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The Mitochondria-targeted Peptide, Bendavia, Attenuated Ischemia/Reperfusion-induced Stroke Damage.
https://gifu-pu.repo.nii.ac.jp/records/14155
https://gifu-pu.repo.nii.ac.jp/records/14155586ec1c4-5a25-4ed7-bcbb-d1c4ce791c8a
| Item type | 研究室原著論文(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2020-09-11 | |||||
| タイトル | ||||||
| タイトル | The Mitochondria-targeted Peptide, Bendavia, Attenuated Ischemia/Reperfusion-induced Stroke Damage. | |||||
| 言語 | en | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | journal article | |||||
| アクセス権 | ||||||
| アクセス権 | metadata only access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
| 抄録 | ||||||
| 値 | After ischemic stroke, oxygen and nutrition depletion induce mitochondrial dysfunction, which aggravates brain injury. Bendavia, a mitochondria-targeted tetra-peptide, has anti-oxidative and anti-inflammatory activities. We previously reported that bendavia protected human brain microvascular endothelial cells against oxygen/glucose deprivation (OGD)-induced damage via preserving mitochondrial function. The effects of bendavia on mitochondrial function include the inhibition of reactive oxygen species (ROS) production, inhibition of apoptosis, and restoration of adenosine tri-phosphate synthesis. However, the influence of bendavia on the blood-brain barrier (BBB) and neurons after brain ischemia/reperfusion damage is unclear. The aim of this study was to investigate whether bendavia has protective effects against ischemia/reperfusion damage using both in vivo and in vitro models. The in vivo experiments were conducted in mice, which were subjected to transient middle cerebral occlusion (t-MCAO) to induce brain ischemia/reperfusion damage. After t-MCAO, the cerebral blood flow (CBF), neurological deficits, infarct volume, BBB permeability, and microglia/macrophage activation were assessed. Compared to the vehicle group, bendavia administration (administered twice; immediately after reperfusion and 4 h later) attenuated the sensori-motor dysfunction and infarct formation independent of CBF variation. In addition, bendavia decreased BBB hyper-permeability and microglia/macrophage activation. The in vitro experiments were conducted utilizing two models: (1) OGD/re-oxygenation (OGD/R) or (2) hydrogen peroxide (H2O2)-induced neuron damage. In both models, bendavia inhibited neuronal cell death induced by OGD/R or H2O2. These findings indicated that bendavia attenuated brain ischemia/reperfusion damage and has direct neuroprotective effects against cell injury. Therefore, bendavia may be a novel therapeutic agent to improve ischemic stroke patient outcome. Keywords: bendavia; blood–brain barrier; brain ischemia; microglia/macrophage; neuron; oxygen-glucose deprivation/re-oxygenation (OGD/R). |
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| 書誌情報 |
en : Neuroscience 巻 443, p. 110-119, 発行日 2020-09-01 |
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| DOI | ||||||
| 値 | 10.1016/j.neuroscience.2020.07.044 | |||||
