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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 observe the effect of anti-depressant citalopram on the expression of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in cultured microglial cells in vitro and to investigate the effects of citalopram on microglial cells The role of mitogen-activated protein kinase family p38 (p38MAPK) and c-jun amino-terminal kinase (JNK). Methods Lipopolysaccharide (LPS) induced the expression of TNF-α and IL-1β in BV2 microglial cells. After pretreatment with citalopram (20μmol / L) for 4 hours, the expression of TNF-αmRNA and IL-1βmRNA were detected by qRTPCR. After pretreatment for 24 h, the levels of TNF-α and IL- Culture supernatant concentration; 30min after pretreatment cells were harvested to observe the citalopram p38MAPK and JNK phosphorylation. Results Citalopram significantly inhibited the mRNA and protein expression of TNF-α and IL-1β in microglial cells. Citalopram inhibited LPS-induced phosphorylation of p38MAPK and JNK. Conclusion Citalopram may play an immunosuppressive role on microglia by inhibiting the MAPK pathway.