Brazilian
propolis is rich in
cinnamic acid derivatives and reportedly reduces intestinal
inflammation in rodents; however, the underlying mechanisms remain unclear. We hypothesized that the regulation of tight junction (TJ) barrier, Th17 cell differentiation, and/or, macrophage activation by
cinnamic acid derivatives were involved in the
propolis-mediated anti-inflammatory effect. Mice were orally administered 2%
dextran sodium sulfate (DSS) in combination with either the feeding control or a diet containing 0.3%
ethanol extract of Brazilian
propolis for 9 days. DSS administration induced acute
colitis in mice, whereas the
propolis extract mitigated DSS-induced
weight loss; colon shortening; increased plasma levels of
lipopolysaccharide-binding protein; reduced expression of TJ
proteins, such as zonula occludens,
junctional adhesion molecule-A,
occludin, and
claudins; and increased expression of inflammatory
cytokines, such as
tumor necrosis factor (TNF) α,
interleukin (IL) 6, and
IL-17a.
Cinnamic acid derivatives, such as
artepillin C and
caffeic acid phenethyl ester, present in the
propolis extract suppressed the
IL-17 production from cultured murine splenocytes through decreased
retinoic acid-related orphan receptor gT expression.
Baccharin,
drupanin, and culifolin, which are also present in Brazilian
propolis, reduced the TNF-α and/or
IL-6 production by suppressing inflammatory signaling in murine RAW 264.7 macrophages. Taken together, the regulation of Th17 differentiation and macrophage activation by
cinnamic acid derivatives, at least in part, contribute to the anti-inflammatory effect mediated by Brazilian
propolis.