Hashioka Sadayuki, McGeer Patrick L, Monji Akira, Kanba Shigenobu
Department of Psychiatry, The University of British Columbia, Vancouver, Canada.
Cent Nerv Syst Agents Med Chem. 2009 Mar;9(1):12-9. doi: 10.2174/187152409787601897.
Increasing evidence of pro-inflammatory mediator expression in major depressions indicate that inflammatory changes may play a role. If this is true, the efficacy of antidepressants may be partially attributable to suppression of inflammation. Various types of antidepressants can suppress serum and plasma levels of pro-inflammatory mediators in patients with major depression. Therefore they can inhibit the production of pro-inflammatory mediators by immune cells. These include glial cells, which are the main sources and targets of cytokines in the brain. This review summarizes the evidence showing that antidepressants have an anti-inflammatory potential. The putative mechanisms are also discussed. Because of the anti-inflammatory effects of antidepressants, they might also act as preventives for neurodegenerative dementias including Alzheimer's disease, where the pathogenesis involves chronic inflammation associated with activated microglia.
越来越多的证据表明，在重度抑郁症中促炎介质表达增加，这表明炎症变化可能起作用。如果这是真的，那么抗抑郁药的疗效可能部分归因于对炎症的抑制。各类抗抑郁药可降低重度抑郁症患者血清和血浆中促炎介质的水平。因此，它们可以抑制免疫细胞产生促炎介质。这些免疫细胞包括神经胶质细胞，而神经胶质细胞是大脑中细胞因子的主要来源和靶点。本综述总结了表明抗抑郁药具有抗炎潜力的证据，并对其可能的机制进行了讨论。由于抗抑郁药的抗炎作用，它们也可能作为包括阿尔茨海默病在内的神经退行性痴呆的预防药物，而阿尔茨海默病的发病机制涉及与活化小胶质细胞相关的慢性炎症。
