Abstract
ObjectiveTo investigate the effect of intraventricular injection of human dental pulp stem cells (DPSCs) on hypoxic-ischemic brain damage (HIBD) in neonatal rats.MethodsThirty-six neonatal rats (postnatal day 7) were assigned to control, HIBD, or HIBD+DPSC groups (n = 12 each group). For induction of HIBD, rats underwent left carotid artery ligation and were exposed to 8% to 10% oxygen for 2 h. Hoechst 33324-labeled human DPSCs were injected into the left lateral ventricle 3 days after HIBD. Behavioral assays were performed to assess hypoxic-ischemic encephalopathy (HIE), and on postnatal day 45, DPSC survival was assessed and expression of neural and glial markers was evaluated by immunohistochemistry and Western blot.ResultsThe HIBD group showed significant deficiencies compared to control on T-maze, radial water maze, and postural reflex tests, and the HIBD+DPSC group showed significant improvement on all behavioral tests. On postnatal day 45, Hoechst 33324-labeled DPSC nuclei were visible in the injected region and left cortex. Subsets of DPSCs showed immunostaining for neuronal (neuron-specific enolase [NSE], Nestin) and glial markers (glial fibrillary acidic protein [GFAP], O4). Significantly decreased staining/expression for NSE, GFAP, and O4 was found in the HBID group compared to control, and this was significantly increased in the HBID+DPSC group.ConclusionIntraventricular injection of human DPSCs improves HIBD in neonatal rats.
Highlights
Hypoxic-ischemic encephalopathy (HIE) is caused by partial or complete anoxia, a reduction of cerebral blood flow, or a temporary occlusion
Similar changes were observed in BrdU-positive neuronal cells and BrdU-positive glial cells. These results indicated that hypoxicischemic brain damage (HIBD) decreased proliferation and that dental pulp stem cells (DPSCs) administration was able to ameliorate this to a large extent
Results of the present study showed that intraventricular DPSC injection exerted significant ameliorative effects with respect to HIBD-induced behavioral dysfunction and expression of neural and glial markers in neonatal rats
Summary
Hypoxic-ischemic encephalopathy (HIE) is caused by partial or complete anoxia, a reduction of cerebral blood flow, or a temporary occlusion. The effectiveness of stem cell transplant for HIE treatment has been reported in animal models, and clinical trials are currently being performed (reviewed in [2,3,4]). Cells used in animal models include, but are not limited to, embryonic stem cells, neural stem cells, bone marrow mesenchymal stem cells, and umbilical cord blood stem cells. In terms of use in humans, some of these stem cells are associated with issues in terms of limited donor sources, host-graft rejection, expense, and ethical concerns. Stem cells such as umbilical cord blood stem cells and mesenchymal stem cells in the bone marrow are derived from the mesoderm. The ability of mesodermal stem cells to eventually differentiate to ectodermally derived neurons remains uncertain
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