In this study, we investigated the effect of (+)-rhododendrol (1) and epi-rhododendrin (2) isolated from Acer nikoense Maxim. (Aceraceae) on nitric oxide (NO) production in mouse peritoneal macrophages elicited by bacillus Calmette-Guerin and in vitro stimulated by lipopolysaccharide. The NO production was not affected by an oral administration of methanol extract at a dose of 100 mg/kg/day. However, the AcOEt soluble fraction significantly reduced the NO production. (+)-Rhododendrol (1) isolated as an active substance from the AcOEt fraction suppressed the NO production. epi- Rhododendrin (2), the glucoside of (+)-rhododendrol (1) isolated from the n- BuOH fraction, also suppressed the NO production. As NO is one of the critical mediators in inflammation, these results suggest that (+)- rhododendrol (1) and epi-rhododendrin (2) contribute in part to the anti- inflammatory effect of A. nikoense.
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