rhG-CSF联合胞磷胆碱处理对大鼠脑缺血再灌注后Bcl-2,Bax的影响

目的观察rhG-CSF、胞磷胆碱处理分别对大鼠大脑局灶性脑缺血再灌注损伤后Bcl-2和Bax表达规律的影响,明确rhG-CSF、胞磷胆碱对大鼠大脑局灶性脑缺血再灌注损伤后的脑保护作用,并探讨其脑保护作用的机制。方法 72只成年雄性wistar大鼠(230±10g),随机分为4组,模型组(n=18)、rhG-CSF给药组(n=18)、胞磷胆碱给药组(n=18)、rhG-CSF联合胞磷胆碱给药组(n=18)。每组又分为6h、24h、72h三个亚组。采用线栓法制备大鼠大脑中动脉局灶缺血再灌注模型,采用DNA原位末端缺口标记法(TUNEL)检测神经元凋亡;HE染色观察脑组织形态病理学变化;免疫组化法测定大鼠脑缺血再灌注不同时间Bax和Bcl-2的平均光密度值。结果与手术组相比,给药组均能改善脑缺血大鼠神经损伤症状,减轻脑缺血再灌注的病理损伤,减少凋亡表达,增加Bcl-2,减少Bax的表达。且联合用药组与rhG-CSF组、胞磷胆碱组比较,各时间点Bcl-2的增加与Bax的减少,差异有统计学意义。结论 rhG-CSF、胞磷胆碱能减轻脑梗死后细胞凋亡,其机制可能与上调Bcl-2,降低Bax表达有关,联合用药治疗效果优于单独用药。

The expression of Bcl-2 and Bax on rat brain after focal cerebral ischemia-reperfusion injury by treating with rhG-CSF and citicoline

Objective To observe the expression of Bcl-2 and Bax on rat brain after focal cerebral ischemia-reperfusion injury by treating with rhG-CSF and citicoline respectively,clear the cerebral protective effect of rhG-CSF and citicoline on rat brain after focal cerebral ischemia-reperfusion injury and explore its mechanism of cerebral protective effect.Methods 72 adult male Wistar rats(230±10g),were randomly divided into 4 groups,the model group(n=18),rhG-CSF group(n=18),citicoline group(n=18),rhG-CSF combined with citicoline group(n=18).Each group was subdivided into 6h,24h,72h three subgroups.Prepare the rats model of focal ischemia-reperfusion by lining the middle cerebral artery,detection of neuronal apoptosis with TdT-Mediated dUTP Nick-End Labeling(TUNEL),observe the morphology and pathological changes of brain tissue with HE staining and determine the average optical density value of Bax and Bcl-2 at different times in rats brain after focal cerebral ischemia-reperfusion using immunohistochemical method.Results Compared with the model group,medication group can improve symptoms of nerve injury in rats with cerebral ischemia,release the pathological damage in rats with cerebral ischemia-reperfusion,reduce the expression of apoptosis,increase the expression of Bcl-2,and reduce the expression of Bax.And compared with the rhG-CSF group and citicoline group,the Bcl-2 were increased and Bax were reduced at each time point in the combined group.The difference was statistically significant.Conclusion The apoptosis of brain cell after cerebral infarction can be reduced with the rhG-CSF and citicoline treatment.The mechanism may be related to increased the expression of Bcl-2 and reduced the expression of Bax.The combination therapy is better than medication alone.