(-RHODODENDROL AND EPI-RHODODENDRIN SUPPRESS THE NO PRODUCTION BY ACTIVATED MACROPHAGES IN-VIVO())

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 lipopolysaccha ride. The NO production was not affected by an oral administration of methanol extract at a dose of 100 mg/kg/day. However, the AcOEt solubl e 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 (+)-rhododen drol (1) isolated from the n-BuOH fraction, also suppressed the NO pro duction. As NO is one of the critical mediators in inflammation, these results suggest that (+)-rhododendrol (1) and epi-rhododendrin (2) co ntribute in part to the anti-inflammatory effect of A. nikoense.