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<0.05). The p-p38 protein in the inhibitor group and edaravone groups was decreased significantly (\P<0.05) when compared with that in model control group. The
