Dental pulp stem cell transplantation facilitates neuronal neuroprotection following cerebral ischemic stroke

Objectives: This study aimed to identify and evaluate the intracranial transplantation of dental pulp stem cells (DPSCs) as a possible ischemic stroke therapy that mitigates neuronal death/apoptosis. Materials and methods: DPSCs were isolated from the impacted third molars of healthy volunteers and...

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Bibliographic Details
Main Authors: Pian Gong, Qi Tian, Yan He, Peibang He, Jianfeng Wang, Yujia Guo, Qingsong Ye, Mingchang Li
Format: Article
Language:English
Published: Elsevier 2022-08-01
Series:Biomedicine & Pharmacotherapy
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Online Access:http://www.sciencedirect.com/science/article/pii/S0753332222006230
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Summary:Objectives: This study aimed to identify and evaluate the intracranial transplantation of dental pulp stem cells (DPSCs) as a possible ischemic stroke therapy that mitigates neuronal death/apoptosis. Materials and methods: DPSCs were isolated from the impacted third molars of healthy volunteers and then intracranially injected at 24 h post-ischemic stroke to Sprague Dawley rats that had been subjected to 2 h of middle cerebral artery occlusion. Neurological functional deficits were assessed using the modified neurological severity score (mNSS), and cerebral edema was quantified using brain water content. Neuronal death/apoptosis was indicated by TdT-mediated dUTP Nick-End Labeling (TUNEL) staining, NeuN immunofluorescence and immunohistochemistry, and Western blot analysis of the protein expression of anti-apoptotic indicator of Bcl-2 and apoptotic indicators of Bax and caspase 3. Results: DPSC transplantation could ameliorate neurological dysfunction and brain edema, reduce infarct volume, decrease the percentage of TUNEL-positive nuclei, increase the number and percentage of NeuN-positive cells in ischemic penumbra, increase the ratio of Bcl-2 and Bax and down-regulate the production of caspase 3 in the cortical infarct zone. Conclusions: DPSC therapy via intracranial injection exerted remarkably neuroprotection mainly by inhibiting neuronal death/apoptosis.
ISSN:0753-3322