Hashmi Ali Madeeh, Butt Zeeshan, Umair Muhammad
Department of Psychiatry, King Edward Medical University/Mayo Hospital, Lahore.
J Pak Med Assoc. 2013 Jul;63(7):899-906.
The current review examines the relationship between depression and the inflammatory immune response. Mood disorders are a significant cause of morbidity and the etiology of depression is still not clearly understood. Many studies have shown links between inflammatory cytokines and mood disorders, including elevated level of cytokines like tumour necrosis factor-alpha (TNF alpha), Interleukins (IL-1,IL-6) and others. Raised levels of cytokines have been shown to increase depressive behaviour in animal models, while many anti-depressants reverse this behaviour alongside reducing the Central Nervous System (CNS) inflammatory response and reduction in the amounts of inflammatory cytokines. Cytokines reduce neurogenesis, Brain Derived Neurotrophic Factor (BDNF) and neuronal plasticity in the CNS, while many anti-depressants have been shown to reverse these processes. The considerations of anti-depressants as anti-inflammatory agents, and implication of other anti-inflammatory therapeutics for the treatment of depression are pointed out.
本综述探讨了抑郁症与炎症免疫反应之间的关系。情绪障碍是发病的重要原因，而抑郁症的病因仍未完全明确。许多研究表明炎症细胞因子与情绪障碍之间存在联系，包括肿瘤坏死因子-α（TNFα）、白细胞介素（IL-1、IL-6）等细胞因子水平升高。研究表明，细胞因子水平升高会增加动物模型中的抑郁行为，而许多抗抑郁药在减少中枢神经系统（CNS）炎症反应和炎症细胞因子数量的同时，会逆转这种行为。细胞因子会减少神经发生、脑源性神经营养因子（BDNF）和中枢神经系统中的神经元可塑性，而许多抗抑郁药已被证明可以逆转这些过程。文中指出了将抗抑郁药视为抗炎药的考量，以及其他抗炎疗法对抑郁症治疗的意义。
