Song C, Halbreich U, Han C, Leonard B E, Luo H
Department of Biomedical Sciences, University of Prince Edward Island, Charlottetown, Canada.
Pharmacopsychiatry. 2009 Sep;42(5):182-8. doi: 10.1055/s-0029-1202263. Epub 2009 Sep 1.
An increase in inflammatory response and an imbalance between T-helper (Th) 1 and 2 functions have been implicated in major depression. The aims of the present study were to 1) study the relationship between pro- and anti-inflammatory cytokines and between Th1 and Th2 produced cytokines in depressed patients and 2) evaluate and compare the effect of treatments with electroacupuncture (EA) and fluoxetine on these cytokines.
95 outpatients with major depressive disorder were treated for 6 weeks with EA, fluoxetine or placebo. Hamilton Depression Rating Scale (HDRS) and Clinical Global Impression (CGI) were used to assess severity and therapeutic effects. 30 volunteers served as controls. Serum cytokine concentrations were measured by ELISA.
Increased proinflammatory cytokine interleukin (IL)-1beta and decreased anti-inflammatory cytokine IL-10 were found in the depressed patients. By contract, Th1 produced proinflammatory cytokines, tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma were decreased, and Th2 produced cytokine IL-4 was significantly increased in depressed patients. The ratio of IFN/IL-4 was also increased. Both acupuncture and fluoxetine treatments, but not the placebo, reduced IL-1beta concentrations in responders. However, only acupuncture attenuated TNF-alpha concentration and INF-gamma/IL-4 ratio towards the control level.
These results suggest that an imbalance between the pro- and anti-inflammatory cytokines (IL-1 and IL-10), and between Th1 and Th2 cytokines (INF-gamma or TNF-alpha and IL-4) occurred in untreated depressed patients. Both EA and fluoxetine had an anti-inflammatory effect by reducing IL-1beta. EA treatment also restored the balance between Th1 and Th2 systems by increasing TNF-alpha and decreasing IL-4.
炎症反应增加以及辅助性T细胞(Th)1和Th2功能失衡与重度抑郁症有关。本研究的目的是:1)研究抑郁症患者促炎和抗炎细胞因子之间以及Th1和Th2产生的细胞因子之间的关系;2)评估并比较电针(EA)和氟西汀治疗对这些细胞因子的影响。
95名重度抑郁症门诊患者接受了为期6周的EA、氟西汀或安慰剂治疗。采用汉密尔顿抑郁量表(HDRS)和临床总体印象量表(CGI)评估严重程度和治疗效果。30名志愿者作为对照。通过酶联免疫吸附测定法(ELISA)测量血清细胞因子浓度。
抑郁症患者促炎细胞因子白细胞介素(IL)-1β升高,抗炎细胞因子IL-10降低。相比之下,抑郁症患者中Th1产生的促炎细胞因子肿瘤坏死因子(TNF)-α和干扰素(IFN)-γ降低,Th2产生的细胞因子IL-4显著升高。IFN/IL-4的比值也升高。针刺和氟西汀治疗(而非安慰剂治疗)均降低了有效应答者的IL-1β浓度。然而,只有针刺使TNF-α浓度以及INF-γ/IL-4比值降至对照水平。
这些结果表明,未经治疗的抑郁症患者促炎和抗炎细胞因子(IL-1和IL-10)之间以及Th1和Th2细胞因子(INF-γ或TNF-α和IL-4)之间存在失衡。EA和氟西汀均通过降低IL-1β发挥抗炎作用。EA治疗还通过增加TNF-α和降低IL-4恢复了Th1和Th2系统之间的平衡。