阿司匹林 & 重症抑郁症
重症抑郁症促炎细胞因子TNF-α的水平显著高 。另外，抑郁症患者有抗炎细胞因子的水平较低。
8周左洛复治疗能够降低见于抑郁症患者一些促炎细胞因子。在抑郁症患者,左洛复增加抗炎细胞因子。
患者中50％以上的响应这样的组合治疗--抗抑郁 + 阿司匹林。在研究结束时80％以上响应消炎的进入缓解。
patients with major depressive disorder had significantly higher levels of the pro-inflammatory cytokine TNF-alpha . In addition, patients with depression had low levels of anti-inflammatory cytokines.
eight weeks of Zoloft treatment was able to decrease some pro-inflammatory cytokines seen in depressed patients. On Zoloft, the depressed patients also saw an increase in anti-inflammatory cytokines.
A study involving depressed patients classified as non-responders supplemented the patients' standard antidepressant treatment with the addition of aspirin, an anti-inflammatory. More than 50% of these patients responded to this combination treatment. At the end of the study more than 80% of the group responsive to the anti-inflammatory went into remission.
看来，炎症和免疫系统的化学信使称为细胞因子的复杂集合在脑功能发挥重要作用，并可能导致心理症状。
It appears that inflammation and the complicated collection of immune system chemical messengers called cytokines play an important role in brain function and may cause psychological symptoms.
当大脑被任何紧张源，感染，外伤，中风，毒药，或营养缺乏加重炎症刺激促炎细胞因子的释放，这可能会影响心情。
When the brain is aggravated by any source-stress, infections, trauma, stroke, poisons, or nutritional deficiencies-inflammation spurs the release of pro- inflammatory cytokines, which may affect mood.
细胞因子激活的酶，吲哚胺2,3 - 双加氧酶（IDO），这会降低血清素,导致神经递质水平低。 IDO也降低了前驱体对血清素，色氨酸。神经递质血清素的水平降低可能促进抑郁症状的发展。炎症过程对血清素的恒定破坏 减小恢复的机会。
Cytokines activate an enzyme, indoleamine 2,3-dioxygenase (IDO), which degrades serotonin resulting in low levels of the neurotransmitter. IDO also degrades the precursor to serotonin, tryptophan. Decreased levels of the neurotransmitter serotonin are likely the contributing factor to the development of depressive symptoms. The inflammatory process' contribution to the constant destruction of serotonin decreases the chances of recovery.
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