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1.
Probiotics Antimicrob Proteins ; 12(2): 451-460, 2020 06.
Article in English | MEDLINE | ID: mdl-31111440

ABSTRACT

The probiotic effect of Enterococcus faecalis-1 (isolated from healthy chickens) on growth performance, immune response, and modulation of the intestinal microbiota of broilers was assessed with a total of 100-day-old commercial Cobb chicks. The chicks were randomly divided into two equal groups. The control group received a basal diet, while the test group received a basal diet and was orally supplied with E. faecalis at a dose of 108 CFU/bird/day. Results showed that E. faecalis-1 supplement significantly (P < 0.05) improved the body weight and feed conversion ratio of treated broilers compared with the control ones. The mortality percentage was reduced in E. faecalis-1-supplemented group. The total IgY serum level was significantly (P < 0.05) increased in broilers receiving E. faecalis-1 supplement (7.1 ± 0.39) compared with the control group (5.8 ± 0.3), while the serum avidin level was significantly (P < 0.05) decreased in E. faecalis-1-supplemented broilers (76 ± 11.1). There was no significant change in the immune response towards avian influenza and Newcastle vaccines in both groups. The total Lactobacillus and Enterococcus counts were significantly (P < 0.05) higher in the cecal contents of broilers given E. faecalis-1 than those that received the control treatment. E. faecalis-1 supplement enhanced the enzyme activities, antioxidant system, and liver functions of treated broilers compared with those in the control group. Collectively, these results showed that E. faecalis-1 could promote growth performance and immunological status and convey beneficial modulation of the cecal microbiota in broilers.


Subject(s)
Animal Nutritional Physiological Phenomena , Chickens , Enterococcus faecalis , Gastrointestinal Microbiome , Immunity , Probiotics/administration & dosage , Animals , Chickens/growth & development , Chickens/immunology
2.
Am J Physiol Cell Physiol ; 301(4): C895-902, 2011 Oct.
Article in English | MEDLINE | ID: mdl-21775707

ABSTRACT

In this study, the effect of lipopolysaccharide (LPS) on protein synthesis (PS) and intracellular signaling factors that regulate it have been investigated in C2C12 murine-derived myotubes. In particular, the role of Akt/mammalian target of rapamycin (mTOR) and the mitogen-activated protein kinases (MAPKs) [p38 and extracelluar regulated protein kinase (ERK1/2)] have been examined. The direct effect of LPS on PS was measured at 3 and 18 h. LPS significantly decreased PS at 3 h but not at the 18-h time point. This effect was preceded by decreased Akt phosphorylation at 5 and 30 min after LPS administration. The mTOR phosphorylation exhibited a long time dose-dependent increase at all the time points. Similarly, the activity-related phosphorylation of p38 and ERK1/2 significantly increased in a time- and dose-dependent manner at all the time points. Polymyxin B abolished the LPS-induced decrease in PS rate. The phosphatidylinositol 3-kinase inhibitor LY-0294002 in combination with LPS significantly decreased the rate of PS by 81% and alone by 66%, respectively, for the 3- and 18-h time points, whereas p38 and ERK inhibitors in combination with LPS significantly decreased the rate PS rate at the 18-h time point by 41% and 59%, respectively, compared with control cells. In conclusion, LPS alone transiently decreased the rate of PS by 50% at 3 h; this effect is most likely mediated via the Toll-like receptor 4 (TLR4)-Akt/mTOR pathway, and both p38 and ERK when inhibited in the presence of LPS at 3 h have a similar effect in preventing the LPS-induced reduction in PS.


Subject(s)
Gene Expression Regulation/drug effects , Lipopolysaccharides/pharmacology , Mitogen-Activated Protein Kinase Kinases/metabolism , Muscle Fibers, Skeletal/metabolism , Muscle Proteins/metabolism , Proto-Oncogene Proteins c-akt/metabolism , Animals , Cell Line , Dose-Response Relationship, Drug , Lipopolysaccharides/administration & dosage , Mice , Mitogen-Activated Protein Kinase Kinases/genetics , Muscle Fibers, Skeletal/drug effects , Muscle Proteins/genetics , Myoblasts , Phosphorylation , Proto-Oncogene Proteins c-akt/genetics , Signal Transduction , TOR Serine-Threonine Kinases/genetics , TOR Serine-Threonine Kinases/metabolism , Time Factors
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