Kinsmen Laboratory of Neurological Research, Department of Psychiatry, The University of British Columbia, Vancouver, B.C., Canada.
Mini Rev Med Chem. 2011 Jun;11(7):555-64. doi: 10.2174/138955711795906888.
Neuroinflammation is traditionally defined as the brain's innate immune response and is also considered to be a glial-cell propagated inflammation. Increasing evidence indicates that neuroinflammation plays an important role in some cases of major depression and also that antidepressants possess anti-neuroinflammatory properties. Inhibition of neuroinflammation may represent a novel mechanism of action of antidepressant treatment. In vivo studies with animal models of neurological conditions have shown that various types of antidepressants exert inhibitory effects on the expression of inflammatory mediators, including cytokines, as well as on both microgliosis and astrogliosis in the inflamed CNS. In vitro studies using pathologically activated rodent microglia or mixed glial cells have demonstrated that various types of antidepressants diminish glial generation of inflammatory molecules. One of the most plausible mechanisms of such anti-neuroinflammatory efficacy of the drugs, as well as their antidepressant actions, seems to involve elevated intracellular cAMP levels. But the exact mechanism has still to be elucidated.
神经炎症传统上被定义为大脑的固有免疫反应，也被认为是一种神经胶质细胞介导的炎症。越来越多的证据表明，神经炎症在某些重度抑郁症病例中起着重要作用，而且抗抑郁药具有抗炎特性。抑制神经炎症可能代表抗抑郁治疗的一种新的作用机制。对神经疾病动物模型的体内研究表明，各种类型的抗抑郁药对炎症介质（包括细胞因子）的表达以及中枢神经系统炎症中的小胶质细胞增生和星形胶质细胞增生都有抑制作用。使用病理性激活的啮齿动物小胶质细胞或混合神经胶质细胞进行的体外研究表明，各种类型的抗抑郁药可减少神经胶质细胞产生炎症分子。这些药物的抗炎作用以及抗抑郁作用的最合理机制之一似乎涉及细胞内 cAMP 水平的升高。但确切的机制仍有待阐明。
