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Oregonin from the Bark of Alnus japonica Restrained Ischemia–Reperfusion‐Induced Mesentery Oxidative Stress by Inhibiting NADPH Oxidase Activation
Author(s) -
Tung Nguyen Huu,
Sun Kai,
Fan JingYu,
Shoyama Yukihiro,
Han JingYan
Publication year - 2014
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1111/micc.12147
Subject(s) - nadph oxidase , degranulation , oxidative stress , reactive oxygen species , chemistry , ischemia , superior mesenteric artery , microbiology and biotechnology , biochemistry , medicine , biology , receptor
Objective NADPH oxidase activation results in ROS overproduction that is the pathological basis of I/R injury. This study aimed to investigate potential effects of ORG on I/R‐induced ROS production in rat mesenteric microvasculature and underlying mechanisms. Methods Mesenteric I/R in Male Wistar rats (200~250 g) was induced by ligation of the mesenteric artery and vein for 10 minutes followed by reperfusion for 60 minutes by releasing of the occlusion. The rats were infused intravenously with or without ORG (5 mg/kg per hour) 10 minutes before ischemia (pretreatment) or 20 minutes after reperfusion (posttreatment). The DHR fluorescence intensity on, the leukocytes adherent to, and mast cell degranulation out of mesenteric venules were determined using an intravital microscope. NADPH oxidase subunit p47 phox membrane translocation in intestine tissues was detected by Western blotting. Results Pre‐ or posttreatment with ORG inhibited I/R‐induced DHR fluorescence intensity on the venular walls and leukocytes adhesion, ORG pretreatment inhibited mast cell degranulation as well. Furthermore, the translocation of p47 phox from cytosol to membrane was suppressed markedly by ORG after I/R. Conclusions The results suggested that ORG restrained I/R‐induced ROS production, which might be correlated with its inhibitive effect on NADPH activation.