The Role of IL-17 Promotes Spinal Cord Neuroinflammation via Activation of the Transcription Factor STAT3 after Spinal Cord Injury in the Rat
Study Design. In this study, we investigated the role of IL-17 via activation of STAT3 in the pathophysiology of SCI. Objective. The purpose of the experiments is to study the expression of IL-17 and related cytokines via STAT3 signaling pathways, which is caused by the acute inflammatory response f...
Saved in:
| Main Authors: | , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2014-01-01
|
| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2014/786947 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1832549223149600768 |
|---|---|
| author | Shaohui Zong Gaofeng Zeng Ye Fang Jinzhen Peng Yong Tao Keke Li Jingmin Zhao |
| author_facet | Shaohui Zong Gaofeng Zeng Ye Fang Jinzhen Peng Yong Tao Keke Li Jingmin Zhao |
| author_sort | Shaohui Zong |
| collection | DOAJ |
| description | Study Design. In this study, we investigated the role of IL-17 via activation of STAT3 in the pathophysiology of SCI. Objective. The purpose of the experiments is to study the expression of IL-17 and related cytokines via STAT3 signaling pathways, which is caused by the acute inflammatory response following SCI in different periods via establishing an acute SCI model in rat. Methods. Basso, Beattie, and Bresnahan hind limb locomotor rating scale was used to assess the rat hind limb motor function. Immunohistochemistry was used to determine the expression levels of IL-17 and p-STAT3 in spinal cord tissues. Western blotting analysis was used to determine the protein expression of p-STAT3 in spinal cord tissue. RT-PCR was used to analyze the mRNA expression of IL-17 and IL-23p19 in the spleen tissue. ELISA was used to determine the peripheral blood serum levels of IL-6, IL-21, and IL-23. Results. Compared to the sham-operated group, the expression levels of IL-17, p-STAT3, IL-6, IL-21, and IL-23 were significantly increased and peaked at 24 h after SCI. The increased levels of cytokines were correlated with the SCI disease stages. Conclusion. IL-17 may play an important role in promoting spinal cord neuroinflammation after SCI via activation of STAT3. |
| format | Article |
| id | doaj-art-311d92b581544e7e9cf569de4d269bed |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2014-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-311d92b581544e7e9cf569de4d269bed2025-02-03T06:11:45ZengWileyMediators of Inflammation0962-93511466-18612014-01-01201410.1155/2014/786947786947The Role of IL-17 Promotes Spinal Cord Neuroinflammation via Activation of the Transcription Factor STAT3 after Spinal Cord Injury in the RatShaohui Zong0Gaofeng Zeng1Ye Fang2Jinzhen Peng3Yong Tao4Keke Li5Jingmin Zhao6Department of Spine Osteopathia, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, ChinaCollege of Public Hygiene of Guangxi Medical University, Nanning, Guangxi 530021, ChinaGraduate School of Guangxi Medical University, Nanning, Guangxi 530021, ChinaGraduate School of Guangxi Medical University, Nanning, Guangxi 530021, ChinaGraduate School of Guangxi Medical University, Nanning, Guangxi 530021, ChinaGraduate School of Guangxi Medical University, Nanning, Guangxi 530021, ChinaDepartment of Osteopathia, The First Affiliated Hospital of Guangxi Medical University, No. 22 Shuangyong Road, Nanning, Guangxi 530021, ChinaStudy Design. In this study, we investigated the role of IL-17 via activation of STAT3 in the pathophysiology of SCI. Objective. The purpose of the experiments is to study the expression of IL-17 and related cytokines via STAT3 signaling pathways, which is caused by the acute inflammatory response following SCI in different periods via establishing an acute SCI model in rat. Methods. Basso, Beattie, and Bresnahan hind limb locomotor rating scale was used to assess the rat hind limb motor function. Immunohistochemistry was used to determine the expression levels of IL-17 and p-STAT3 in spinal cord tissues. Western blotting analysis was used to determine the protein expression of p-STAT3 in spinal cord tissue. RT-PCR was used to analyze the mRNA expression of IL-17 and IL-23p19 in the spleen tissue. ELISA was used to determine the peripheral blood serum levels of IL-6, IL-21, and IL-23. Results. Compared to the sham-operated group, the expression levels of IL-17, p-STAT3, IL-6, IL-21, and IL-23 were significantly increased and peaked at 24 h after SCI. The increased levels of cytokines were correlated with the SCI disease stages. Conclusion. IL-17 may play an important role in promoting spinal cord neuroinflammation after SCI via activation of STAT3.http://dx.doi.org/10.1155/2014/786947 |
| spellingShingle | Shaohui Zong Gaofeng Zeng Ye Fang Jinzhen Peng Yong Tao Keke Li Jingmin Zhao The Role of IL-17 Promotes Spinal Cord Neuroinflammation via Activation of the Transcription Factor STAT3 after Spinal Cord Injury in the Rat Mediators of Inflammation |
| title | The Role of IL-17 Promotes Spinal Cord Neuroinflammation via Activation of the Transcription Factor STAT3 after Spinal Cord Injury in the Rat |
| title_full | The Role of IL-17 Promotes Spinal Cord Neuroinflammation via Activation of the Transcription Factor STAT3 after Spinal Cord Injury in the Rat |
| title_fullStr | The Role of IL-17 Promotes Spinal Cord Neuroinflammation via Activation of the Transcription Factor STAT3 after Spinal Cord Injury in the Rat |
| title_full_unstemmed | The Role of IL-17 Promotes Spinal Cord Neuroinflammation via Activation of the Transcription Factor STAT3 after Spinal Cord Injury in the Rat |
| title_short | The Role of IL-17 Promotes Spinal Cord Neuroinflammation via Activation of the Transcription Factor STAT3 after Spinal Cord Injury in the Rat |
| title_sort | role of il 17 promotes spinal cord neuroinflammation via activation of the transcription factor stat3 after spinal cord injury in the rat |
| url | http://dx.doi.org/10.1155/2014/786947 |
| work_keys_str_mv | AT shaohuizong theroleofil17promotesspinalcordneuroinflammationviaactivationofthetranscriptionfactorstat3afterspinalcordinjuryintherat AT gaofengzeng theroleofil17promotesspinalcordneuroinflammationviaactivationofthetranscriptionfactorstat3afterspinalcordinjuryintherat AT yefang theroleofil17promotesspinalcordneuroinflammationviaactivationofthetranscriptionfactorstat3afterspinalcordinjuryintherat AT jinzhenpeng theroleofil17promotesspinalcordneuroinflammationviaactivationofthetranscriptionfactorstat3afterspinalcordinjuryintherat AT yongtao theroleofil17promotesspinalcordneuroinflammationviaactivationofthetranscriptionfactorstat3afterspinalcordinjuryintherat AT kekeli theroleofil17promotesspinalcordneuroinflammationviaactivationofthetranscriptionfactorstat3afterspinalcordinjuryintherat AT jingminzhao theroleofil17promotesspinalcordneuroinflammationviaactivationofthetranscriptionfactorstat3afterspinalcordinjuryintherat AT shaohuizong roleofil17promotesspinalcordneuroinflammationviaactivationofthetranscriptionfactorstat3afterspinalcordinjuryintherat AT gaofengzeng roleofil17promotesspinalcordneuroinflammationviaactivationofthetranscriptionfactorstat3afterspinalcordinjuryintherat AT yefang roleofil17promotesspinalcordneuroinflammationviaactivationofthetranscriptionfactorstat3afterspinalcordinjuryintherat AT jinzhenpeng roleofil17promotesspinalcordneuroinflammationviaactivationofthetranscriptionfactorstat3afterspinalcordinjuryintherat AT yongtao roleofil17promotesspinalcordneuroinflammationviaactivationofthetranscriptionfactorstat3afterspinalcordinjuryintherat AT kekeli roleofil17promotesspinalcordneuroinflammationviaactivationofthetranscriptionfactorstat3afterspinalcordinjuryintherat AT jingminzhao roleofil17promotesspinalcordneuroinflammationviaactivationofthetranscriptionfactorstat3afterspinalcordinjuryintherat |