ERK通路参与蛇毒型神经生长因子诱导的中枢神经保护作用 |
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引用本文: | 石胜良,陈仕检,梁森,李鑫,毕桂南,刘唐威. ERK通路参与蛇毒型神经生长因子诱导的中枢神经保护作用[J]. 神经疾病与精神卫生, 2010, 10(5): 458-461. DOI: 10.3969/j.issn.1009-6574.2010.05.008 |
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作者姓名: | 石胜良 陈仕检 梁森 李鑫 毕桂南 刘唐威 |
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作者单位: | 广西医科大学第一附属医院神经内科,530021 |
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基金项目: | 桂科自0728133,博士后流动站基金 20702011046 |
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摘 要: | 目的观察经侧脑室给予蛇毒型神经生长因子(vNGF)对脑缺血再灌注损伤后细胞外信号调节激酶(extracellular signal—regulated kinase,ERK)表达的影响,探讨外源性vNGF通过影响ERK的表达减轻神经元损伤的可能机理。方法取健康清洁级雄性Wistar大鼠,按随机分组原则分为2d组(n=30)、7d组(n=30)、14d组(n=30)。每个时间点再分为五个亚组vNGF25U、vNGF50U、vNGF100U、生理盐水对照组、以及假手术组,每个亚组6只大鼠。生理盐水对照组和vNGF各亚组大鼠采用大脑中动脉线栓法建立局灶性脑缺血-再灌注损伤模型,术后各时间点vNGF亚组采用改良的侧脑室置管术法给予相应剂量蛇毒型神经生长因子,生理盐水对照组给予等渗盐水。采用免疫组织化学法测定术后第2d、第7d以及第14d缺血皮质周围和海马CA3/DG区ERK阳性细胞数。结果(1)与对照组相比,经侧脑室给予蛇毒型神经生长因子各组大鼠神经功能明显改善,显示了外源性补充蛇毒型神经生长因子的明显正性干预作用。(2)ERK免疫组织化学结果显示:经侧脑室给予vNGF各亚组ERK阳性细胞在缺血皮质周围和海马CA3/DG区第2d表达为高峰,第7d明显下降,第14d恢复基线水平。与相应时间点对照组相比,呈明显下降趋势。结论局灶性脑缺血再灌注后磷酸化ERK表达增加,NGF可能通过抑制ERK途径而发挥神经保护作用。
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关 键 词: | 卒中 脑缺血再灌注 神经保护 蛇毒型神经生长因子 ERK |
Erk pathway involved in NGF-induced pprotective effect of the central nervous system |
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Affiliation: | SHI Sheng-liang CHEN Shi-jian, LIANG Sen, et al.( Neurology Department of The First Affiliated Hospital Guangxi Medical University, Nanning 530021 ,China) |
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Abstract: | Objective To investigate the effect of intracereb --roventricular administration of vevom nerve growth factor on the effect s of phosphorylated extraeellular signal--regulated kinase in rats with cerebral ischemical reperfusion injury. Methods Wistar rats were randomly divided into three groups: 2 days group, 7 days group and 14 days group ( n =30 in each group) ,then each group randomly assigned to vNGF 25U , vNGF 50U , vNGF 100U , sham--operation, and ischemia/reperfusion control subgroups ( n = 6 in each subgroup) . Then , a focal cerebral ischemia / reperfusion model was induced by middle cerebral artery intraluminal suture occlusion (MCAO) method in the I/R control and vNGF subgroups. Normal saline or Different concentrations vNGF was administered via intracerebroven- tricular to the I/R control or vNGF subgroups rats per day according to the corresponding time points. The numbers of positive cells of ERK+ cells in the Peri--ischemic cortex and Hippoeampus CA3/DG were assessed by immunohistochemical method in the corresponding time points. Results As compared with control subgroups, snake venom nerve growth factor subgroups which was administered via intrace- rebroventricular, the neurological function began to recover in the first two days. which showed its positive intervention effects markedly. The results of ERK immuno-- histochemistry showed that., the num- bers of ERK positive cells in Peri-ischemic cortex and Hippocampus CA3/DG of snake venom nerve growth factor subgroups reach the peak at 2 days after the procedures, began to decline at 7 days, then restored baseline levels at 14 days. As compared with the I/R control subgroups, snake venom nerve growth factor subgroups showed a clear downward trend. Conclusions Focal cerebral ischemia-- reperfusion injury can induces the expression of phosphorylated ERK, NGF may play a neuroprotective effect via inhibit ERK signal transduction pathways. |
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Keywords: | ERK |
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