Inflammation is a defense mechanism that protects the body from
infections. However, chronic
inflammation causes damage to body tissues. Thus, controlling
inflammation and investigating anti-inflammatory mechanisms are keys to preventing and treating inflammatory diseases, such as
sepsis and
rheumatoid arthritis. In continuation with our work related to the discovery of bioactive natural products, a
polyphenol, catechin-7,4'-O-digallate (CDG), was isolated from Woodfordia uniflora, which has been used as a
sedative and remedy for skin
infections in the Dhofar region of Oman. Thus far, no study has reported the anti-inflammatory compounds derived from W. uniflora and the mechanisms underlying their action. To investigate the effects of CDG on the regulation of
inflammation, we measured the reduction in
nitric oxide (NO) production following CDG treatment in immortalized mouse Kupffer cells (ImKCs). CDG treatment inhibited NO production through the downregulation of
inducible nitric oxide synthase expression in
lipopolysaccharide (LPS)-stimulated ImKCs. The anti-inflammatory effects of CDG were mediated via the inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, an important inflammatory-response-associated signaling pathway. Moreover, CDG treatment has regulated the expression of pro-inflammatory
cytokines, such as
IL-6 and IL-1β. These results suggested the anti-inflammatory action of CDG in LPS-stimulated ImKCs.