Cinnamomum camphora Sieb (Lauraceae) has long been prescribed in
traditional medicine for the treatment of
inflammation-related diseases such as
rheumatism,
sprains,
bronchitis and muscle pains. In this study, therefore, we aimed to investigate the inhibitory effects of Cinnamomum camphora on various inflammatory phenomena to explore its potential anti-inflammatory mechanisms under non-cytotoxic (less than 100 microg/ml) conditions. The total
crude extract (100 microg/ml) prepared with 80%
methanol (MeOH extract) and its fractions (100 microg/ml) obtained by
solvent partition with
hexane and
ethyl acetate (EtOAc) significantly blocked the production of
interleukin (IL)-1 beta,
IL-6 and the
tumor necrosis factor (
TNF)-alpha from RAW264.7 cells stimulated by
lipopolysaccharide (LPS) up to 20-70%. The
hexane and EtOAc extracts (100 microg/ml) also inhibited
nitric oxide (NO) production in LPS/
interferon (IFN)-gamma-activated macrophages by 65%. The MeOH extract (100 microg/ml) as well as two fractions (100 microg/ml) prepared by
solvent partition with
n-butanol (BuOH) and EtOAc strongly suppressed the
prostaglandin E(2) (
PGE(2)) production in LPS/IFN-gamma-activated macrophages up to 70%. It is interesting to note that
hexane, BuOH and EtOAc extracts (100 microg/ml) also inhibited the functional activation of beta1-integrins (CD29) assessed by U937 homotypic aggregation up to 70-80%. Furthermore, EtOAc and BuOH extracts displayed strong anti-oxidative activity with IC(50) values of 14 and 15 microM, respectively, when tested by the
1,1-diphenyl-2-picrylhydrazyl (DPPH) and
xanthine oxide (XO) assays. Taken together, these data suggest that the anti-inflammatory actions of Cinnamomum camphora may be due to the modulation of
cytokine, NO and
PGE(2) production and oxidative stress, and of the subfractions tested, the EtOAc extract may be further studied to isolate the active anti-inflammatory principles.