摘要
目的本研究主要探讨姜黄素(curcumin,Cur)对暴露于β淀粉样蛋白(β-amyloid,Aβ)中的小胶质细胞激活水平的影响,并观察上述作用是否通过细胞因子信号抑制蛋白1(suppressor of cytokine signaling 1,SOCS1)分子介导。方法将细胞分为4组,分别为正常培养的对照组(Control组)、10μmol的Aβ刺激组(Aβ组)、50μg/ml的Cur和10μmol的Aβ共同处理组(Cur+Aβ组)和50μg/ml的Cur单独暴露组(Cur组),培养24 h后,通过酶联免疫吸附试验(enzyme-linked immunosorbent assay,ELISA)检测培养基中炎症因子水平、Western blot检测诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)和SOCS1表达、免疫细胞染色观察细胞iNOS水平。结果与对照组相比,10μmol的Aβ处理24 h可显著增加培养基内肿瘤坏死因子α(tumor necrosis factor alpha,TNF-α)、白细胞介素1β(interleukin-β,IL-1β)和白细胞介素6(interleukin 6,IL-6)水平(P<0.05),并显著上调细胞iNOS蛋白表达(P<0.05),50μg/ml的Cur可显著降低上述炎症因子和iNOS表达水平(P<0.05),SOCS1-siRNA可显著逆转Cur的上述作用。结论 Cur可显著减轻Aβ对小胶质细胞的激活,上述作用可能通过SOCS1分子介导。
Objective To investigate curcumin（Cur）-induced effects on microglia exposed toβ-amyloid（Aβ）,and explore the role of suppressor of cytokine signaling 1（SOCS1）in the process.Methods Microglial cells were divided into control group（normal cultivated）,Aβgroup（10μmol）Aβ-activated）and Cur＋Aβgroup（50μg/ml Cur-and 10μmol Aβ-treated）.After 24 hour＇s treatment,inflammatory factors were measured by enzyme-linked immunosorbent assay（ELISA）,inducible nitric oxide synthase（iNOS）and SOCS1 expression was detected by Western blot,and levels of iNOS were observed in immunocytochemistry.Results Compared with control group,the levels of tumor necrosis factor alpha（TNF-α）,interleukin-β（IL-1β）and interleukin 6（IL-6）and iNOS expression were increased with 10μmol Aβtreatment for 24 hours.The above-mentioned inflammatory cytokines and iNOS expression levels were decreased with50μg/ml Cur（P〈0.05）.However,the above-mentioned effects of Cur were reversed by SOCS1-siRNA（P〈0.05）.Conclusion The research shows Cur can alleviate microglial cell activation,because of SOCS1 molecule mediating.
出处
《华南国防医学杂志》
CAS
2016年第10期627-631,共5页
Military Medical Journal of South China
