蛋白激酶C在抑郁症神经免疫炎症机制中的研究进展

Research progress of protein kinase C in the neuroimmune-inflammatory mechanism of depression

近年来,“炎症假说”颇受关注,该假说认为炎症反应参与抑郁症的发病。小神经胶质细胞作为中枢神经系统的免疫细胞,激活时会增加炎症细胞因子的释放,引发机体的炎症状态,进而参与抑郁症的发生发展。蛋白激酶在调节小胶质细胞的激活中发挥重要作用,其中蛋白激酶C(PKC)可能是此过程中最重要的一种激酶。此外,PKC的表达水平和活动变化可能均与抑郁症的发病机制密切相关。文章对PKC进行简要概述,并通过总结动物及临床研究证据来明确PKC与抑郁症之间的关系,进一步对可能参与抑郁症发病机制的PKC相关信号通路进行重点阐述,以期为抑郁症免疫炎症假说提供研究思路,为寻找抗抑郁治疗新靶点提供科学依据。

Much attention has been paid to the"inflammatory hypothesis"in recent years,which suggests that inflammation is involved in the pathogenesis of depression.Activation of microglia,the immune cells of the central nervous system,increases the release of inflammatory cytokines and triggers an inflammatory state in the body,which in turn is involved in the development of depression.Protein kinases have been found to play an important role in regulating microglia activation,and protein kinase C(PKC)is probably the most important kinase in this process.In addition,it was found that changes in both PKC expression levels and activity may be closely related to the pathogenesis of depression.Therefore,we will first provide a brief overview of PKC,and then clarify the relationship between PKC and depression by summarizing evidence from animal and clinical studies.Finally,we will focus on PKC-related signaling pathways involved in the pathogenesis of depression to provide research ideas for the immuno inflammatory hypothesis of depression and provide scientific basis for finding new targets for antidepressant therapy.