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目的探讨促红细胞生成素(EPO)对大鼠局灶性脑缺血再灌注后脑梗死面积变化及信号转导与转录激活子-1(STAT1)、磷酸化STAT1(P-STAT1)、信号转导与转录激活子-3(STAT3)、磷酸化STAT3(P-STAT3)蛋白表达的影响。方法雄性健康SD大鼠40只,随机分为假手术组(A)、脑缺血再灌注组(B)、生理盐水治疗组(C)、EPO治疗组(D),采用线栓法阻断大鼠一侧大脑中动脉血流2 h,再灌注24 h,建成局灶性脑缺血再灌注损伤模型。治疗组于脑缺血刚开始时腹腔注射EPO或等量生理盐水,于24 h时行MRI检查观察脑梗死面积,采用Western blotting检测STAT1、P-STAT1、STAT3、P-STAT3蛋白表达水平的变化。结果与B、C组相比,D组脑梗死面积减小(P<0.05),STAT3磷酸化水平增加(P<0.05),STAT1磷酸化水平有所减少。结论 EPO可能通过影响JAK/STAT信号转导通路减小脑梗死面积。
Objective To investigate the effects of erythropoietin (EPO) on the changes of cerebral infarction area and the expressions of signal transducers and activators of transcription-1 (STAT1), phosphorylated STAT1 (P-STAT1), signal transduction And transcriptional activator-3 (STAT3), phosphorylated STAT3 (P-STAT3) protein expression. Methods Forty male Sprague-Dawley rats were randomly divided into sham operation group (A), cerebral ischemia-reperfusion group (B), saline control group (C) and EPO treatment group (D) Rat middle cerebral artery blood flow 2 h, reperfusion 24 h, built a focal cerebral ischemia-reperfusion injury model. At the beginning of cerebral ischemia, the treatment group were intraperitoneally injected with EPO or normal saline, and the cerebral infarction area was observed by MRI at 24 hours. The expression of STAT1, P-STAT1, STAT3 and P-STAT3 protein were detected by Western blotting . Results Compared with group B and group C, the area of infarction in group D was decreased (P <0.05), the level of STAT3 phosphorylation was increased (P <0.05), and the level of STAT1 phosphorylation was decreased. Conclusion EPO may reduce the area of cerebral infarction by affecting JAK / STAT signal transduction pathway.