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[Apocynin relieves inflammation in dextran sulfate sodium-induced ulcerative colitis mice: the role of NOXs-ROS-p38MAPK pathway.] [Article in Chinese]

WEI Dan-Dan, LIN Xu-Hong, WANG Hui-Chao, WANG Bin, BAI Chun-Yang, WANG Ya-Qiang, LI Guo-En, REN Xue-Qun

Department of Clinical Laboratory, Huaihe Hospital Affiliated to Henan University, Kaifeng 475000, China； Department of Nephrology, the First Hospital Affiliated to Henan University, Kaifeng 475000, China； Department of Digestive Medicine, Huaihe Hospital Affiliated to Henan University, Kaifeng 475000, China； Department of General Surgery, Huaihe Hospital Affiliated to Henan University, Kaifeng 475000, China

Abstract

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.

Key words: apocynin; NADPH oxidase; reactive oxygen species

Received: 2014-07-10　　Accepted: 2014-08-21

Corresponding author: 任学群　　E-mail: lxh80726@126.com

Citing This Article：

WEI Dan-Dan, LIN Xu-Hong, WANG Hui-Chao, WANG Bin, BAI Chun-Yang, WANG Ya-Qiang, LI Guo-En, REN Xue-Qun. [Apocynin relieves inflammation in dextran sulfate sodium-induced ulcerative colitis mice: the role of NOXs-ROS-p38MAPK pathway.] [Article in Chinese]. Acta Physiol Sin 2015; 67 (1): 74-82 (in Chinese with English abstract).