NADPH oxidase 2 does not contribute to early reperfusion-associated reactive oxygen species generation following transient focal cerebral ischemia
Autor: | Jian-Ming Wu, Yuan Zhang, Ting Wang, Ke Yang, Wenlan Liu, Ji Xu |
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Rok vydání: | 2016 |
Předmět: |
0301 basic medicine
Pathology medicine.medical_specialty Nox family Central nervous system Ischemia nerve regeneration NADPH oxidase cerebral ischemia reactive oxygen species reperfusion central nervous system stroke blood flow neural regeneration Pharmacology lcsh:RC346-429 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Developmental Neuroscience medicine Lucigenin Stroke lcsh:Neurology. Diseases of the nervous system chemistry.chemical_classification Reactive oxygen species biology business.industry medicine.disease 030104 developmental biology medicine.anatomical_structure Cerebral blood flow chemistry biology.protein business Reperfusion injury 030217 neurology & neurosurgery Research Article |
Zdroj: | Neural Regeneration Research, Vol 11, Iss 11, Pp 1773-1778 (2016) Neural Regeneration Research |
ISSN: | 1673-5374 |
Popis: | Excess production of reactive oxygen species (ROS) critically contributes to occurrence of reperfusion injury, the paradoxical response of ischemic brain tissue to restoration of cerebral blood flow. However, the enzymatic sources of ROS generation remain to be unclear. This study examined Nox2-containing NADPH oxidase (Nox2) expression and its activity in ischemic brain tissue following post-ischemic reperfusion to clarify the mechanism of enzymatic reaction of ROS. Male Sprague-Dawley rats were subjected to 90-minute middle cerebral artery occlusion, followed by 3 or 22.5 hours of reperfusion. Quantitative reverse transcriptase PCR and western blot assay were performed to measure mRNA and protein expression of Nox2. Lucigenin fluorescence assays were performed to assess Nox activity. Our data showed that Nox2 mRNA and protein expression levels were significantly increased (3.7-fold for mRNA and 3.6-fold for protein) in ischemic brain tissue at 22.5 hours but not at 3 hours following post-ischemic reperfusion. Similar results were obtained for the changes of NADPH oxidase activity in ischemic cerebral tissue at the two reperfusion time points. Our results suggest that Nox2 may not contribute to the early burst of reperfusion-related ROS generation, but is rather an important source of ROS generation during prolonged reperfusion. |
Databáze: | OpenAIRE |
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