l-Arginine stimulates proliferation and prevents endotoxin-induced death of intestinal cells |
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Authors: | Bie Tan Yulong Yin Xiangfeng Kong Peng Li Xilong Li Haijun Gao Xinguo Li Ruilin Huang Guoyao Wu |
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Institution: | (1) Hunan Engineering Technology Research Center of Healthy Animal Husbandry and Laboratory for Agro-ecological Processes in Subtropical Region, Institute of Subtropical Agriculture, Chinese Academy of Sciences, 410125 Hunan, China;(2) Department of Animal Science, Texas A&M University, College Station, TX 77843, USA;(3) The Graduate School of the Chinese Academy of Sciences, 100039 Beijing, China;(4) Hunan Institute of Animal Husbandry and Veterinary Medicine, Changsha, 410131 Hunan, China; |
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Abstract: | This study tested the hypothesis that l-arginine (Arg) may stimulate cell proliferation and prevent lipopolysaccharide (LPS)-induced death of intestinal cells. Intestinal
porcine epithelial cells (IPEC-1) were cultured for 4 days in Arg-free Dulbecco’s modified Eagle’s-F12 Ham medium (DMEM-F12)
containing 10, 100 or 350 μM Arg and 0 or 20 ng/ml LPS. Cell numbers, protein concentrations, protein synthesis and degradation,
as well as mammalian target of rapamycin (mTOR) and Toll-like receptor 4 (TLR4) signaling pathways were determined. Without
LPS, IPEC-1 cells exhibited time- and Arg-dependent growth curves. LPS treatment increased cell death and reduced protein
concentrations in IPEC-1 cells. Addition of 100 and 350 μM Arg to culture medium dose-dependently attenuated LPS-induced cell
death and reduction of protein concentrations, in comparison with the basal medium containing 10 μM Arg. Furthermore, supplementation
of 100 and 350 μM Arg increased protein synthesis and reduced protein degradation in both control and LPS-treated IPEC-1 cells.
Consistent with the data on cell growth and protein turnover, addition of 100 or 350 μM Arg to culture medium increased relative
protein levels for phosphorylated mTOR and phosphorylated ribosomal protein S6 kinase-1, while reducing the relative levels
of TLR4 and phosphorylated levels of nuclear factor-κB in LPS-treated IPEC-1 cells. These results demonstrate a protective
effect of Arg against LPS-induced enterocyte damage through mechanisms involving mTOR and TLR4 signaling pathways, as well
as intracellular protein turnover. |
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