ArticleMolecular genetics & genomic medicine2019
SOD3 overexpression alleviates cerebral ischemia-reperfusion injury in rats.
Article in Molecular genetics & genomic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
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- The ER Stress Induced in Human Neuroblastoma Cells Can Be Reverted by Lumacaftor, a CFTR Corrector.Current issues in molecular biology · 2024Article
- Deciphering Proteomic Expression in Inflammatory Disorders: A Mass Spectrometry Exploration Comparing Infectious, Noninfectious, and Traumatic Brain Injuries in Human Cerebrospinal Fluid.Neurotrauma reports · 2024Article
- The Applications and Mechanisms of Superoxide Dismutase in Medicine, Food, and Cosmetics.Antioxidants (Basel, Switzerland) · 2023Review
- Adenosine receptor A1 enhanced mitochondrial biogenesis and exerted neuroprotection after cerebral ischemia through PGC-1α.Experimental brain research · 2023Article
- MSC based gene delivery methods and strategies improve the therapeutic efficacy of neurological diseases.Bioactive materials · 2023Review
- All roads lead to Rome - a review of the potential mechanisms by which exerkines exhibit neuroprotective effects in Alzheimer's disease.Neural regeneration research · 2022Review
- Clinical Observation of Salvianolic Acid Combined with Panax Notoginseng Saponins Combined with Basic Nursing Intervention on Cerebral Ischemia-Reperfusion Injury in Rats.Journal of healthcare engineering · 2022Article
- Genetic Modification of Mesenchymal Stem Cells for Neurological Disease Therapy: What Effects Does it Have on Phenotype/Cell Behavior, Determining Their Effectiveness?Molecular diagnosis & therapy · 2020Review
- Improved therapeutics of modified mesenchymal stem cells: an update.Journal of translational medicine · 2020Review
- SOD3 overexpression alleviates cerebral ischemia-reperfusion injury in rats.Molecular genetics & genomic medicine · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIschemic stroke is a deadly disease that poses a serious threat to human life. Superoxide dismutase 3 (SOD3, ECSOD) is the main antioxidant enzyme that removes superoxide anions from cells. This study aimed to investigate the effect of SOD3 overexpression on cerebral ischemia-reperfusion injury in rats.
methodsGV230-EGFP-ECSOD, the recombinant SOD3-overexpressed vector, was constructed by genetic engineering technology, and mesenchymal stem cells (MSCs) were infected with lentiviral packaging. In animal experiment, cerebral ischemia-reperfusion injury model rats were successfully established. ECSOD-MSCs are the MSCs that successfully transfected with SOD3 overexpression vector. The animals were injected with ECSOD-MSCs (ECSOD-MSC group), normal MSCs (MSCs group), PBS (PBS group), and not do any processing (Model group) via the tail vein. Then MRI was used to detect the infarct volume of rats, modified Neurological Severity Scores (mNSS), and immunohistochemistry were used to evaluate the expression of neurological function and apoptosis-related genes in rats.
resultsWestern blot analysis revealed that the SOD3 was highly expressed in MSCs. Animal experiments showed that the transplantation of ECSOD-MSCs significantly reduced the infarct volume of ischemic stroke rats (p < 0.05), significantly improved neurological function in rats (p < 0.05), and found proapoptotic gene, Bax, expression was significantly decreased (p < 0.05), the expression of anti-apoptotic gene, Bcl-2, was significantly increased (p < 0.05). The highly expressed SOD3 has no correction with brain infarct volume, and the highly expressed SOD3 has a positive correlation with cell apoptosis. It is speculated that overexpression of SOD3 affects the expression of Bax and Bcl-2, and improves apoptosis to alleviate ischemic stroke.
conclusionOur results indicated that MSCs transfected with SOD3 can effectively alleviate cerebral ischemia-reperfusion injury in rats.
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