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张桂莲, 郭英英, 张磊等. 依达拉奉对Aβ\25-35诱导的PC12细胞MAPKs信号通路的影响[J]. koko体育app 学报（医学版）, 2015, 46(2): 179-184.
引用本文: 张桂莲, 郭英英, 张磊等. 依达拉奉对Aβ\25-35诱骗的PC12体细胞MAPKs卫星信号环路的反应[J]. 河北大学时学报（医学界版）, 2015, 46(2): 179-184.
ZHANG Gui-lian, GUO Ying-ying, ZHANG Lei. et al. The Effect of Edaravone on MAPKs Signal Pathway Associated with Aβ\25-35 Treatment in PC12 Cells[J]. Journal of Sichuan University (Medical Sciences), 2015, 46(2): 179-184.
Citation: ZHANG Gui-lian, GUO Ying-ying, ZHANG Lei. et al. The Effect of Edaravone on MAPKs Signal Pathway Associated with Aβ\25-35 Treatment in PC12 Cells[J]. Journal of Sichuan University (Medical Sciences), 2015, 46(2): 179-184.

依达拉奉对Aβ\25-35诱导的PC12细胞MAPKs信号通路的影响

The Effect of Edaravone on MAPKs Signal Pathway Associated with Aβ\25-35 Treatment in PC12 Cells

  • 摘要: 目的 探讨自由基清除剂依达拉奉通过丝裂原活化蛋白激酶（MAPKs）信号转导通路发挥细胞保护作用的途径，为阿尔茨海默病（AD）发病机制及AD治疗新药的研发增添理论依据。方法 培养肾上腺嗜铬瘤细胞（PC12细胞），根据不同的干预措施将细胞分为4组。阴性对照组（高糖DMEM组）；AD模型组（30 μmol/L Aβ\25-35处理组）；抑制剂对照组：10 μmol/L SB203580〔丝裂原活化蛋白激酶p38(p38)抑制剂〕、10 μmol/L SP600125〔c-Jun氨基末端激酶（JNK）抑制剂〕或10 μmol/L PD98059〔细胞外调节蛋白激酶（ERK）抑制剂〕处理组；依达拉奉低、中、高剂量组：依达拉奉20、40、80 μmol/L及30 μmol/L Aβ\25-35共同孵育组。Western blot检测各组细胞p-p38、p-JNK及p-ERK蛋白的表达；RT-PCR法检测以上各组（抑制剂对照组仅加入SB203580 10 μmol/L）p38 mRNA的表达。结果 ① 与阴性对照组比，AD模型组p-p38 蛋白表达增高（\P\P\P\P\P\P\P>0.05）。④ 与阴性对照组比，AD模型组的p38 mRNA表达增加，而抑制剂对照组的p38 mRNA表达减少（分别\P\P\P\25-35可能直接激活MAPK信号通路，尤其p38及JNK，损伤PC12细胞。依达拉奉可能同时在mRNA水平及蛋白质水平，阻断p38信号转导通路，发挥抗Aβ\25-35引起的PC12细胞损伤作用，有望成为治疗AD的新药。  
    Abstract: Objective To explore whether edaravone protects cells damage via mitogen-activated protein kinases (MAPKs) signal pathway, and which procedure of p38 be affected so as to add theories for AD pathogenesis and treatments. Methods According to different drugs treated, PC12 cells \in vitro were divided into four groups. Negative control group: cells were treated with media alone. AD model group: cells were treated with 30 μmol/L Aβ\25-35. Inhibitor control group: cells were treated with 10 μmol/L SB203580 〔p38 mitogen-activated protein kinase (p38) inhibitor〕, 10 μmol/L SP600125 〔c-Jun NH2 terminal kinase (JNK) inhibitor〕, or 10 μmol/L PD98059 extracelular signal regulated kinase (ERK) inhibitor〕. Low-dose, middle-dose and high-dose edaravone group: cells plated for 24 hours treated with 30 μmol/L Aβ\25-35 and co-treated with 20, 40, 80 μmol/L edaravone 3 hours, respectively. The morphology of the treated cells were observed, the p-p38, p-JNK and p-ERK proteins in each group were tested by the Western blot. The p38 mRNA were tested in each group above (only add SB203580 10 μmol/L in third group) by the real time PCR. Results ① The p-p38 protein was significantly increased in model control group compared with that in negative control group (\P\P<0.05) when compared with that in model control group. The  
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