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      SOD3 overexpression alleviates cerebral ischemia‐reperfusion injury in rats

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          Abstract

          Background

          Ischemic 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.

          Methods

          GV230‐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.

          Results

          Western 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.

          Conclusion

          Our results indicated that MSCs transfected with SOD3 can effectively alleviate cerebral ischemia‐reperfusion injury in rats.

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          Mesenchymal stem cells promote proliferation of endogenous neural stem cells and survival of newborn cells in a rat stroke model.

          Byoung Kim, Seung-Schik Yoo, Moo Lee … (2008)
          Mesenchymal stem cells (MSCs) secrete bioactive factors that exert diverse responses in vivo. In the present study, we explored mechanism how MSCs may lead to higher functional recovery in the animal stroke model. Bone marrow-derived MSCs were transplanted into the brain parenchyma 3 days after induction of stroke by occluding middle cerebral artery for 2 h. Stoke induced proliferation of resident neural stem cells in subventricular zone. However, most of new born cells underwent cell death and had a limited impact on functional recovery after stroke. Transplantation of MSCs enhanced proliferation of endogenous neural stem cells while suppressing the cell death of newly generated cells. Thereby, newborn cells migrated toward ischemic territory and differentiated in ischemic boundaries into doublecortin+ neuroblasts at higher rates in animals with MSCs compared to control group. The present study indicates that therapeutic effects of MSCs are at least partly ascribed to dual functions of MSCs by enhancing endogenous neurogenesis and protecting newborn cells from deleterious environment. The results reinforce the prospects of clinical application using MSCs in the treatment of neurological disorders.
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            Effects of transplantation with bone marrow-derived mesenchymal stem cells modified by Survivin on experimental stroke in rats

            Nan Liu, Yixian Zhang, Lin Fan … (2011)
            Background This study was performed to determine whether injury induced by cerebral ischemia could be further improved by transplantation with bone marrow-derived mesenchymal stem cells (MSCs) modified by Survivin (SVV). Methods MSCs derived from bone marrow of male Sprague-Dawley rats were infected by the self-inactive lentiviral vector GCFU carrying green fluorescent protein (GFP) gene and SVV recombinant vector (GCFU-SVV). In vitro, vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) were detected in infected MSCs supernatants under hypoxic conditions by ELSIA. In vivo, experiments consisted of three groups, one receiving intravenous injection of 500 μl of phosphate-buffered saline (PBS) without cells (control group) and two groups administered the same volume solution with either three million GFP-MSCs (group GFP) or SVV/GFP-MSCs (group SVV). All animals were submitted to 2-hour middle cerebral artery occlusion (MCAO) and then reperfusion. Differentiation and survival of the transplanted MSCs were determined by confocal microscope. Western blot was used to detect the expression of VEGF and bFGF in ischemic tissue. A 2,3,5-triphenyltetrazolium chloride (TTC) staining was used to assess the infarct volume. Evaluation of neurological function was performed using a modified Neurological Severity Score (mNSS). Results In vitro, modification with SVV further increased secretion of VEGF and bFGF under hypoxic condition. In vivo, only very few transplantated cells co-expressed GFP and NeuN. The survival transplanted cells in the group SVV was 1.3-fold at 4 days after transplantation and 3.4-fold higher at 14 days after transplantation, respectively, when compared with group GFP. Expression of VEGF and bFGF in the ischemic tissue were further up-regulated by modification with SVV. Moreover, modification with SVV further reduced the cerebral infarct volume by 5.2% at 4 days after stroke and improved post-stroke neurological function at 14 days after transplantation. Conclusion Modification with SVV could further enhance the therapeutic effects of MSCs possibly through improving the MSCs survival capacity and up-regulating the expression of protective cytokines in the ischemic tissue.
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              Ellagic acid protects against neuron damage in ischemic stroke through regulating the ratio of Bcl-2/Bax expression

              Qing-shan Liu, Ran Deng, Shuran Li … (2017)
              An oxygen-glucose deprivation and reoxygenation model in primary cultured rat cortical neurons was developed for this study to investigate the effects of ellagic acid (EA), a low-molecular-weight polyphenol, on neuron cells and their function, and to evaluate whether EA can be safely utilized by humans as a functional food or therapeutic agent. Administration of EA significantly decreased the volume of cerebrum infarction and the neurological deficit scores of the rats; EA treatment also increased the number of Bcl-2-positive cells and the ratio of Bcl-2-positive to Bax-positive neurons in the semidarkness zone near the brain ischemic focus in the photothrombotic cerebral ischemia model. Treatment of EA resulted in increased neuron viability, cell nuclear integrity, and the ratio of Bcl-2/Bax expression in the primary cultured neuron model; EA treatment also lead to a decrease in the number of apoptotic cells. Our results therefore suggest a specific mechanism for the beneficial effects of EA, providing new insights into how it provides neuroprotection. To the best of our knowledge, these results represent new insights on the mechanisms of the brain cell protective activity of EA. Thus, EA may be used in functional foods or medicines to help treat nerve dysfunction, neurodegenerative disease, and aging.
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                Author and article information

                Contributors
                Ying Xia:
                ORCID: https://orcid.org/0000-0001-8018-4935
                yingxiahainan@163.com
                Journal
                Journal ID (nlm-ta): Mol Genet Genomic Med
                Journal ID (iso-abbrev): Mol Genet Genomic Med
                Journal ID (doi): 10.1002/(ISSN)2324-9269
                Journal ID (publisher-id): MGG3
                Title: Molecular Genetics & Genomic Medicine
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Electronic): 2324-9269
                Publication date (Electronic): 28 August 2019
                Publication date Collection: October 2019
                Volume: 7
                Issue: 10 ( doiID: 10.1002/mgg3.v7.10 )
                Electronic Location Identifier: e00831
                Affiliations
                [ 1 ] Department of Neurosurgery Haikou People’s Hospital, Xiangya Medical College Affiliated Haikou Hospital, Central South University Haikou China
                [ 2 ] Department of Neurosurgery Yiyang Central Hospital Hunan China
                Author notes
                [*] [* ] Correspondence

                Ying Xia, # 43 Renmin avenue, Haidian island, Haikou, Hainan570208, China.

                Email: yingxiahainan@ 123456163.com

                Author information
                https://orcid.org/0000-0001-8018-4935
                Article
                Publisher ID: MGG3831
                DOI: 10.1002/mgg3.831
                PMC ID: 6785449
                PubMed ID: 31461803
                SO-VID: 3e10148e-92bc-478f-9a06-7c63006576b5
                Copyright © © 2019 The Authors. Molecular Genetics & Genomic Medicine published by Wiley Periodicals, Inc.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 14 November 2018
                Date revision received : 28 March 2019
                Date accepted : 07 April 2019
                Page count
                Figures: 4, Tables: 0, Pages: 9, Words: 4767
                Funding
                Funded by: National Natural Science Foundation of China
                Award ID: 81360190
                Categories
                Subject: Original Article
                Subject: Original Articles
                Custom metadata
                source-schema-version-number 2.0
                component-id mgg3831
                cover-date October 2019
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:5.7.0 mode:remove_FC converted:09.10.2019

                Keywords: ischemic stroke,mesenchymal stem cells,protection,sod3
                Data availability:
                Keywords: ischemic stroke, mesenchymal stem cells, protection, sod3

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