Cu,Zn-Superoxide Dismutase Increases the Therapeutic Potential of Adipose-derived Mesenchymal Stem Cells by Maintaining Antioxidant Enzyme Levels |
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| Authors: | Dae Young Yoo Dae Won Kim Jin Young Chung Hyo Young Jung Jong Whi Kim Yeo Sung Yoon In Koo Hwang Jung Hoon Choi Goang-Min Choi Soo Young Choi Seung Myung Moon |
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| Affiliation: | 1.Departments of Anatomy and Cell Biology, College of Veterinary Medicine, and Research Institute for Veterinary Science,Seoul National University,Seoul,South Korea;2.Departments of Biochemistry and Molecular Biology, Research Institute of Oral Sciences, College of Dentistry,Gangneung-Wonju National University,Gangneung,South Korea;3.Departments of Veterinary Internal Medicine and Geriatrics, College of Veterinary Medicine and Institute of Veterinary Science,Kangwon National University,Chuncheon,South Korea;4.Department of Anatomy, College of Veterinary Medicine and Institute of Veterinary Science,Kangwon National University,Chuncheon,South Korea;5.Departments of Thoracic and Cardiovascular Surgery, Chuncheon Sacred Heart Hospital, College of Medicine,Hallym University,Chuncheon,South Korea;6.Department of Biomedical Sciences, and Research Institute for Bioscience and Biotechnology,Hallym University,Chuncheon,South Korea;7.Department of Neurosurgery, Dongtan Sacred Heart Hospital, College of Medicine,Hallym University,Hwaseong,South Korea |
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| Abstract: | In the present study, we investigated the ability of Cu, Zn-superoxide dismutase (SOD1) to improve the therapeutic potential of adipose tissue-derived mesenchymal stem cells (Ad-MSCs) against ischemic damage in the spinal cord. Animals were divided into four groups: the control group, vehicle (PEP-1 peptide and artificial cerebrospinal fluid)-treated group, Ad-MSC alone group, and Ad-MSC-treated group with PEP-1-SOD1. The abdominal aorta of the rabbit was occluded for 30 min in the subrenal region to induce ischemic damage, and immediately after reperfusion, artificial cerebrospinal fluid or Ad-MSCs (2?×?105) were administered intrathecally. In addition, PEP-1 or 0.5 mg/kg PEP-1-SOD1 was administered intraperitoneally to the Ad-MSC-treated rabbits. Motor behaviors and NeuN-immunoreactive neurons were significantly decreased in the vehicle-treated group after ischemia/reperfusion. Administration of Ad-MSCs significantly ameliorated the changes in motor behavior and NeuN-immunoreactive neuronal survival. In addition, the combination of PEP-1-SOD1 and Ad-MSCs further increased the ameliorative effects of Ad-MSCs in the spinal cord after ischemia. Furthermore, the administration of Ad-MSCs with PEP-1-SOD1 decreased lipid peroxidation and maintained levels of antioxidants such as SOD1 and glutathione peroxidase compared to the Ad-MSC alone group. These results suggest that combination therapy using Ad-MSCs and PEP-1-SOD1 strongly protects neurons from ischemic damage by modulating the balance of lipid peroxidation and antioxidants. |
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