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目的:观察脑出血(ICH)后粒细胞集落刺激因子(G-CSF)对炎症因子NF-κB和IL-1β表达的影响,探讨G-CSF对ICH后脑组织继发性炎症损伤的保护机制。方法:将健康成年雄性SD大鼠随机分为假手术组、模型组和G-CSF治疗组(治疗组),每组10只。采用注入自体血方法复制脑出血模型。Garcia等方法进行神经功能障碍评分;干湿重法检测脑组织含水量;免疫组织化学SP法检测NF-κB和IL-1β蛋白的表达;免疫印迹检测NF-κB和IL-1β蛋白的表达水平。结果:与假手术组比较,大鼠脑出血后神经功能障碍评分降低,NF-κB和IL-1β阳性表达和脑含水量明显增多(P<0.05);G-CSF干预后NF-κB和IL-1β阳性表达和脑含水量显著下调(P<0.05),与脑神经功能障碍评分上调相一致。结论:粒细胞集落刺激因子可能通过抑制炎症因子NF-κB和IL-1β的表达,减轻脑出血血肿周围组织的炎性反应,改善神经功能损伤,起到神经保护作用。
Objective: To observe the effect of granulocyte-colony stimulating factor (G-CSF) on the expression of inflammatory factors NF-κB and IL-1β after intracerebral hemorrhage (ICH), and to explore the protective mechanism of G-CSF on secondary inflammatory injury induced by intracerebral hemorrhage in ICH. Methods: Healthy adult male Sprague-Dawley rats were randomly divided into sham operation group, model group and G-CSF treatment group (treatment group), with 10 rats in each group. Intracerebral hemorrhage was made by injection of autologous blood. Garcia and other methods for neurological dysfunction score; wet and dry method to detect brain water content; immunohistochemical SP method to detect the expression of NF-κB and IL-1β protein; Western blot detection of NF-κB and IL-1β protein expression . Results: Compared with the sham group, the scores of neurological dysfunction decreased, the expression of NF-κB and IL-1β and brain water content increased significantly after ICH (P <0.05), while the levels of NF-κB and IL -1β expression and brain water content were significantly down-regulated (P <0.05), which was consistent with the upregulation of neurological dysfunction score. Conclusion: Granulocyte-colony stimulating factor may play a neuroprotective role by inhibiting the expression of inflammatory factors NF-κB and IL-1β, relieving the inflammatory reaction around the hematoma of intracerebral hemorrhage, and improving the neurological function.