{'fraction_non_alphanumeric': 0.028551532033426183, 'fraction_numerical': 0.012534818941504178, 'mean_word_length': 5.415178571428571, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
NADPH oxidase mediates the expression of MMP-9 in cerebral tissue after ischemia–reperfusion damage

Abstract Oxygen free radicals and their reactive lipid peroxidation are known to be elements promoting ischemia–reperfusion damage. NADPH oxidase is a major factor in peroxide production. Excessive production of oxygen free radicals is considered as an important mechanism in the expression of matrix metalloproteinase (MMP)-9 and in damage to the blood–brain barrier (BBB). In this study, we evaluated changes in the expression of the NADPH oxidase catalytic subunit gp91phox and oxidase activity, as well as the involvement of NADPH oxidase catalysis in the expression of MMP-9 in cerebral tissue after ischemia–reperfusion damage. A middle cerebral artery occlusion (MCAO) model was established using male Sprague-Dawley (SD) rats. Brain tissue was isolated for triphenyltetrazolium chloride (TTC) staining, gp91phox mRNA quantitative PCR analysis, western blot analysis, NADPH oxidase activity determination (detection), and MMP-9 gelatin zymography analysis. In the MCAO rats, gp91phox and MMP-9 expression was upregulated in the ischemic hemisphere of the brain tissue after 90 minutes of MCAO with 22·5 hours of reperfusion. Inhibition of NADPH oxidase with apocynin reduced the increase in MMP-9. These results suggest that NADPH oxidase is a major precipitating factor for the expression of MMP-9 in the ischemic brain tissue.