Effects of over-expression of SOD2 in bone marrow-derived mesenchymal stem cells on traumatic brain injury

被引:25
作者
Shi, Xiaodong [1 ,2 ]
Bai, Yunan [2 ]
Zhang, Guodong [2 ]
Liu, Yuguang [1 ]
Xiao, Hang [2 ]
Liu, Xiaogang [2 ]
Zhang, Wei [1 ]
机构
[1] Qilu Hosp, Wenhuaxi Rd, Jinan 250014, Shandong, Peoples R China
[2] Weifang Yidu Cent Hosp, Dept Neurosurg, 4138 Linglongshan Rd, Qingzhou 262500, Shandong, Peoples R China
关键词
Traumatic brain injury (TBI); Mesenchymal stem cell (MSC); Superoxide dismutase 2 (SOD2); Oxidative stress; Antioxidant; OXIDATIVE STRESS; STROMAL CELLS; PHASE-I; THERAPY; DISEASE; CANCER; OVEREXPRESSION; IMPACT; RAT;
D O I
10.1007/s00441-017-2716-7
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Intravenous administration of bone marrow-derived mesenchymal stem cells (BM-MSCs) has been shown to promote nerve cell regeneration following traumatic brain injury (TBI). As the anti-oxidant defense systems in neuronal tissue including superoxide dismutase 2 (SOD2) are crucial to defend cell against oxidative stress. We proposed a new stratege to increase the therapeutic effect of MSCs by preventing cells death from oxidative stress. We overexpressed SOD2 in BM-MSCs, transplanted these MSCs into TBI model mice, assessed the protective effect of SOD2 against oxidation-induced apoptosis in BM-MSCs both in vitro and in vivo, evaluated brain functional recovery by the rotarod behavioral test, and tested the oxidation status of TBI mice brain after BM-MSCs transplantation by monitoring the superoxide dismutase, glutathione and malonaldehyde level. We found over-expression of SOD2 protected BM-MSCs from H2O2-induced cell apoptosis. Injection of SOD2 over-expressed BM-MSCs attenuated neuro-inflammation in the ipsilateral cortex of TBI mice, and protected TBI mice against loss of blood-brain barrier integrity. Furthermore, the rotarod behavioral test showed functional recovery of TBI mice after MSC treatment. Our experiments indicated that SOD2-over-expressed BM-MSCs have an improved therapeutic effect on brain injury treatment in TBI mice.
引用
收藏
页码:67 / 75
页数:9
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