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机构地区:[1]金华市中心医院神经内科,浙江金华321000 [2]温州医学院附属第二医院神经内科,浙江温州325000
出 处:《中风与神经疾病杂志》2011年第6期541-543,共3页Journal of Apoplexy and Nervous Diseases
摘 要:目的研究粒细胞集落刺激因子(G-CSF)对脑出血大鼠模型出血灶周脑组织中炎症反应的影响,并初步探讨G-CSF抗炎作用的可能作用机制。方法 36只成年雄性Wistar大鼠随机分成两组:对照组和G-CSF治疗组,每组各18只大鼠。自体血注入法建立大鼠脑出血模型。术后2h和12h,G-CSF治疗组分别给予粒细胞集落刺激因子50μg/kg)皮下注射;对照组注入等量生理盐水。于术后24h、7d、14d每组分别取6只大鼠,处死取脑,免疫组化染色计数TNF-α、IL-1β阳性细胞;Western blot检测NF-κB/IκBα蛋白含量。结果脑出血灶周组织中的IL-1β阳性细胞和TNF-α阳性细胞在出血24h后最多,7d、14d较前下降。G-CSF组与对照组相比,IL-1β和TNF-α阳性细胞数在24h和7d时下降明显,差异显著性(P<0.01),而14d下降不明显;G-CSF组与对照组相比,24h时NF-κB表达减少而IκB表达增加,差异有统计学意义(P<0.05)。结论 G-CSF通过NF-κB途径,减轻血肿周围脑组织中TNF-α、IL-1β的生成,发挥抗炎症作用从而在脑出血后发挥神经保护作用。Objective To study the effects and mechanisms of G-CSF on anti-inflammatory in tissues around the hematoma of rats after intracerebral hemorrhage.Methods 36 male Wistar rats were randomly divided into 2 groups:the control group and G-CSF group,18 rats in each group.Autologous blood was injected into the rats' brain to establish the experimental animal models.2h and 12h after injection,G-CSF group were given granulocyte colony-stimulating factor(50μg/kg) while the control group were given equivalent saline.6 rats from each group were sacrificied on 1d,7d and 14d after injection.TNF alpha and IL-1 beta expression was detected by immunohistochemical method.And the contents of NF-κB and IκB were detected by western blot.Results IL-1β and TNF-α positive cells around the hematoma reached the peak at 24h after bleeding,then decreased on 7d and 14d.IL-1β and TNF-α positive cells were significantly less at 24h and 7d in the G-CSF group than in the control group(P0.01).The content of NF-κB were lower but IκB levels were higher in the G-CSF group than in the control group(P0.05).Conclusion G-CSF could reduce the inflammation by antagonizing NF-κB pathway to exert neuroprotective effects.
关 键 词:脑出血 粒细胞集落刺激因子 肿瘤坏死因子 白细胞介素
分 类 号:R743.34[医药卫生—神经病学与精神病学]
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