摘要
目的探讨小檗碱处理对大鼠脑缺血后单核细胞趋化蛋白-1(MCP-1)表达的影响及小檗碱对脑缺血的神经保护作用。方法建立大鼠短暂性全脑缺血模型,采用尼氏体亚甲蓝染色观察脑缺血后大鼠脑海马CA1区神经元存活情况;采用免疫荧光染色方法检测脑缺血后大鼠缺血脑组织中MCP-1的表达情况。结果(1)与假手术组比较,脑缺血组大鼠脑海马CA1区神经元明显缺失,而小檗碱处理组大鼠脑海马CA1区神经元存活数明显多于缺血对照组;(2)与假手术组比较,脑缺血组大鼠脑缺血区MCP-1表达显著增多,而小檗碱处理显著降低了大鼠脑缺血区MCP-1的阳性表达。结论脑缺血引起MCP-1表达上调,提示MCP-1可能参与脑缺血损伤。小檗碱可抑制缺血脑组织MCP-1的表达,推测其可能经此途径减轻脑缺血的炎症反应而发挥一定的神经保护作用。
Objective To investigate the neuroprotective mechanism of berberine in the effect on the expression of Monocyte chemoattractant protein-1 （MCP-1） in rats after cerebral ischemia. Methods The model of transient global cerehral isehemia was established by 10 rain of bilateral common carotid artery occlusion and hypotension in rat. The neuronal absence in the CA1 section of the hippocampus was observed by nissel body stain. The immunoreactivity of MCP-1 was evaluated by immuno-fiucrescent staining. Results （1）The hippocampal CA1 neurons in the cerebral ischemic group were significantly absent while compared with the shamoperating group. And the absence of hippocampal CA1 neurons in the berberine group was more alleviative than ischemic contral group （P〈0. 01 ）. （2）The positive MCP-1 immunostain cells were observed in the ischemic brain in both cerebral ischemic group and berberine groups, but the quantity of positive MCP-1 cells in berberine group was significantly lower than that in the ischemic contral group. Conclusions It is suggested that up regulation of MCP-1 may be a key event in the neuronal injury induced by cerebral ischemia. And it is indicated that the berberine can inhibit the expression of MCP-1. So the alleviation of inflammation is assumed to be a neuroprotective mechanism of berberine in cerebral ischemia.
出处
《卒中与神经疾病》
2008年第6期323-326,共4页
Stroke and Nervous Diseases
基金
教育部博士点基金(0040533053)
2006年福建省青年科技创新人才基金(2006F3047)
关键词
脑缺血
单核细胞趋化蛋白-1
小檗碱
大鼠
Cerebral isehemia Monoeyte Chemoattraetant Protein-1 Berberine Rat
