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Selenium Alleviates Cerebral Ischemia/Reperfusion Injury by Regulating Oxidative Stress, Mitochondrial Fusion and
Yuanyuan Shi1, Lijian Han2, Xianxian Zhang2
1Department of Central Laboratory, The Yancheng School of Clinical Medicine of Nanjing Medical University (Yancheng Third People's Hospital), Yancheng, 224008, Jiangsu, China.
Abstract:
To clarify the potential role of selenium (Se) on cerebral ischemia/reperfusion (I/R) injury, we utilized mouse middle cerebral artery occlusion (MCAO) followed by reperfusion as an animal model and oxygen-glucose deprivation and reoxygenation (OGD/R) to treat N2a cells as a cell model, respectively. MCAO model was established in mice and then divided into different groups with or without Se treatment. TTC staining was used to observe whether the cerebral I/R modeling was successful, and the apoptosis level was determined by TUNEL staining. The expression of GPx-4 and p22phox was assessed by western blot. In vitro experiments, the OGD/R induced oxidative stress in N2a cells was assessed by levels of GSH/GSSG, malondialdehyde, superoxide dismutase and iron content, respectively. QRT-PCR was used to detect the mRNA levels of Cox-2, Fth1, Mfn1 and mtDNA in N2a cells. JC-1 staining and flow cytometry was performed to detect the mitochondrial membrane potential. Se treatment alleviated cerebral I/R injury and improved the survival rate of mice. Additionally, Se treatment apparently attenuated oxidative stress and inhibited iron accumulation in MCAO model mice and OGD/R model of N2a cells. In terms of its mechanism, Se could up-regulate Mfn1 expression to alleviate oxidative stress and ferroptosis by promoting mitochondrial fusion in vivo and vitro. These findings suggest that Se may have great potential in alleviating cerebral I/R injury.
Insights
Selenium (Se) supplementation alleviates cerebral ischemia/reperfusion (I/R) injury by reducing oxidative stress and iron accumulation. Se promotes mitochondrial fusion, offering potential therapeutic benefits for I/R injury.
Area of Science:
- Neuroscience
- Biochemistry
- Cell Biology
Background:
- Cerebral ischemia/reperfusion (I/R) injury is a significant cause of neurological damage.
- Oxidative stress and ferroptosis play critical roles in the pathogenesis of I/R injury.
- The therapeutic potential of selenium (Se) in mitigating I/R injury remains to be fully elucidated.
Purpose of the Study:
- To investigate the protective effects of selenium (Se) against cerebral ischemia/reperfusion (I/R) injury.
- To explore the underlying mechanisms by which Se influences oxidative stress, ferroptosis, and mitochondrial dynamics in I/R injury models.
Main Methods:
- Established mouse middle cerebral artery occlusion (MCAO) and N2a cell oxygen-glucose deprivation/reoxygenation (OGD/R) models.
- Assessed I/R injury using TTC and TUNEL staining, western blot for GPx-4 and p22phox.
- Quantified oxidative stress markers (GSH/GSSG, MDA, SOD, iron content) and mitochondrial membrane potential (JC-1 staining).
- Analyzed mRNA levels of Cox-2, Fth1, Mfn1, and mtDNA using qRT-PCR.
Main Results:
- Se treatment significantly alleviated cerebral I/R injury in mice, improving survival rates.
- Se administration attenuated oxidative stress and inhibited iron accumulation in both MCAO and OGD/R models.
- Se upregulated Mfn1 expression, promoting mitochondrial fusion and reducing oxidative stress and ferroptosis.
Conclusions:
- Selenium demonstrates significant neuroprotective effects against cerebral I/R injury.
- Se mitigates I/R injury by inhibiting oxidative stress and iron accumulation through enhanced mitochondrial fusion.
- Selenium holds considerable therapeutic potential for managing cerebral I/R injury.
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