首发精神分裂症和首发抑郁症患者血浆白细胞介素及其可溶性受体的对照研究

The comparative study on plasma interleukin and soluble interleukin receptors between first-episode schizophrenic patients and first-episode depressive patients

目的在细胞因子水平探讨精神分裂症和抑郁症病理机制的异同。方法首发精神分裂症和首发抑郁症患者各30例,分别单一接受利培酮(6mg/d)、帕罗西汀(20mg/d)治疗6周,治疗前后用阳性和阴性症状量表(PANSS)评估精神分裂症患者,并用汉密尔顿抑郁量表(HAMD)评估抑郁症患者。用酶联免疫吸附(ELISA)法测定治疗前后患者组和30名正常对照的血浆白细胞介素-2(IL-2)、可溶性白细胞介素-2受体(sIL-2R)、白细胞介素-6(IL-6)、可溶性白细胞介素-6受体(sIL-6R)的浓度。结果治疗前,2个患者组的血浆IL-2、sIL-2R、IL-6、sIL-6R均高于正常对照组(P<0.05);精神分裂症组血浆sIL-2R高于抑郁症组(P<0.05),而IL-2、IL-6、sIL-6R低于抑郁症组(P<0.05)。②治疗后,精神分裂症组血浆IL-2、sIL-6R较治疗前下降(P<0.05),抑郁症组血浆IL-2、sIL-2R、IL-6、sIL-6R均较治疗前下降(P<0.05);精神分裂症组血浆sIL-2R高于抑郁症组(P<0.05),而IL-2、sIL-6R低于抑郁症组(P均小于0.05)。③精神分裂症组治疗前后血浆IL-2变化率与PANSS总分减分率正相关(r=0.64,P<0.001);抑郁症组治疗前后血浆IL-2和IL-6的变化率均与HAMD总分减分率正相关(r=0.42,P=0.02;r=0.54,P=0.002)。结论精神分裂症和抑郁症细胞因子均存在异常,提示二者可能存在共同的病理机制,但细胞因子表达的差异可能与二者存在不同的生物学基础有关。

Objective To explore the pathogenesis of schizophrenia and depressive disorder at cellular level. Methods Thirty first-episode schizophrenic patients and 30 first-episode depressive patients were recruited and treated with either risperdone （6 mg/d） or paroxetine hydrocbloride （20mg/d） , respectively for 6 weeks. Thirty healthy people served as normal controls. The Positive and Negative Syndrome Scale （PANSS） was utilized to evaluate the schizophrenic patients before and after treatment; Hamilton Depression Scale （HAMD） was used for evaluation of depressive patients before and after treatment. Enzyme-labeled immunosorbent assay （ELISA） was also used to measure the concentrations of IL-2,sIL- 2R,IL-6 ,sIL-6R in blood plasma. Results （1） Prior to treatment, the concentrations of the IL-2,sIL-2R,IL-6 ,sIL-6 from schizophrenia and depressive disorder groups were all higher than those from normal control group （ P 〈 0. 05 ） ; the concentration of the sIL-2R from schizophrenia group was higher than that from depressive disorder group （ P 〈 0. 05 ） , whereas the concentrations of the IL-2 ,IL-6 ,sIL-6R from schizophrenia group were lower than those from depressive disorder group（ P 〈 0. 05 ）. （2） After treatment, the concentrations of the IL-2, sIL-6R from schizophrenia group and the concentrations of the IL-2,IL-6 ,sIL-2R and sIL-6R from depressive disorder group decreased （ P 〈 0. 05 ）. The concentration of sIL-2R from schizophrenia group was higher than that from depressive disorder group （ P 〈 0. 05 ） ; the concentrations of the IL-2,sIL-6R from schizophrenia group were lower than those from depressive disorder group （P 〈 0. 05 ）. （3） In schizophrenia group, the IL-2 variation rates after treatment was positively associated with the decrease rate of PANSS total score （ r = 0. 64, P 〈 0. 001 ）. In depressive disorder group, the variation rates of IL-2 and IL-6 after trentment were positively associated with the decrease rates of HAMD total scores （ r = 0. 42, P = 0. 02 ; r = 0. 54, P = 0. 002）. Conclusions Cytokine abnormalities are present in both schizophrenia and depressive disorder, which suggest a common underlying pathogenesis of both schizophrenia and depressive disorder. The difference in expression patterns of cytokines suggests that schizophrenia and depressive disorder may have different neural substrates.