大鼠抑郁障碍与心血管组织炎性标记物的相关性研究

目的探讨强迫游泳抑郁模型大鼠抑郁障碍与炎性标记物的相关性。方法健康SD大鼠随机抽签分为对照组和模型组,应用21 d强迫游泳试验建立大鼠抑郁模型,模型组大鼠包括SS组(9只,应激+生理盐水腹腔注射)、SF组(8只,应激+氟西汀腹腔注射)和SI组(8只,应激+丙咪嗪腹腔注射)。对照组大鼠包括CS组(10只,生理盐水腹腔注射),CI组(7只,丙咪嗪腹腔注射)。应用透射免疫比浊法和酶联免疫法检测外周血炎性标记物高敏C反应蛋白(hsCRP)、单核细胞趋化因子1(MCP-1)水平,应用免疫组织化学染色法和蛋白印迹法检测血管组织核因子-κB(NF-κB)p65、抑制蛋白κB(IκB)-α、MCP-1表达水平。结果应激后模型组外周血hsCRP和MCP-1含量明显高于CS、CI组,SS组与CS组hsCRP水平分别为(0.26±0.07)mg/L和(0.15±0.06)mg/L(P<0.01),SS组与CS组MCP-1水平分别为(52.02±18.83)ng/L和(22.52±8.45)ng/L(P<0.01)。血管组织中MCP-1、NF-κB p65表达显著增强,SS组与CS组MCP-1水平分别为(1.78±0.36)mg/L和(0.85±0.15)mg/L,SS组与CS组NF-κB p65水平分别为(0.88±0.16)和(0.12±0.04)(P<0.01),胞浆中IκB-α表达显著减少,SS组与CS组IκB-α水平分别为(0.48±0.07)和(2.07±0.48)(P<0.01)。结论抑郁障碍通过NF-κB表达增强来启动炎症反应。

Relationship between depressive disorder and inflammation markers in depression rat model

Objective To investigate the relationship between depressive disorder and inflammation markers in depression rat model. Methods Depression rat model was made by Forced Swimming Test(FST) in 21days.A total of 50 Sprague-Dawley rats were randomly divided into 5 groups: CS group(n=10,control group,treated with saline),CI group(n=10,control group,treated with imipramine),SS group(n=10,model group,treated with saline),SF group(n=10,model group,treated with fluoxetine) and SI group(n=10,model group,treated with imipramine).Monocyte chemoattractant protein-1(MCP-1) in peripheral blood was measured by enzyme linked immunoassay(ELISA) and hypertensive C-reaction protein(hsCRP) by immunoturbidimetric assay.The expression of MCP-1,nuclear factor-kappa B(NF-κB) p65 and inhibitory kappa B(IκB)-α in aorta tissue were observed by immunohistochemistry and western blot. Results Eight rats died during the study(3 in CI group,1 in SS group,2 in SF group and 2 in SI group).Serum concentration of hsCRP and MCP-1 in peripheral blood was significantly higher (0.26±0.07) mg/L vs.(0.15±0.06) mg/L for hsCRP and(52.02±18.83) ng/L vs.(22.52±8.45) ng/L for MCP-1,both P<0.01] and expression of MCP-1 and NF-κB p65 in aorta tissue was significantly increased in SS group than in CS group(1.78±0.36) vs.(0.85±0.15) for MCP-1 and(0.88±0.16)vs.(0.12±0.04) for NF-κB p65,both P<0.01].The expression of IκB-α was significantly decreased in aorta tissue in SS group than in CS group (0.48±0.07) vs.(2.07±0.48),P<0.01]. Conclusions Depression disorder activates inflammatory reaction by increasing expression of NF-κB.