| 王 琦,武秀权,戴舒惠,高翔宇,豆雅楠,罗 鹏,李 新.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[J].,2019,19(15):2845-2849 |
| 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 |
| Effects of α7nAChR in Regulation of STAT3 Phosphorylation after Astrocytic Mechanical Injury-induced Inflammation |
| 投稿时间：2019-02-18 修订日期：2019-03-15 |
| DOI：10.13241/j.cnki.pmb.2019.15.009 |
| 中文关键词: 创伤性脑损伤 星形胶质细胞 炎症反应 烟碱型乙酰胆碱受体 ?琢7 亚单位 信号传导及转录活化因子3 |
| 英文关键词: Traumatic brain injury Astrocyte Inflammation Nicotinic acetylcholine receptor alpha 7 subunit Signal transducer and activator of transcription 3 |
| 基金项目:国家自然科学基金青年科学基金项目（81601149）；陕西省高校科协青年人才托举计划项目（20180305）；陕西省自然科学基金项目（2017JQ8038） |
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| 中文摘要: |
| 摘要 目的：通过建立星形胶质细胞机械性损伤模型，研究烟碱型乙酰胆碱受体 α7 亚单位（α7nAChR）在创伤性脑损伤后星形胶质细胞炎症反应中的作用及调控机制。方法：建立星形胶质细胞机械性损伤模型，通过ELISA检测炎症因子IL-1β、TNF-α、IL-10和TGF-β的表达；利用α7nAChR抑制剂α-BGT和激动剂PHA-543613处理星形胶质细胞，检测相关炎症因子表达，并通过Western blot检测信号传导及转录活化因子3（STAT3）和磷酸化STAT3（p-STAT3）的表达；利用α-BGT和STAT3抑制剂Stattic处理星形胶质细胞，检测相关炎症因子表达。结果：①星形胶质细胞机械性损伤后，促炎因子IL-1β、TNF-α表达增加，抗炎因子IL-10、TGF-β表达降低（P<0.05）。②利用α-BGT抑制α7nAChR可增加损伤后IL-1β、TNF-α的表达，减少IL-10、TGF-β的表达（P<0.05）；而利用PHA-543613激活α7nAChR功能，则发挥相反作用（P<0.05）。③α-BGT可促进STAT3磷酸化，而PHA-543613抑制STAT3磷酸化（P<0.05）。④STAT3抑制剂Stattic可减少IL-1β和TNF-α的表达，增加IL-10和TGF-β的表达，并部分阻断α-BGT对IL-1β、TNF-α、IL-10及TGF-β表达的影响（P<0.05）。结论：机械性损伤后，激活α7nAChR可减轻星形胶质细胞炎症反应，而抑制STAT3磷酸化是其重要的下游机制。 |
| 英文摘要: |
| 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-1β and 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-1β and TNF-α after 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). ③Administration of α-BGT increased the phosphorylation of STAT3, while administration of PHA-543613 decreased the phosphorylation of STAT3 (P<0.05). ④Administration of STAT3 antagonist (Stattic) decreased the expressions of IL-1β and 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). Conclusion: After mechanical injury, activation of α7nAChR reduces the inflammation in astrocytes. Inhibition of STAT3 phosphorylation acted as an important downstream mechanism of this process. |
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