Abstract
BackgroundBecause there is little research on the effects of transplanted stem cells on neuronal metabolites in infarct areas, we transplanted human umbilical cord blood mesenchymal stem cells (hUCB-MSCs) into cerebral ischemic rabbits and examined the neuronal metabolites.ResultsRabbits (n = 40) were equally divided into sham, middle cerebral artery occlusion (MCAO), hUCB-MSC, and saline groups. The rabbit ischemic model was established by MCAO. The effects of hUCB-MSC transplantation were assessed by proton magnetic resonance spectroscopy (1H-MRS), neurological severity scores (NSSs), infarct area volume, neuronal density, and optical density (OD) of microtubule-associated protein 2 (MAP2)-positive cells. We also evaluated complete blood cell counts(CBCs) and serum biochemical parameters. NSSs in the hUCB-MSC group at 7 and 14 days after reperfusion were lower than in MCAO and saline groups (p < 0.05). Compared with MCAO and saline groups at 2 weeks after MCAO, the infarction volume in the hUCB-MSC group had decreased remarkably (p < 0.05). Significant neuronal metabolic changes occurred in the infarct area at 24 h and 2 weeks after MCAO. 1H-MRS revealed an elevation in the lactate (Lac)/creatine including phosphocreatine (Cr) ratio and a decrease in the N-acetylaspartate (NAA)/Cr and choline-containing phospholipids (Cho)/Cr ratios at 24 h after MCAO in the MCAO group (p < 0.01). Compared with saline and MCAO groups at 24 h and 2 weeks after MCAO, NAA/Cr and Cho/Cr ratios had increased significantly, whereas the Lac/Cr ratio had decreased significantly in the hUCB-MSC group (p < 0.01). Neuronal density and OD of MAP2-positive cells in the MCAO group were significantly lower than those in the sham group, whereas the neuronal density and OD of MAP2-positive cells in the hUCB-MSC group were higher than those in MCAO and saline groups (p < 0.05). CBCs and biochemical parameters were unchanged in the MCAO group at 24 h and 2 weeks after hUCB-MSC transplantation.ConclusionsTransplanted hUCB-MSCs might ameliorate ischemic damage by influencing neuronal metabolites in the infarct area, providing additional evidence for neuroprotection by stem cells. No significant changes were observed in CBCs or serum biochemical parameters, suggesting that intravenous infusion of hUCB-MSCs is safe for rabbits in the short-term.
Highlights
Because there is little research on the effects of transplanted stem cells on neuronal metabolites in infarct areas, we transplanted human umbilical cord blood mesenchymal stem cells into cerebral ischemic rabbits and examined the neuronal metabolites
Phenotype of hUCB-MSCs The cells picked from clones could be passaged successfully and the cells grew as a fusiform or fibroblast-like shape, whereas the subclones developed like a whirlpool (Figure 1)
Isolated hUCB-MSCs were characterized by flow cytometric analysis of specific surface antigens. hUCB-MSCs expressed surface antigens CD29 and CD44, but not CD34 and CD45, which was consistent with the surface antigens of bone marrow-derived MSCs (Figure 2)
Summary
Because there is little research on the effects of transplanted stem cells on neuronal metabolites in infarct areas, we transplanted human umbilical cord blood mesenchymal stem cells (hUCB-MSCs) into cerebral ischemic rabbits and examined the neuronal metabolites. Cerebral vascular diseases are a major cause of mortality and disability worldwide. At least 1,500,000 patients are affected by cerebrovascular diseases annually, and approximately 30% of these patients become severely and permanently disabled. Once cell damage from stroke has been established, little can be done to restore pre-stroke conditions. In this regard, hundreds of studies have described the therapeutic potential of either endogenous or transplanted stem cells in experimental models of stroke [2]. Various proposed mechanisms have been investigated in preclinical stroke models, including formation of new neuronal circuitry, reductions of apoptosis and inflammation, and promotion of angiogenesis, neurogenesis, and other endogenous repair processes [3,4,5,6]
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