CAJ | 학술논문

目的初步探讨急性缺血性卒中患者血浆120种细胞因子蛋白水平与卒中后抑郁（post-stroke depression，PSD）发生的关系。方法入组PSD及非PSD患者各12例，均为卒中发生后3 d内入院的急性缺血性卒中患者，随访至卒中后2周，对患者进行神经功能，认知功能及抑郁、焦虑严重程度评估。患者入院后1d[卒中后（1.5±0.9） d]清晨6∶30留取空腹时静脉血浆标本，利用人类细胞因子蛋白表达微阵列芯片进行120种细胞因子蛋白组学检测。结果与非PSD组相比，PSD组4个细胞因子血浆中点信号强度（spot signal intensity，SIs）显示降低，差异有显著性，分别为胰岛素样生长因子1受体（insulin-like growth factor 1 receptor, IGF-I SR）（P=0.021），巨噬细胞炎症蛋白-3β（macrophage inflammatory protein-3 beta，MIP-3 beta）（P=0.033），胎盘生长因子（placental growth factor，PIGF）（P=0.021），血管内皮生长因子（vascular endothelial growth factor，VEGF）（P=0.015），但均未通过错误发现率多重校正，多因素Logistic回归分析无阳性发现。血浆胰岛素样生长因子1受体蛋白SIs与患者入院时Barthel指数呈负相关（r=-0.641， P=0.025），与2周后PSD患者汉密尔顿抑郁量表评分（r=0.478，P=0.005）及汉密尔顿焦虑量表评分（r=0.674，P=0.016）呈正相关。结论本研究的数据尚未发现能独立预测卒中急性期PSD风险的血浆细胞因子，但3种生长因子水平的异常提示PSD可能存在突触可塑及神经再生障碍。
목적초보탐토급성결혈성졸중환자혈장120충세포인자단백수평여졸중후억욱（post-stroke depression，PSD）발생적관계。방법입조PSD급비PSD환자각12례，균위졸중발생후3 d내입원적급성결혈성졸중환자，수방지졸중후2주，대환자진행신경공능，인지공능급억욱、초필엄중정도평고。환자입원후1d[졸중후（1.5±0.9） d]청신6∶30류취공복시정맥혈장표본，이용인류세포인자단백표체미진렬심편진행120충세포인자단백조학검측。결과여비PSD조상비，PSD조4개세포인자혈장중점신호강도（spot signal intensity，SIs）현시강저，차이유현저성，분별위이도소양생장인자1수체（insulin-like growth factor 1 receptor, IGF-I SR）（P=0.021），거서세포염증단백-3β（macrophage inflammatory protein-3 beta，MIP-3 beta）（P=0.033），태반생장인자（placental growth factor，PIGF）（P=0.021），혈관내피생장인자（vascular endothelial growth factor，VEGF）（P=0.015），단균미통과착오발현솔다중교정，다인소Logistic회귀분석무양성발현。혈장이도소양생장인자1수체단백SIs여환자입원시Barthel지수정부상관（r=-0.641， P=0.025），여2주후PSD환자한밀이돈억욱량표평분（r=0.478，P=0.005）급한밀이돈초필량표평분（r=0.674，P=0.016）정정상관。결론본연구적수거상미발현능독립예측졸중급성기PSD풍험적혈장세포인자，단3충생장인자수평적이상제시PSD가능존재돌촉가소급신경재생장애。
Objective To investigate the association between post-stroke depression (PSD) and the level of cytokines in plasma. Methods Plasma spot signal intensity (SIs) of 120 cytokines were measured by Human Cytokine Antibody Array G-Series 1000 in 12 patients with PSD and 12 non-PSD controls who admitted to the hospital within the ifrst 3 days after stroke onset. The diagnoses of PSD were made in accordance with DSM-IV criteria. The 17-item Hamilton Depression Rating Scale (HAMD) and Hamilton Anxiety Scale (HAMA) were used to screen for depressive and anxiety symptoms on days 14 after admission. Results Plasma SIs of 4 cytokines (insulin-like growth factor 1 receptor [IGF-I SR], macrophage inflammatory protein-3 beta [MIP-3 beta], placental growth factor [PIGF], vascular endothelial growth factor [VEGF]) were signiifcantly lower in PSD patients than in non-PSD patients, although these findings were not significant after the false discovery rate (FDR) correction for multiple testing to be applied. No cytokine was independently associated with incidence of PSD at the acute stage of stroke. Plasma SIs of IGF-I SR showed a negative correlation with the Barthel index (r=-0.641, P=0.025) 1 day after admission and showed positive correlations with the HAMD (r=0.478, P=0.005) and HAMA scores (r=0.674, P=0.016) 14 days after admission. Conclusion Plasma levels of cytokines after ischemic stroke can't serve as a biological marker to predict the incidence of PSD. Dysfunction of synaptic plasticity and neurogenesis may play a causative role in PSD.