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Glucosamine Sulfate Inhibits TNF- and IFN--Induced Production of ICAM-1 in Human Retinal Pigment Epithelial Cells In Vitro

¹From the Department of Ophthalmology, Tri-Service General Hospital, Taipei, Taiwan; the ²Department of Ophthalmology, National Defense Medical Center, Taipei, Taiwan; and the ³Institute of Aerospace Medicine, National Defense Medical Center, Taipei, Taiwan, Republic of China.

PURPOSE. Glucosamine sulfate (GS) is a naturally occurring sugar that possesses some immunosuppressive effects in vitro and in vivo, but its mechanism is unknown. We investigated whether GS could modulate the proinflammatory cytokine-induced expression of the gene for intercellular adhesion molecule (ICAM)-1, an inflammatory protein in human retinal pigment epithelial (RPE) cells.

METHODS. ARPE-19 cells were used as a model to determine the effects of GS on the expression of the ICAM-1 gene upregulated by TNF- or IFN-, by Western blot analysis and semiquantitative reverse transcription polymerase chain reaction (RT-PCR). The activation and nuclear translocation of the nuclear factors NF-B and STAT1 were evaluated by immunocytochemistry, Western blot analysis, and electrophoretic mobility shift assay (EMSA).

RESULTS. Both TNF- and IFN- increased the expression of ICAM-1 at the mRNA and protein levels in a time- and dose-dependent manner in ARPE-19 cells. GS effectively downregulated the TNF-- or IFN--induced expression of ICAM-1 in the protein and mRNA level in a dose-dependent manner. GS further inhibited the nuclear translocation of p65 proteins in TNF- and phosphorylated STAT1 in IFN--stimulated ARPE-19 cells.

CONCLUSIONS. GS inhibits the expression of the ICAM-1 gene in ARPE-19 cell stimulated with TNF- or IFN- through blockade of NF-B subunit p65 and nuclear translocation of STAT1. This study has demonstrated a potentially important property of GS in reducing ICAM-1 mediated inflammatory mechanisms in the eye.

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