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Targeting Smox Is Neuroprotective and Ameliorates Brain Inflammation in Cerebral Ischemia/Reperfusion Rats
Jiawei Fan1, Mei Chen2, Xiyan Wang1
1School of Basic Medical Science.
Abstract:
Spermine oxidase (Smox) is a member of the polyamine oxidases and has been demonstrated to be involved in ischemic brain damage. In this study, we found that Smox expression was increased in a rat middle cerebral artery occlusion (MCAO) model and in cultured primary neurons after oxygen-glucose deprivation and reoxygenation (OGD/R). Smox downregulation by the adeno-associated virus RNA interference system significantly reduced the MCAO-induced brain infarct volume and neurological deficits and decreased neuronal apoptosis and inflammatory reactions. In addition, significant microglial activation and increased IL-6 and TNF-α expression were observed in microglia treated with supernatant from neurons after OGD/R. However, a significant reduction in microglial activation as well as IL-6 and TNF-α expression was observed in microglia treated with supernatant from Smox downregulated neurons after OGD/R. Therefore, the results indicated that Smox is an important mediator of cerebral ischemia injury and may be a therapeutic target for cerebral ischemia patients.
Insights
Spermine oxidase (Smox) is elevated in ischemic brain injury. Reducing Smox lessens stroke damage, neuronal death, and inflammation, indicating Smox is a potential therapeutic target for cerebral ischemia.
Area of Science:
- Neuroscience
- Biochemistry
Background:
- Spermine oxidase (Smox) is implicated in ischemic brain damage.
- Polyamines and their catabolizing enzymes play roles in cellular stress responses.
Purpose of the Study:
- To investigate the role of Smox in cerebral ischemia.
- To evaluate Smox as a potential therapeutic target for stroke.
Main Methods:
- Utilized a rat middle cerebral artery occlusion (MCAO) model.
- Employed oxygen-glucose deprivation and reoxygenation (OGD/R) in cultured neurons.
- Used adeno-associated virus RNA interference to downregulate Smox.
- Assessed infarct volume, neurological deficits, neuronal apoptosis, and inflammatory markers (IL-6, TNF-α).
- Examined microglial activation.
Main Results:
- Smox expression increased in MCAO and OGD/R models.
- Smox downregulation significantly reduced infarct volume and neurological deficits.
- Reduced neuronal apoptosis and inflammatory reactions were observed post-Smox downregulation.
- Smox downregulation decreased microglial activation and pro-inflammatory cytokine expression (IL-6, TNF-α).
Conclusions:
- Smox is a key mediator in cerebral ischemia injury.
- Targeting Smox offers a potential therapeutic strategy for cerebral ischemia patients.
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