抑郁症患者血清白细胞介素-1β,6的水平及其发病机制的对照研究  

A controlled study between plasma interleukin-1 beta,6 levels and its mechanisn of onset in depressed patients.

作　　者：王从杰[1] 宋波[1] 周娟[1] 杨丽[1] 李湖[1] 王建文[1] 陈汇[1] 杨海英[1] 

机构地区：[1]江苏省淮安市第三人民医院,223001

出　　处：《四川精神卫生》2004年第2期65-66,共2页Sichuan Mental Health

摘　　要：目的　探讨抑郁症的细胞免疫改变及其可能的发病机制。方法　采用酶联免疫吸附法 ,对 31例抑郁症患者在抗抑郁治疗前后分别进行HAMD评定及IL - 1β ,IL - 6的检测 ,并以 2 1例健康者作对照。 结果　抑郁症治疗前IL - 1β及IL - 6水平显著高于正常对照组 (P <0 0 5 ) ,且经 4～ 10周左右治疗后 ,二者明显下降。但疗前HAMD评分高低与疗前IL - 1β及IL - 6水平并无相关性 (P >0 0 5 )。 结论　免疫系统激活及炎症反应确实参与抑郁症的发病过程 ,但本研究尚不能确定抑郁症严重度 (HAMD评分 )与血清IL - 1β及IL - 6水平存在相关性。Objective To study cellular immunity changes of depression and its possible mechanism of onset.Method Plasma interleukin-1 beta,6(IL-1β,6)levels were measured with ELISA in 31 depressed patients whose clinical evaluation was peformed by the Hamilton rating scale for depression(HAMD) before and after treatment with antidepressants respectively.Meanwhile,they were compared with those of 21 control subjects.Results Plasma interleukin-1 beta,6 levels in depressed patients before treatment both were obviousely higher than that in controls( P <0.05),and remarkblely decreased after 4～10 weeks of treatments;But the positive correlation before treatments was not found between the severity of depression(the scores of HAMD)and plasma IL-1 beta and 6.Conclusions These findings further show that an activation of the immune-inflammatory system is involved in the pathophysiology of depressive disorders,but now it could not be determined that the severity of depression was associated with plasma concentrations of IL-1 beta,6 before treatment.

关 键 词：抑郁症白细胞介素-1β白细胞介素-6 

分 类 号：R749.3[医药卫生—神经病学与精神病学]