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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。
Objective To observe the effects of rhG-CSF and citicoline on the expression of Bcl-2 and Bax after focal cerebral ischemia / reperfusion injury in rats, and to investigate the effect of rhG-CSF and citicoline on the brain Cerebral protection after focal cerebral ischemia-reperfusion injury and its mechanism of cerebral protection. Methods 72 male Wistar rats (230 ± 10g) were randomly divided into 4 groups: model group (n = 18), rhG-CSF administration group (n = 18) and citicoline administration group (n = 18), rhG-CSF plus citicoline (n = 18). Each group is divided into 6h, 24h, 72h three subgroups. The rat middle cerebral artery occlusion (MCAO) model of ischemia-reperfusion was established by thread occlusion. Neuronal apoptosis was detected by TUNEL method. Morphological and pathological changes of brain were observed by HE staining. Immunohistochemistry Mean optical density values of Bax and Bcl-2 at different time points after cerebral ischemia reperfusion in rats. Results Compared with the operation group, the administration group could improve the symptoms of nerve injury, alleviate the pathological injury of cerebral ischemia-reperfusion injury, reduce the expression of apoptosis, increase Bcl-2 and decrease the expression of Bax. Compared with rhG-CSF group and citicoline group, Bcl-2 and Bax decreased at each time point in combination therapy group, the difference was statistically significant. Conclusions rhG-CSF and citicoline can ameliorate the apoptosis of the cells after cerebral infarction. The mechanism may be related to the up-regulation of Bcl-2 and the decrease of Bax expression. Combination therapy is better than single therapy.