| The translocation of lipopolysaccharide in the digestive tract seriously affects the production performance of lactating animals.However,most studies on the mechanism of lipopolysaccharide translocation and injury are focused on the acute stress model.At present,there are few studies on chronic stimulation of lipopolysaccharide in the digestive tract before translocation,and recent studies have found that oral lipopolysaccharide has an effect of promoting immune function.The aim of this study was to investigate the effects of chronic stimulation of digestive tract by lipopolysaccharide on lactating animals and its contribution to translocation.In this test,the concentration of lipopolysaccharide in the digestive tract of lactating mothers was increased by long-term addition of lipopolysaccharide in drinking water of mice.After delivery,32 pregnant rats of SPF grade were randomly divided into four groups,with 8 offspring in each litter:control group(CON)without lipopolysaccharide in drinking water,LPS-10 group with 10 ug/ml concentration,LPS-20 group with 20 ug/ml concentration and LPS-40 group with 40 ug/ml concentration.This test examined the production performance,inflammation and immune factors,hormone levels and biochemical indicators,intestinal health and appetite regulation genes in lactating mice..Result:Chronic stimulation of LPS promoted the increase of feed intake in lactating mice(P=0.015),which was dose-dependent in the range of concentration set in the experiment.The treatment promoted the expression of appetite-promoting regulatory gene agouti gene-related protein(P=0.0025),but had no effect on the expression of neuropeptide Y(P=0.1032).Compared with the control group,the test treatment had the effect of promoting the increase of litter weight gain(P=0.0087),and the effect was weakened as the concentration increased.Chronic stimulation of LPS caused inflammatory damage to the stomach of lactating mice;no significant damage was caused to the duodenum and jejunum.The concentration of plasma lipopolysaccharide(P<0.001),lipopolysaccharide binding protein(P=0.0095),and haptoglobin(P<0.0042)in the LPS-treated group was significantly decreased,while serum amyloid A concentration was not changed.The levels of interferon-gamma(P < 0.0001),tumor necrosis factor-alpha(P = 0.0047)and interleukin-8(P< 0.0001)were significantly decreased in LPS treatment group,while the levels of interleukin-1 beta(P = 0.0307)and interleukin-10(P < 0.0001)were increased,while the levels of interleukin-6 remained unchanged.Moreover,the cortisol concentration of the LPS treatment group was significantly decreased(P < 0.0001).Chronic stimulation of LPS resulted in a significant increase in plasma immunoglobulin A,immunoglobulin G,and immunoglobulin M levels(P < 0.0001).Lipopolysaccharide treatment caused a significant decrease in total protein(P < 0.0001),albumin(P = 0.0299)and free fatty acids(P = 0.0002).However,it did not have a significant effect on the levels of blood sugar,aspartate aminotransferase,alanine aminotransferase,urea,triglyceride,total cholesterol and?-hydroxybutyrate,but there was a tendency to increase the level of ?-hydroxybutyrate.Lipopolysaccharide treatment significantly reduced the level of glucagon in plasma and increased the levels of insulin,insulin-like growth factor 1,growth hormone and prolactin(P< 0.01).For leptin and glucagon-like peptide 1,the level in LPS-10 was significantly lower than that in the control group,while the levels in LPS-20 and LPS-40 were significantly higher than those in the control group.Conclusion:Chronic stimulation of LPS in digestive tract can stimulate the increase of feeding intake and lactation performance of lactating mice;significantly reduce the levels of proinflammatory factors tumor necrosis factor-alpha,interleukin-8 and interferon-gamma in plasma,reduce cortisol concentration and increase the levels of the anti-inflammato ry factors interleukin-10 and immunoglobulins(IgA,IgG,IgM);significantly reduced plasma total protein and albumin levels,affecting the body's protein metabolism. |
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