Attenuation of Ischemic Stroke-Caused Brain Injury by a Monoamine Oxidase Inhibitor Involves Improved Proteostasis and Reduced Neuroinflammation
| العنوان: | Attenuation of Ischemic Stroke-Caused Brain Injury by a Monoamine Oxidase Inhibitor Involves Improved Proteostasis and Reduced Neuroinflammation |
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| المؤلفون: | Hongmin Wang, Kalpana Subedi, Yanying Liu, Shelley Feng |
| المصدر: | Mol Neurobiol |
| بيانات النشر: | Springer Science and Business Media LLC, 2019. |
| سنة النشر: | 2019 |
| مصطلحات موضوعية: | 0301 basic medicine, Nialamide, Monoamine Oxidase Inhibitors, medicine.drug_class, Monoamine oxidase, Neuroscience (miscellaneous), Ischemia, Pharmacology, medicine.disease_cause, Neuroprotection, Article, Mice, 03 medical and health sciences, Cellular and Molecular Neuroscience, 0302 clinical medicine, medicine, Animals, Neuroinflammation, Inflammation, Neurons, Monoamine oxidase inhibitor, Chemistry, Brain, Recovery of Function, medicine.disease, Mitochondria, Stroke, Oxidative Stress, 030104 developmental biology, Proteostasis, Neurology, Astrocytes, Brain Injuries, 030217 neurology & neurosurgery, Oxidative stress, medicine.drug |
| الوصف: | Mitochondrial dysfunction and oxidative stress play a key role in ischemia/reperfusion (I/R) induced brain injury. We previously showed that ubiquilin-1 (Ubqln1), a ubiquitin-like protein, improves proteostasis and protects brains against oxidative stress and I/R induced brain injury. We demonstrate here that nialamide (NM), a non-selective monoamine oxidase (MAO) inhibitor, upregulated Ublqn1 and protected neurons from oxygen-glucose deprivation- and I/R-caused cell death in in vitro and in vivo, respectively. Post-ischemic administration of the NM in a stroke mouse model even at 3 h following I/R still reduced neuronal injury and improved functional recovery and survival. Treating stroke animals with NM also increased the association of Ubqln1 with mitochondria and decreased the total oxidized and polyubiquitinated protein levels. Intriguingly, NM-enhanced proteostasis was also associated with reduced I/R-caused neuroinflammation, as reflected by attenuated activation of microglia and astrocytes as well as reduced TNF-α level. Thus, our results suggest that MAO inhibition-induced neuroprotection following I/R involves improved proteostasis and reduced neuroinflammation. |
| تدمد: | 1559-1182 0893-7648 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0a4df0764d8f5225c67577ba0b960f11Test https://doi.org/10.1007/s12035-019-01788-2Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....0a4df0764d8f5225c67577ba0b960f11 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15591182 08937648 |
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