We are analyzing https://link.springer.com/article/10.1007/s11064-022-03643-8.

Title:
Selenium Alleviates Cerebral Ischemia/Reperfusion Injury by Regulating Oxidative Stress, Mitochondrial Fusion and Ferroptosis | Neurochemical Research
Description:
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.
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Keywords {🔍}

treatment, cells, pubmed, cerebral, injury, article, ferroptosis, mfn, oxidative, stress, google, scholar, brain, ogdr, mcao, fig, mitochondrial, mice, group, expression, cell, iron, level, content, selenium, detected, cas, kit, central, assay, staining, fusion, model, apoptosis, significantly, wang, data, chen, china, tissues, mda, ischemiareperfusion, zhang, gpx, levels, protein, sod, showed, mouse, induced,

Topics {✒️}

lentiviral vector plko-trc-puro pink1/parkin-mediated mitophagy clearance quantitative real-time pcr cerebral ischemia-reperfusion injury prevent ischemia-reperfusion injury tdt enzyme andfluorescein-12-dutp fundc1-dependent mitophagy induced roles/writing—original draft article download pdf total glutathione/oxidized glutathione cerebral ischemia/reperfusion cerebral ischemia-reperfusion mitochondrial fusion/fission dynamics mcao + se + si-nc group ischemia/reperfusion injuries mcao + se + si-mfn1 group autophagy-lysosomal pathway anti-oxidative stress caused central nervous system ischemia reperfusion injury middle cerebral artery mcao + se + si-nc scientific research project qrt-pcr assay showed ischemic cerebrovascular disease full access qrt-pcr result showed common carotid artery privacy choices/manage cookies mcao + se + si-mfn1 oxygen–glucose deprivation pathogen-free cages writing—review & editing redox biology protects cerebral neurons catalyzing redox reaction transcriptional adaptive program search search cell death triggered total protein concentrations se alleviated cerebral glutathione/oxidized glutathione multiple biological functions ischemia/reperfusion iron-dependent form cerebral infarction area mcao + se treatment group external carotid artery internal carotid artery dixon sj

Questions {❓}

Steinbrenner H, Klotz LO (2020) Selenium and zinc: “antioxidants” for healthy aging?

Schema {🗺️}

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         description: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.
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      headline:Selenium Alleviates Cerebral Ischemia/Reperfusion Injury by Regulating Oxidative Stress, Mitochondrial Fusion and Ferroptosis
      description: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.
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      name:Department of Neurology, The Yancheng School of Clinical Medicine of Nanjing Medical University (Yancheng Third People’s Hospital), Yancheng, China
      name:Department of Central Laboratory, The Yancheng School of Clinical Medicine of Nanjing Medical University (Yancheng Third People’s Hospital), Yancheng, China
      name:Department of Central Laboratory, The Yancheng School of Clinical Medicine of Nanjing Medical University (Yancheng Third People’s Hospital), Yancheng, China

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