[No authors listed]
CONTEXT:Compound K (CK, 20-O-d-glucopyranosyl-20(S)-protopanaxadiol), a novel ginsenoside metabolite, is structurally a member of the dammarane-type triterpene saponins. Several studies have identified the anti-inflammatory activity of CK. Our previous study demonstrated that CK exerted its anti-inflammatory effect via inhibition of abnormal activation and differentiation of T cells. However, its mechanism of action on B cells remains unclear. OBJECTIVE:The objective of this study is to investigate the effect and underlying mechanisms of CK's effects on memory B cells in the setting of adjuvant-arthritis (AA). MATERIALS AND METHODS:Complete Freund's adjuvant was used to induce AA in rats. Rats were administered, either CK (10, 40, and 160âmg/kg), once daily for 15âd, or methotrexate (MTX; 0.5âmg/kg) once every 3âd, for a total of six times. To evaluate the anti-inflammatory effect of CK, a global assessment and a swollen joint count of AA rats were performed every 3âd. Spleen index and histopathology were examined. Subsets of B cells including CD45R(+)IgM(+) (total B cells) and CD45R(+)CD27(+) (memory B cells) and expression of CD40 and CD40L were assayed by flow cytometry. RESULTS:Compared with the AA rats, global assessment scores and swollen joint counts were significantly lower in the treated groups received CK (40 and 160âmg/kg; pâ<â0.05 and pâ<â0.01, respectively). CK (40 and 160âmg/kg) decreased the spleen index (pâ<â0.01), and alleviated hyperplasia of lymph nodes (pâ<â0.05 and pâ<â0.01, respectively) and marginal zone (pâ<â0.05) in the spleen. In addition, CK (40 and 160âmg/kg) suppressed memory B cell subsets (pâ<â0.05), and suppressed CD40L expression on T cells and CD40 expression on B cells (pâ<â0.05 and pâ<â0.01, respectively). DISCUSSION AND CONCLUSION:This study demonstrated that CK downregulated memory B cells in AA rats, and this down-regulation may be T-cell dependent.
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