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- Title
α7nAChR 调控STAT3 磷酸化在星形胶质细胞机械性 损伤后炎症反应中的作用.
- Authors
王琦; 武秀权; 戴舒惠; 高翔宇; 豆雅楠; 罗鹏; 李新
- Abstract
Objective: To investigate the role of nicotinic acetylcholine receptor alpha 7 subunit (α7nAChR) in astrocyte-associated inflammation after traumatic brain injury via establishment of astrocytic mechanical injury model. Methods: After establishment of astrocytic mechanial injury, expressions of inflammatory factors, including IL-1β, TNF-α, IL-10, and TGF-β, were detected by ELISA assay. After administration of α7nAChR antagonist (α-BGT) and α7nAChR agonist (PHA-543613), expressions of inflammatory factors were detected by ELISA assay and expressions of STAT3 and STAT3 phosphorylation (p-STAT3) were detected by Western blot. After administration of α-BGT and STAT3 antagonist (Stattic), expressions of inflammatory factors were detected by ELISA assay. Results: 1) After astrocytic mechanial injury, expressions of pro-inflammatory factors, IL-1βand TNF-α, were increased, while expressions of anti- inflammatory factors, IL-10 and TGF-β, were decreased (P<0.05). 2) Inhibition of α7nAChR by α-BGT increased the expressions of IL-1βand TNF-αafter injury and decreased the expressions of IL-10 and TGF-β(P<0.05), while activation of α7nAChR by PHA-543613 showed the reverse effects on these inflammatory facoters (P<0.05). 3) Administration of α-BGT increased the phosphorylation of STAT3, while administration of PHA-543613 decreased the phosphorylation of STAT3 (P<0.05). 4) Administration of STAT3 antagonist (Stattic) decreased the expressions of IL-1βand TNF-α, increased the expressions of IL-10 and TGF-β, and partially reversed the effects of α-BGT on expressions of IL-1β, TNF-α, IL-10, and TGF-β(P<0.05). Conclusions: After mechanical injury, activation of α7nAChR reduces the inflammation in astrocytes. Inhibition of STAT3 phosphorylation acted as an important downstream mechanism of this process.
- Subjects
NICOTINIC acetylcholine receptors; BRAIN injuries; MECHANICAL models; WESTERN immunoblotting; PHOSPHORYLATION
- Publication
Progress in Modern Biomedicine, 2019, Vol 19, Issue 15, p2845
- ISSN
1673-6273
- Publication type
Article
- DOI
10.13241/j.cnki.pmb.2019.15.009