2012Int J ImmunolRequires access

Mechanism of Th17 and IL-17 in Cerebral Ischemic Injury

Dandan Wang, Zhe Zhang, Qingfei Kong, Jinghua Wang, Guangyou Wang, Yumei Liu, Hulun Li

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Abstract

Objective To investigate the expression of Th17 in ischemic brain tissue and the mechanism of IL-17 in potentiating neuronal injury induced by oxygen-glucose deprivation.Methods Set up the permanent middle cerebral artery occlusion (pMCAO)model by an intraluminal nylon introduction.Investigate the Th17 cells in the ischemic brain tissue by immunofluorescence detection.oxygen-glucose deprivation (OGD) was induced in primary hippocampus cell cultures to modify ischemia microenvironment.Different dose of recombined IL-17 administration with or without IL-17R inhibitor was carried out to explore the mechanism of IL-17 in potentiating neuronal injury under OGD.Results Animal model of pMCAO was successfully set up with large cerebral infarctions after TTC stain.Infiltration of Th17 cells was observed according to the double-immunofluorescence for CD4 and IL-17.Exogenous IL-17 facilitated OGD-mediated neuronal cell death which could be blocked using IL-17R inhibitor.Conclusion There was Th17 cells infiltration in the ischemic brain of pMCAO mice.IL-17 secreted from Th17 cells was relevant to OGD-induced neuronal injury. Key words: Ischemia;  Th17 ;  IL-17 ;  Oxygen-Glucose Deprivation;  Hippocampus neurons

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Objective To investigate the expression of Th17 in ischemic brain tissue and the mechanism of IL-17 in potentiating neuronal injury induced by oxygen-glucose deprivation.Methods Set up the permanent middle cerebral artery occlusion (pMCAO)model by an intraluminal nylon introduction.Investigate the Th17 cells in the ischemic brain tissue by immunofluorescence detection.oxygen-glucose deprivation (OGD) was induced in primary hippocampus cell cultures to modify ischemia microenvironment.Different dose of recombined IL-17 administration with or without IL-17R inhibitor was carried out to explore the mechanism of IL-17 in potentiating neuronal injury under OGD.Results Animal model of pMCAO was successfully set up with large cerebral infarctions after TTC stain.Infiltration of Th17 cells was observed according to the double-immunofluorescence for CD4 and IL-17.Exogenous IL-17 facilitated OGD-mediated neuronal cell death which could be blocked using IL-17R inhibitor.Conclusion There was Th17 cells infiltration in the ischemic brain of pMCAO mice.IL-17 secreted from Th17 cells was relevant to OGD-induced neuronal injury. Key words: Ischemia;  Th17 ;  IL-17 ;  Oxygen-Glucose Deprivation;  Hippocampus neurons

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Available abstract

Objective To investigate the expression of Th17 in ischemic brain tissue and the mechanism of IL-17 in potentiating neuronal injury induced by oxygen-glucose deprivation.Methods Set up the permanent middle cerebral artery occlusion (pMCAO)model by an intraluminal nylon introduction.Investigate the Th17 cells in the ischemic brain tissue by immunofluorescence detection.oxygen-glucose deprivation (OGD) was induced in primary hippocampus cell cultures to modify ischemia microenvironment.Different dose of recombined IL-17 administration with or without IL-17R inhibitor was carried out to explore the mechanism of IL-17 in potentiating neuronal injury under OGD.Results Animal model of pMCAO was successfully set up with large cerebral infarctions after TTC stain.Infiltration of Th17 cells was observed according to the double-immunofluorescence for CD4 and IL-17.Exogenous IL-17 facilitated OGD-mediated neuronal cell death which could be blocked using IL-17R inhibitor.Conclusion There was Th17 cells infiltration in the ischemic brain of pMCAO mice.IL-17 secreted from Th17 cells was relevant to OGD-induced neuronal injury. Key words: Ischemia;  Th17 ;  IL-17 ;  Oxygen-Glucose Deprivation;  Hippocampus neurons

Key concepts: Ischemia, Infiltration (HVAC), Immunofluorescence, Ischemic injury, Medicine, Pharmacology, Pathology, Chemistry

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