Tsao Chiung-Wen, Lin Yee-Shin, Chen Chwen-Cheng, Bai Chyi-Huey, Wu Shin-Rung
Department of Nursing, Chung Hwa College of Medical Technology, Tainan County, Taiwan.
Prog Neuropsychopharmacol Biol Psychiatry. 2006 Jul;30(5):899-905. doi: 10.1016/j.pnpbp.2006.01.029. Epub 2006 Mar 6.
Altered cytokine secretion as a mechanism in the etiology of depression is still obscure. The serotonin transporter (5-HTT) may play an important role in the termination of serotonergic neurotransmission by serotonin (5-HT) uptaking into presynaptic neurons and representing as an initial action site for selective 5-HTT reuptake inhibitors (SSRI). In our study, we evaluated whether cytokines and 5-HTT acted as biological markers for depression. Blood samples were collected from 42 participants. The differences in cytokine and 5-HTT mRNA expressions of leukocytes were assessed between the patients with major depression (n=20) and the healthy controls (n=22), along with the measurements prior and after treatment with a SSRI, fluoxetine, for 3 months in the follow-up patient group (n=8). The results revealed that the mRNA expressions of IL-1beta, IL-6, IFNgamma, TNFalpha, and 5-HTT were higher in the depressed patients than those of the healthy controls. The higher level of mRNA expressions of IFNgamma and 5-HTT diminished after fluoxetine treatment. Furthermore, we found a positive correlation between 5-HTT and cytokines mRNA expressions in total participants, which suggested that pro-inflammatory cytokines and 5-HTT might play critical roles in the pathogenesis of major depression and that their levels were affected by chronic treatment with 5-HTT inhibitors.
细胞因子分泌改变作为抑郁症病因的一种机制仍不清楚。血清素转运体(5-HTT)可能在血清素(5-HT)摄取到突触前神经元从而终止血清素能神经传递过程中发挥重要作用,并作为选择性5-HTT再摄取抑制剂(SSRI)的初始作用位点。在我们的研究中,我们评估了细胞因子和5-HTT是否作为抑郁症的生物学标志物。从42名参与者采集血样。评估了重度抑郁症患者(n = 20)和健康对照者(n = 22)白细胞中细胞因子和5-HTT mRNA表达的差异,以及随访患者组(n = 8)中8名患者在使用SSRI氟西汀治疗3个月前后的测量结果。结果显示,抑郁症患者中IL-1β、IL-6、IFNγ、TNFα和5-HTT的mRNA表达高于健康对照者。氟西汀治疗后,IFNγ和5-HTT的mRNA表达水平降低。此外,我们发现所有参与者中5-HTT与细胞因子mRNA表达之间呈正相关,这表明促炎细胞因子和5-HTT可能在重度抑郁症的发病机制中起关键作用,且它们的水平受5-HTT抑制剂的长期治疗影响。