolism; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D019587:Dietary Supplements; D004926:Escherichia coli; D005347:Fibroblasts / Q000187:drug effects / Q000473:pathology; D022781:Hepatocytes / Q000187:drug effects / Q000473:pathology; D008070:Lipopolysaccharides; D008099:Liver / Q000187:drug effects* / Q000201:enzymology / Q000276:immunology; D008107:Liver Diseases / Q000178:diet therapy* / Q000382:microbiology*; D008315:Malondialdehyde / Q000378:metabolism; D008407:Mast Cells / Q000187:drug effects / Q000473:pathology; D016328:NF-kappa B / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D013552:Swine; D051197:Toll-Like Receptor 4 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D008070:Lipopolysaccharides; D016328:NF-kappa B; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D001120:Arginine; D001219:Aspartate Aminotransferases; D000469:Alkaline Phosphatase