P2Y2 Receptor Mediated Neuronal Regeneration and Angiogenesis to Affect Functional Recovery in Rats with Spinal Cord Injury

The aim of this study was to investigate the effect of the P2Y2 receptor (P2Y2R) signaling pathway on neuronal regeneration and angiogenesis during spinal cord injury (SCI). The rats were randomly divided into 3 groups, including the sham+dimethyl sulfoxide (DMSO), SCI+DMSO, and SCI+P2Y2R groups. Th...

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Main Authors: Ruidong Cheng, Genying Zhu, Chengtao Ni, Rui Wang, Peng Sun, Liang Tian, Li Zhang, Jie Zhang, Xiangming Ye, Benyan Luo
Format: Article
Language:English
Published: Wiley 2022-01-01
Series:Neural Plasticity
Online Access:http://dx.doi.org/10.1155/2022/2191011
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author Ruidong Cheng
Genying Zhu
Chengtao Ni
Rui Wang
Peng Sun
Liang Tian
Li Zhang
Jie Zhang
Xiangming Ye
Benyan Luo
author_facet Ruidong Cheng
Genying Zhu
Chengtao Ni
Rui Wang
Peng Sun
Liang Tian
Li Zhang
Jie Zhang
Xiangming Ye
Benyan Luo
author_sort Ruidong Cheng
collection DOAJ
description The aim of this study was to investigate the effect of the P2Y2 receptor (P2Y2R) signaling pathway on neuronal regeneration and angiogenesis during spinal cord injury (SCI). The rats were randomly divided into 3 groups, including the sham+dimethyl sulfoxide (DMSO), SCI+DMSO, and SCI+P2Y2R groups. The SCI animal models were constructed. A locomotor rating scale was used for behavioral assessments. The apoptosis of spinal cord tissues was detected by TUNEL staining. The expression levels of P2Y2R, GFAP, nestin, Tuj1, and CD34 were detected by immunofluorescence staining, and the expression levels of TNF-α, IL-1β, and IL-6 were detected by enzyme-linked immunosorbent assay. The locomotor score in the model group was significantly lower than the sham group. The expression of P2Y2R was increased after SCI. The expression levels of TNF-α, IL-1β, and IL-6 were increased remarkably in the SCI model group compared with the sham group. The P2Y2R inhibitor relieved neuronal inflammation after SCI. Compared with the sham group, the apoptotic rate of spinal cord tissue cells in the model group was significantly increased. The P2Y2R inhibitor reduced the apoptosis of the spinal cord tissue. The expressions of CD34, Tuj1, and nestin in the model group were decreased, while the expressions of GFAP and P2Y2R were increased. The P2Y2R inhibitor reversed their expression levels. The P2Y2R inhibitor could alleviate SCI by relieving the neuronal inflammation, inhibiting the spinal cord tissue apoptosis, and promoting neuronal differentiation and vascular proliferation after SCI. P2Y2R may serve as a target for the treatment of SCI.
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issn 1687-5443
language English
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spelling doaj-art-063895cb1d5d4c04a549117a1e8812bd2025-02-03T06:05:32ZengWileyNeural Plasticity1687-54432022-01-01202210.1155/2022/2191011P2Y2 Receptor Mediated Neuronal Regeneration and Angiogenesis to Affect Functional Recovery in Rats with Spinal Cord InjuryRuidong Cheng0Genying Zhu1Chengtao Ni2Rui Wang3Peng Sun4Liang Tian5Li Zhang6Jie Zhang7Xiangming Ye8Benyan Luo9Department of Neurology & Brain Medical CenterDepartment of Neurology & Brain Medical CenterGraduate SchoolGraduate SchoolRehabilitation Medicine CenterRehabilitation Medicine CenterRehabilitation Medicine CenterRehabilitation Medicine CenterRehabilitation Medicine CenterDepartment of Neurology & Brain Medical CenterThe aim of this study was to investigate the effect of the P2Y2 receptor (P2Y2R) signaling pathway on neuronal regeneration and angiogenesis during spinal cord injury (SCI). The rats were randomly divided into 3 groups, including the sham+dimethyl sulfoxide (DMSO), SCI+DMSO, and SCI+P2Y2R groups. The SCI animal models were constructed. A locomotor rating scale was used for behavioral assessments. The apoptosis of spinal cord tissues was detected by TUNEL staining. The expression levels of P2Y2R, GFAP, nestin, Tuj1, and CD34 were detected by immunofluorescence staining, and the expression levels of TNF-α, IL-1β, and IL-6 were detected by enzyme-linked immunosorbent assay. The locomotor score in the model group was significantly lower than the sham group. The expression of P2Y2R was increased after SCI. The expression levels of TNF-α, IL-1β, and IL-6 were increased remarkably in the SCI model group compared with the sham group. The P2Y2R inhibitor relieved neuronal inflammation after SCI. Compared with the sham group, the apoptotic rate of spinal cord tissue cells in the model group was significantly increased. The P2Y2R inhibitor reduced the apoptosis of the spinal cord tissue. The expressions of CD34, Tuj1, and nestin in the model group were decreased, while the expressions of GFAP and P2Y2R were increased. The P2Y2R inhibitor reversed their expression levels. The P2Y2R inhibitor could alleviate SCI by relieving the neuronal inflammation, inhibiting the spinal cord tissue apoptosis, and promoting neuronal differentiation and vascular proliferation after SCI. P2Y2R may serve as a target for the treatment of SCI.http://dx.doi.org/10.1155/2022/2191011
spellingShingle Ruidong Cheng
Genying Zhu
Chengtao Ni
Rui Wang
Peng Sun
Liang Tian
Li Zhang
Jie Zhang
Xiangming Ye
Benyan Luo
P2Y2 Receptor Mediated Neuronal Regeneration and Angiogenesis to Affect Functional Recovery in Rats with Spinal Cord Injury
Neural Plasticity
title P2Y2 Receptor Mediated Neuronal Regeneration and Angiogenesis to Affect Functional Recovery in Rats with Spinal Cord Injury
title_full P2Y2 Receptor Mediated Neuronal Regeneration and Angiogenesis to Affect Functional Recovery in Rats with Spinal Cord Injury
title_fullStr P2Y2 Receptor Mediated Neuronal Regeneration and Angiogenesis to Affect Functional Recovery in Rats with Spinal Cord Injury
title_full_unstemmed P2Y2 Receptor Mediated Neuronal Regeneration and Angiogenesis to Affect Functional Recovery in Rats with Spinal Cord Injury
title_short P2Y2 Receptor Mediated Neuronal Regeneration and Angiogenesis to Affect Functional Recovery in Rats with Spinal Cord Injury
title_sort p2y2 receptor mediated neuronal regeneration and angiogenesis to affect functional recovery in rats with spinal cord injury
url http://dx.doi.org/10.1155/2022/2191011
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