西酞普兰对小胶质细胞的免疫调节作用  

Immune regulatory effect of citalopram on microglial cells

作　　者：王姗姗[1] 陈海英[1] 解恒革[1] 

机构地区：[1]解放军总医院南楼神经内科,北京100853

出　　处：《细胞与分子免疫学杂志》2013年第12期1251-1253,1257,共4页Chinese Journal of Cellular and Molecular Immunology

基　　金：国家自然科学基金(81101011)

摘　　要：目的观察抗抑郁药物西酞普兰对体外培养的小胶质细胞中肿瘤坏死因子α(TNF-α)和白细胞介素1β(IL-1β)表达的影响,探讨西酞普兰对小胶质细胞丝裂原活化的蛋白激酶家族p38(p38MAPK)和c-jun氨基末端激酶(JNK)的作用。方法脂多糖(LPS)诱导BV2小胶质细胞表达TNF-α和IL-1β。西酞普兰组(20μmol/L)预处理4 h后,采用实时定量PCR(qRTPCR)观察TNF-αmRNA和IL-1βmRNA的表达;预处理24 h后,ELISA检测TNF-α和IL-1β在细胞培养上清的浓度;预处理30min后收获细胞,观察西酞普兰对p38MAPK和JNK磷酸化的影响。结果西酞普兰显著抑制小胶质细胞TNF-α和IL-1β的mRNA和蛋白表达;西酞普兰抑制LPS诱导的p38MAPK和JNK的磷酸化。结论西酞普兰可能是通过抑制MAPK途径对小胶质细胞发挥免疫抑制作用。Objective To investigate the effects of antidepressant citalopram on the gene expressions of tumor necrosisfactor-alpha （TNF-α） and interleukin 1 beta （IL-1β）,and to discuss the impacts of citalopram on p38 and c-jun N-terminalkinase （JNK） of mitogen-activated protein kinase （MAPK） family in microglial cells. Methods BV2 cells were induced bylipopolysaccharide （LPS） to produce TNF-α and IL-1β. After pretreatment with citalopram （20 μmol/L） for 4 h, the mRNAlevels of TNF-α and IL-1β were measured by quantitative real-time PCR （qRT-PCR） ; after pretreatment for 24 h, the proteinlevels of TNF-α and IL-1β were analyzed by ELISA; the effects of citalopram on the phosphorylation of p38MAPK and JNKwere observed after pretreatment for 30 min. Results Citalopram significantly inhibited the mRNA and protein expressions of TNF-α and IL-1β, and the phosphorylation of p38MAPK and JNK. Conclusion Citalopram may play the anti-inflammatoryrole by inhibiting MAPK pathway in microglial cells.

关 键 词：小胶质细胞 脑卒中后抑郁 西酞普兰 肿瘤坏死因子-Α 白细胞介素1Β 丝裂原活化的蛋白激酶 

分 类 号：R392.11[医药卫生—免疫学] R749.13[医药卫生—基础医学]