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CHPG通过调控mGluR5表达及JNK信号通路抑制LPS诱导的小胶质细胞激活
引用本文:张倩,黄艺滢,谷利,杨荟敏,张红. CHPG通过调控mGluR5表达及JNK信号通路抑制LPS诱导的小胶质细胞激活[J]. 疾病监测, 2015, 30(5): 361-367. DOI: 10.3784/j.issn.1003-9961.2015.05.006
作者姓名:张倩  黄艺滢  谷利  杨荟敏  张红
作者单位:1.首都医科大学基础医学院神经生物学系, 教育部神经变性疾病重点实验室, 北京 100069
基金项目:国家自然科学基金 (No. 81171886, 81372587)北京市自然科学基金(No.7132018)北京市教育委员会科技计划重点项目(No.KZ201310025021)
摘    要:目的 探讨激活mGluR5为什么能够抑制激活小胶质细胞诱导的炎症反应. 方法 在正常的和基因敲减mGluR5的小胶质细胞中,用脂多糖(LPS)建立炎症模型,通过Griess实验、酶联免疫吸附试验、免疫印迹法、流式细胞术等方法,探测CHPG对LPS诱导的炎症反应,mGluR5表达及其下游MAPKs信号分子活性的影响. 结果 LPS诱导炎症反应,引起mGluR5表达量下降,下游JNK活性下降,CHPG逆转上述过程(P=0.0003, P=0.005).在mGluR5敲减的细胞中,CHPG作用消失(P=0.4694, P=0.4407). 结论 激活mGluR5抑制炎症反应是通过上调该受体表达量及其下游的JNK信号通路实现的.

关 键 词:代谢型谷氨酸受体5   CHPG   小胶质细胞   炎症反应   JNK
收稿时间:2015-02-15

CHPG protects against LPS-induced inflammation by modulating mGluR5 and JNK signaling pathway
ZHANG Qian,HUANG Yi-Ying,GU Li,YANG Hui-Min,ZHANG Hong. CHPG protects against LPS-induced inflammation by modulating mGluR5 and JNK signaling pathway[J]. Disease Surveillance, 2015, 30(5): 361-367. DOI: 10.3784/j.issn.1003-9961.2015.05.006
Authors:ZHANG Qian  HUANG Yi-Ying  GU Li  YANG Hui-Min  ZHANG Hong
Affiliation:1.Department of Neurobiology, Capital Medical University, Key Laboratory for Neurodegenerative Disease of the Ministry of Education, Beijing 100069, China2.2. Department of Medical Genetics, Capital Medical University, Beijing 100069, China3.4.Class of Basic Medical Sciences, Capital Medical University, Beijing 100069, China5.Department of Neurobiology, Capital Medical University, Key Laboratory for Neurodegenerative Disease of the Ministry of Education, Beijing 100069, China
Abstract:Objective To investigate the mechanism by which mGluR5 activation suppress the inflammation induced by activated microglia. Methods The effect of (RS)-2-chloro-5-hydroxyphenylglycine (CHPG) on LPS-induced inflammation, the expression of mGluR5 and its downstream MAPK signaling pathways were detected with Griess test, enzyme-linked immunosorbent assay, western blot and flow cytometry. Results CHPG reversed LPS-induced decrease of mGluR5 (P=0.0003) and p-JNK expression (P=0.005) and no such effect of CHPG was observed in mGluR5 knockdown cells (P=0.4694, P=0.4407). Conclusion The anti-inflammation effect of mGluR5 activation is mediated by raising the expression of mGluR5 and its downstream JNK signaling pathway.
Keywords:Metabolic type glutamate receptor 5  (RS)-2-chloro-5-hydroxyphenylglycine  Microglia  Inflammatory response  JNK
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