NADPH oxidase is involved in ischaemia/reperfusion-induced damage in rat gastric mucosa via ROS production--role of NADPH oxidase in rat stomachs

• Published in: Inflammopharmacology Vol. 15; no. 6; pp. 278 - 281
• Main Authors: Nakagiri, A, Sunamoto, M, Murakami, M
• Format: Journal Article
• Language: English
• Published: Switzerland 01-12-2007
• Subjects: Animals; Blotting, Western; Capillary Permeability - drug effects; Cytosol - metabolism; Enzyme Activation - physiology; Gastric Mucosa - enzymology; Gastric Mucosa - pathology; Hydrogen Peroxide - metabolism; Male; NADPH Oxidases - metabolism; NADPH Oxidases - physiology; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species - metabolism; Reperfusion Injury - enzymology; Reperfusion Injury - pathology; Stomach - enzymology; Stomach - physiology
• ISSN: 0925-4692; 1568-5608
• DOI: 10.1007/s10787-007-1587-z

In the process of the oxygen reduction, NADPH oxidase is the enzyme that produces superoxide anion, which subsequently produces reactive oxygen species (ROS) and causes damage in various tissues and microorganisms. NADPH oxidase is demonstrated to exist in several types of cells such as endothelial cells and vascular smooth muscle cells. In the present study, we examined the role of NADPH oxidase in ischaemia/reperfusion (I/R)-induced damage in the rat gastric mucosa. Male SD rats were used after 18 h fasting. Under urethane anaesthesia, the stomach was mounted in an ex-vivo chamber, applied with 100 mM HCl, and a catheter was passed through the left femoral vein. To produce I/R, 4 mL of blood was removed at for 30 min, and then reperfused. DPI was given i.v. 10 min before reperfusion. The combination of ischaemia and reperfusion produced haemorrhagic damage in the rat gastric mucosa. The damage was attenuated by pretreatment of DPI. I/R increased microvascular permeability, the amount of H2O2 and NADPH oxidase activity in the stomach. These increases were suppressed by pretreatment of DPI. As to the presence of a subunit of NADPH oxidase, we detected protein level of p47phox in the gastric mucosa. In conclusion, these results showed that ROS production via NADPH oxidase activity is involved in the pathogenic mechanism of I/R damage in the rat stomach and suggested that activation of NADPH oxidase and the associated ROS product could be a potential target in the gastrointestinal mucosal damage.