title: The role of IL-17 promotes spinal cord neuroinflammation via activation of the transcription factor STAT3 after spinal cord injury in the rat.
abstract: METHODS
  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.
  
  
  CONCLUSIONS
  IL-17 may play an important role in promoting spinal cord neuroinflammation after SCI via activation of STAT3.
authors.affiliation: Department of Spine Osteopathia, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, China.
authors.forename: Shaohui
authors.initials: S
authors.lastname: Zong
authors.affiliation: College of Public Hygiene of Guangxi Medical University, Nanning, Guangxi 530021, China.
authors.forename: Gaofeng
authors.initials: G
authors.lastname: Zeng
authors.affiliation: Graduate School of Guangxi Medical University, Nanning, Guangxi 530021, China.
authors.forename: Ye
authors.initials: Y
authors.lastname: Fang
authors.affiliation: Graduate School of Guangxi Medical University, Nanning, Guangxi 530021, China.
authors.forename: Jinzhen
authors.initials: J
authors.lastname: Peng
authors.affiliation: Graduate School of Guangxi Medical University, Nanning, Guangxi 530021, China.
authors.forename: Yong
authors.initials: Y
authors.lastname: Tao
authors.affiliation: Graduate School of Guangxi Medical University, Nanning, Guangxi 530021, China.
authors.forename: Keke
authors.initials: K
authors.lastname: Li
authors.affiliation: Department of Osteopathia, The First Affiliated Hospital of Guangxi Medical University, No. 22 Shuangyong Road, Nanning, Guangxi 530021, China.
authors.forename: Jingmin
authors.identifier: 0000-0001-5129-6233
authors.initials: J
authors.lastname: Zhao
mesh_terms: D000818:Animals; D001522:Behavior, Animal; D001812:Blood-Brain Barrier; D004797:Enzyme-Linked Immunosorbent Assay; D020869:Gene Expression Profiling; D007150:Immunohistochemistry; D007249:Inflammation / Q000378:metabolism / Q000473:pathology; D020381:Interleukin-17 / Q000378:metabolism*; D053760:Interleukin-23 Subunit p19 / Q000378:metabolism*; D008297:Male; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D050796:STAT3 Transcription Factor / Q000378:metabolism*; D015398:Signal Transduction; D013116:Spinal Cord / Q000473:pathology*; D013119:Spinal Cord Injuries / Q000473:pathology*
chemical_list: C515934:Il17a protein, rat; C508842:Il23a protein, rat; D020381:Interleukin-17; D053760:Interleukin-23 Subunit p19; D012333:RNA, Messenger; D050796:STAT3 Transcription Factor; C494088:Stat3 protein, rat