Oregonin from the Bark of Alnus japonica Restrained Ischemia-Reperfusion-Induced Mesentery Oxidative Stress by Inhibiting NADPH Oxidase Activation

ObjectiveNADPH 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. MethodsMesenteric I/R in Male Wistar rats (200 similar to 250g) was induced by ligation of the mesenteric artery and vein for 10minutes followed by reperfusion for 60minutes by releasing of the occlusion. The rats were infused intravenously with or without ORG (5mg/kg per hour) 10minutes before ischemia (pretreatment) or 20minutes 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. ResultsPre- 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. ConclusionsThe results suggested that ORG restrained I/R-induced ROS production, which might be correlated with its inhibitive effect on NADPH activation.HematologyPeripheral Vascular DiseaseSCI(E)0ARTICLEshoyama@niu.ac.jp; hanjingyan@bjmu.edu.cn8688-6952