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目的研究脑溢安对脑出血大鼠脑内p38丝裂原活化蛋白激酶(Mitogen-activatedproteinkinase,p38MAPK)信号转导通路的影响,探讨中药脑溢安颗粒(简称脑溢安)对脑出血的保护作用机制。方法采用胶原酶注射建立大鼠脑出血模型,应用免疫共沉淀、激酶反应及Westernblot技术检测脑出血大鼠脑内p38MAPK活性变化及脑溢安对p38MAPK活性的影响。结果脑出血损伤后1hp38MAPK活性增强,出血损伤后6h达高峰,12h后下降,至24hp38MAPK活性消失,脑溢安治疗组(简称治疗组)在脑出血损伤后1,6和12h各时间点p38MAPK活性均较模型组减低。结论脑出血大鼠脑内p38MAPK活性增强,脑溢安能抑制脑出血损伤激活的p38MAPK信号转导通路。
Objective To study the effect of Naoyi An on the signal transduction pathway of p38MAPK in the brain of rats with intracerebral hemorrhage, and to explore the protection of cerebral bleeds caused by Nao Yi An granules (abbreviated as Nao Yi An). Mechanism. Methods The rat model of cerebral hemorrhage was established by collagenase injection. The changes of p38MAPK activity in brain of rats with intracerebral hemorrhage and the effects of Nao Yi An on the activity of p38MAPK were detected by co-immunoprecipitation, kinase reaction and Western blot. Results The activity of 1hp38MAPK increased after cerebral hemorrhage and reached the peak at 6h after hemorrhagic injury. The activity of 24hp38MAPK disappeared after 12h. The activity of p38MAPK was detected at 1, 6, and 12h after cerebral hemorrhage in the treatment group (abbreviated as treatment group). Both are lower than the model group. Conclusions The activity of p38MAPK in the brain of rats with intracerebral hemorrhage is enhanced. Nao-yi’an can inhibit the activation of p38MAPK signal transduction pathway induced by cerebral hemorrhage.