| This study was conducted to investigate the regulatory role of arginine (Arg) on lipopolysaccharide (LPS)-induced liver injury in piglets and its mechanism. Eighteen weaned pigs were allotted to three treatments. Each treatment had six replicates, and each replicate had one pig. The three groups included: 1) control (basal diet + sterile saline); 2) LPS-challenged (basal diet + LPS); 3) Arg group (basal diet + 0.5% Arg + LPS). On d 18, pigs were injected with LPS at 100μg/kg of BW or sterile saline. At 4 h post-injection, blood samples were obtained, and then pigs were sacrificed for collection of liver samples. The results showed that: 1) LPS challenge caused liver morphological changes. 0.5% Arg alleviated the liver morphological changes induced by LPS challeng to some extent; 2) LPS increased plasma aspartate aminotransferase (AST), alkaline phosphatase (AKP),γ-glutamate transpeptidase (GGT) activities and the ratio of aspartate aminotransferase/ alanine aminotransferase (AST/ALT) (P<0.05), and reduced plasma glucose (GLU), total protein (TP), albumin (ALB) and globulin content (P<0.05). 0.5% Arg alleviated the increase of AST and AKP activities (P<0.05), and the decrease of TP content induced by LPS (P<0.05); 3) LPS increased hepatic AST, ALT, GGT, AKP and lactate dehydrogenase (LDH) activities (P<0.05), 0.5% Arg alleviated the increase of GGT, AKP and LDH activities (P<0.05); 4) LPS increased malondialdehyde (MDA) content, and superoxide dismutase (SOD) activity in liver (P<0.05). 0.5% Arg alleviated the increase of MDA content induced by LPS (P<0.05); 5)LPS challenge increased tumor necrosis factor-alpha (TNF-α) content of liver (P<0.05). 0.5% Arg alleviated the increase of hepatic TNF-αcontent induced by LPS (P<0.05); 6)LPS increased mast cells number in liver. 0.5% Arg alleviated the increase of mast cells number in liver induced by LPS (P<0.05); 7)LPS increased hepatic NF-κB-positive and TLR4-positive percentage(P<0.05). 0.5% Arg alleviated the increase of hepatic NF-κB-positive and TLR4-positive percentage (P<0.05). These results indicated that LPS could activate the signaling pathway of TLR4/NF-κB to produce proinflammatory cytokines and peroxidation in liver and induced liver morphological and function injury ultimately. 0.5% Arg could attenuate hepatic morphological and function injury induced by LPS challenge in piglets by alleviating the activation of the signaling pathway of TLR4/NF-κB to produce proinflammatory cytokines and peroxidation in liver. |