4.3 Article

Dietary L-arginine supplementation alleviates liver injury caused by Escherichia coli LPS in weaned pigs

Journal

INNATE IMMUNITY
Volume 18, Issue 6, Pages 804-814

Publisher

SAGE PUBLICATIONS LTD
DOI: 10.1177/1753425912441955

Keywords

Arginine; weaned pigs; lipopolysaccharide; Toll-like receptor 4; nuclear factor-kappa B; liver injury

Funding

  1. Program for New Century Excellent Talents in University [NCET-10-0158]
  2. National Natural Science Foundation of China [31172222, 30972109]
  3. Chinese Ministry of Education [209082]
  4. Natural Science Foundation of Hubei Province [2010CDA050, 2009CDB006]
  5. Wuhan Science and Technology Program [201171034320]

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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 mu g/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-alpha, malondialdehyde contents and mast cell number induced by LPS administration (P < 0.05); and it attenuated the elevation of hepatic NF-kappa B 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.

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