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Chronic CXCL10 alters the level of activated ERK1/2 and transcriptional factors CREB and NF-kB in hippocampal neuronal cell culture

机译:慢性CXCL10改变海马神经元细胞培养物中活化的ERK1 / 2和转录因子CREB和NF-kB的水平

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摘要

Signal transduction pathways may be important targets of chemokines during neuroinflammation. In the current study, Western blot analyses show that in rat hippocampal neuronal/glial cell cultures chronic CXCL10 increases the level of protein for ERK1/2 as well as for the transcriptional factors CREB and NF-κB. Bcl-2, an anti-apoptotic protein whose expression can be regulated by a pathway involving ERK1/2, CREB and NF-κB, was also increased in the CXCL10 treated cultures. These results implicate a role for ERK1/2, CREB and NF-κB in effects of CXCL10 on hippocampal cells and suggest that chronic CXCL10 may have a protective role during certain neuroinflammatory conditions.
机译:信号转导途径可能是神经炎症过程中趋化因子的重要靶标。在当前的研究中,蛋白质印迹分析表明,在大鼠海马神经元/神经胶质细胞培养物中,慢性CXCL10增加ERK1 / 2以及转录因子CREB和NF-κB的蛋白质水平。 Bcl-2是一种抗凋亡蛋白,其表达可以通过涉及ERK1 / 2,CREB和NF-κB的途径调节,在CXCL10处理的培养物中也有所增加。这些结果暗示ERK1 / 2,CREB和NF-κB在CXCL10对海马细胞的作用中起作用,并表明慢性CXCL10在某些神经炎性疾病中可能具有保护作用。

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