Differential Effects of Foods Traditionally Regarded as ‘Heating’ and ‘Cooling’ on Prostaglandin E2 Production by a Macrophage Cell LineHuang C.J. · Wu M.C.
Laboratory of Nutritional Biochemistry, Department of Agricultural Chemistry, National Taiwan University, Taipei, Taiwan, ROC
Some components of natural foods may enhance or inhibit prostaglandin formation and potentially affect the inflammation condition. A macrophage cell line, RAW264.7, was employed to examine the effects of foods traditionally regarded as ‘heating’ or ‘cooling’ on the production of PGE2, a well-known proinflammatory mediator. Foods traditionally regarded as ‘heating’ (litchi, longan, and dried longan) or ‘cooling’ (chrysanthemum flower, bitter gourd, and lotus seed plumule) were extracted sequentially with water and ethyl acetate. The water extracts (WE) and ethyl acetate extracts (EAE) were applied to RAW264.7 macrophages in the presence or absence of LPS (lipopolysaccharide). In the absence of LPS, the WEs from the ‘heating foods’, litchi, longan, or dried longan had a dose-dependent enhancing effect on PGE2 production, with respective EC50s of 8.4, 16, and 11 mg/ml. This effect was accompanied by significant induction of COX-2 protein expression, as shown by Western blot analysis. In contrast, LPS-induced PGE2 production was inhibited in a dose-dependent manner by the WEs of the ‘cooling foods’, chrysanthemum flower, bitter gourd, and lotus seed plumule, with respective IC50s of 0.6, 0.13, and 0.08 mg/ml. At the concentrations tested, none of the EAEs had any effect on basal PGE2 production, while LPS-induced PGE2 production was inhibited or increased by the EAE from bitter gourd and longan, respectively. Water-soluble extracts of foods traditionally regarded as ‘heating’ enhanced basal PGE2 production, while those from ‘cooling’ foods significantly inhibited LPS-induced PGE2 production by the macrophage cell line. This subject merits further study to determine whether appropriate food selection may help patients suffering from chronic inflammatory conditions.
© 2002 National Science Council, ROC and S. Karger AG, Basel