The study is aimed to explore the molecular mechanism of the treatment of
apocynin in
dextran sulfate sodium (DSS)-induced
ulcerative colitis (UC) mice. 5% DSS was used to mimic the UC model, and 2%
apocynin was applied to treat the UC mice. HE staining was used for histopathological evaluation. Chemiluminescence technique was used to measure
reactive oxygen species (ROS) production, and the rate of consumption of
NADPH inhibited by DPI was detected to determine the
NADPH oxidases (NOXs) activity. Western blot was applied to identify the level of p38MAPK phosphorylation, Griess reaction assay to analyze NO production, immunoenzymatic method to determine
prostaglandin E2 (
PGE2) production, real time RT-PCR and Western blot to identify the expression of iNOS and COX2, and
enzyme linked
immunosorbent assay to detect inflammatory
cytokines TNF-α,
IL-6, IFN-γ, IL-1β. Rat neutrophils were separated, and then ROS production, NOXs activity, NO and
PGE2 production, NOX1 and p-p38MAPK expression were detected. Compared with the UC group,
apocynin decreased ROS over-production and NOXs activity (P < 0.01), reduced p38MAPK phosphorylation, inhibited NO,
PGE2 and
cytokines production (P < 0.01).
Apocynin also decreased NOXs activity and ROS over-production (P < 0.01), inhibited p38MAPK phosphorylation and NOX1 expression, and reduced NO and
PGE2 production (P < 0.01) in separated neutrophils from UC mice. Therefore,
apocynin could relieve
inflammation in DSS-induced UC mice through inhibiting NOXs-ROS-p38MAPK signal pathway, and neutrophils play an important role.