期刊
PHARMACOLOGICAL REPORTS
卷 61, 期 6, 页码 1105-1112出版社
POLISH ACAD SCIENCES INST PHARMACOLOGY
DOI: 10.1016/S1734-1140(09)70173-2
关键词
amantadine; fluoxetine; imipramine; pro-inflammatory cytokines; interleukin-10
Treatment with amantadine (AMA), an N-methyl-D-aspartate (NMDA) receptor antagonist and anti depressant drug, increased the antidepressant activity of subsequent drugs in experimental studies and in patients Suffering from treatment-resistant depression (TRID). Recent evidence indicates that depression may be accompanied by activation of an inflammatory response. These data indicate that pro-inflammatory cytokines may play a role in the etiology of depression, particularly in TRD. The present in vitro study shows the ability of AMA, used at concentrations between 10(-7) to 10(-5) M, to reduce the production of the pro-inflammatory cytokines, specifically interferon-gamma (IFN-gamma) and turner necrosis factor-alpha (TNF-alpha). In addition, AMA treatment increased the production of the negative immunoregulator, interleukin-10 (IL-10). Furthermore, the combined treatment of AMA with fluoxetine (FLU), but not imipramine (IMI), had a stronger immunomodulatory effect on cytokine production than AMA alone. The above data provide additional rationale for the treatment of patients suffering from depression with a combination of AMA and a selective serotonin reuptake inhibitor.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据