摘要
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大鼠随机分为对照组和模型组,应用21 d强迫游泳实验建立大鼠抑郁模型,模型组大鼠包括SS组(应激+0.9氯化钠注射液腹腔注射)和SI组(应激+丙米嗪腹腔注射)。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hsCRP、MCP-1水平,应用免疫组织化学染色法检测血管组织NF-κB P65、MCP-1表达。结果应激后外周血hsCRP和MCP-1含量明显高于对照组(P<0.05),血管组织中MCP-1为35.6±7.5,NF-κB P65为31.2±6.5,表达显著增强(P<0.05),药物干预组外周血MCP-1显著回降(P<0.05),血管组织炎性标志物表达减少。结论抑郁障碍通过NF-κB表达增强进而启动炎性反应。
Objective To investigate the relationship between depressive disorder and inflammation markers in depressive rats induced by Forced Swimming Test（FST）.Methods SD rats were randomly divided into controlling groups and modelling groups,Depression animal model was reproduced with FST in 21days.Modeling group included SS group（FST rats with 0.9% sodium cloride treated） and SI group（FST rats with imipramine treated）.all peripheral blood serum samples were respectively measured using enzyme linked immunoassay（ELISA） technique for concentration of MCP-1 and immunoturbidimetric assay for hsCRP.The expression of MCP-1 and NF-κB P65 in aorta tissue were observed by immunohistochemistry.Results There was a high level of concentration of hsCRP and MCP-1 in peripheral blood serum samples and increased expression of MCP-1 and NF-κB P65 in aorta tissue of SS groups（P0.05）.SI groups had decreased the expression of inflammation markers in blood and aorta tissue.Conclusion Depressive disorder activate the inflammatory reaction through increased expression of NF-κB.
出处
《基础医学与临床》
CSCD
北大核心
2011年第6期700-703,共4页
Basic and Clinical Medicine
