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目的探讨激活m GluR5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m GluR5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,m GluR5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m GluR5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m GluR5敲减的细胞中,CHPG作用消失(P=0.4694,P=0.4407)。结论激活m GluR5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。
Objective To investigate why activating m GluR5 can inhibit the activation of microglia-induced inflammatory reaction. Methods The model of inflammation was established by lipopolysaccharide (LPS) in normal and gene-knocked-down mGluR5 microglia cells. Griess assay, enzyme-linked immunosorbent assay, Western blot and flow cytometry were used to detect CHPG On the LPS-induced inflammatory response, m GluR5 expression and its downstream MAPKs signaling molecules. Results LPS induced inflammatory reaction, which caused the decrease of GluR5 expression and the decrease of JNK activity in the downstream. CHPG reversed the above process (P = 0.0003, P = 0.005). In m GluR5 knockdown cells, CHPG disappeared (P = 0.4694, P = 0.4407). Conclusion Activation of m GluR5 inhibits the inflammatory response by up-regulating the expression of this receptor and its downstream JNK signaling pathway.