行政院國家科學委員會專題研究計畫成果報告:檳榔成分對T淋巴球細胞激素基因表現之作用與機轉研究
Date Issued
2004
Date
2004
Author(s)
DOI
922320B002093
Abstract
Betel quid chewing is a risk factor for oral squamous cell carcinoma (SCC). Experimental
evidence suggests that the pathogenesis of SCC is associated with immune deterioration. The
objective of the present studies was to investigate the effect of areca nut extract (ANE) on T-cell
proliferation, activation and cytokine expression, and its underlying mechanisms. Murine
splenocytes were pretreated with ANE, arecoline, arecaidine or safrole followed by stimulation
with phorbol-12-myristate-13-acetate plus ionomycin (PMA/Io) or anti-CD3 plus anti-CD28
monoclonal antibodies (CD3/CD28). ANE pretreatment markedly attenuated both the cell
metabolic activity, and the production of interleukin (IL)-2 and interferon (IFN)-γ. In contrast,
ANE pretreatment only slightly inhibited IL-4 secretion. Pretreatment of cells with arecoline,
arecaidine, or safrole (1-100 µM) did not affect the cytokine production. Consistent with the
effect on cytokine production, ANE pretreatment markedly suppressed the steady state mRNA
expression of IL-2 and IFN-γ by CD3/CD28-stimulated splenocytes. The inhibitory effects of
ANE on splenocyte activation and cytokine production were also demonstrated in EL4 cells.
Furthermore, ANE treatment induced the formation of DNA ladder in EL4 cells, indicating
apoptosis of cells in the presence of ANE. Collectively, the present studies demonstrated that Th1
cytokine expression by T cells was attenuated by ANE pretreatment, which was apparently not
mediated by arecoline and arecaidine. The results also suggest that the suppression of cytokine
production by ANE is, at least in part, mediated by induction of T-cell apoptosis.
Subjects
areca quid
immune
T cell activation
cytokine
Publisher
臺北市：國立臺灣大學獸醫學系暨研究所
Type
report
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