粒细胞集落刺激因子对大鼠急性缺血性脑梗死的神经保护作用

Neuro-protective effects of rhG-CSF on focal cerebral infarction in rats

目的初步探讨人重组粒细胞集落刺激因子(rhG-CSF)对大鼠急性缺血性脑梗死的神经保护作用及机制。方法健康雄性Wistar大鼠随机分为缺血组、药物组,同时设立假手术组,神经功能评分后断头取脑,观察病理改变及梗死体积变化,免疫组织化学法检测脑内S-100β表达。结果①缺血组显示神经元细胞核崩解,胞质水肿,胶质细胞增生等;药物组观察到神经细胞及胶质细胞增生明显;4d时血管周围淋巴细胞浸润,形成淋巴套;7d血管密度增高;10d淋巴细胞减少;②药物组神经功能缺损症状较缺血组少(P<0.05),假手术组未见神经功能缺损;③假手术组可见少量S-100β表达,缺血组和药物组明显增加,缺血组增加更为明显。结论G-CSF可减轻大鼠脑梗死体积,减少神经组织损害,发挥脑保护作用。

Objective To explore whether recombinant human granulocyte colony-stimulating factor （rhG-CSF） can be used to protect ischemic cerebral infarction in rats and the mechanism for treatment. Methods Healthy male Wistar rats were randomly assigned to the ischemia group, treatment group and sham operation group. The animals evaluated by neurological deficit score were killed and removed of brains which were sliced to identify the changes in pathology and the size of infarction. Immunohistological staining was used to detect S-100β expression in the brain tissue. Results ①Nuclear disruption and cytoplasm edema neurocytes as well as hyperplasia of gliocytes were seen in the ischemia group, while massive hyperplasia of both neurocytes and gliocytes were found in the treatment group. On day 4 after injury, infiltration of lymphocytes was active around blood vessels with formation of lymphatic sheaths, but subsided on day 10. Furthermore, the density of blood vessels began to increase at 7 d after injury. ②The neurological deficit symptoms appeared more significant in ischemia group than in drug group （P〈0.05）, whereas the sham operation group presented with no symptoms of neurological deficits. ③The expression of S-100β did not increase significantly in the sham operation group. While obvious up-regulation of S-100β was detected in both treatment group and ischemia group, the level of expression was lower in the treatment group than in the ischemia group at every time point. Conclusion G-CSF may reduce the size of infarction and attenuate nerve injury to achieve a significant neuro-protective effect after stroke.