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 microM 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 microM Arg to culture medium dose-dependently attenuated LPS-induced cell death and reduction of protein concentrations, in comparison with the basal medium containing 10 microM Arg. Furthermore, supplementation of 100 and 350 microM 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 microM 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-kappaB 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.
journal_name
Amino Acidsjournal_title
Amino acidsauthors
Tan B,Yin Y,Kong X,Li P,Li X,Gao H,Li X,Huang R,Wu Gdoi
10.1007/s00726-009-0334-8subject
Has Abstractpub_date
2010-04-01 00:00:00pages
1227-35issue
4eissn
0939-4451issn
1438-2199journal_volume
38pub_type
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