摘要
【目的】观察川芎嗪对缺氧大鼠海马神经元凋亡及bcl-2、p53基因表达的影响,探讨脑缺血后神经元损伤途径以及川芎嗪的保护作用机制。【方法】采用大鼠海马神经元体外原代培养法复制缺氧模型。海马神经元培养第14天,分为模型对照组及川芎嗪高、中、低剂量组(剂量分别为800、200、50μg/mL),分别持续缺氧1.5 h。采用流式细胞仪定量分析神经细胞凋亡率,原位杂交法检测海马神经元bcl-2、p53 mRNA的表达。【结果】川芎嗪中剂量组在缺氧1.5 h凋亡率与模型对照组及其他剂量组比较均有显著性差异(P<0.05)。对缺氧1.5 h大鼠海马神经元bcl-2、p53 mRNA原位杂交阳性信号进行分析,川芎嗪中剂量组bcl-2、p53 mRNA的表达与其他各组比较均有显著性差异(P<0.05)。【结论】在无血清培养条件下给予缺氧处理证实了凋亡是脑缺血后神经元损伤途径之一。一定剂量范围的川芎嗪具有抑制神经细胞凋亡的作用,而抑制p53基因的过度表达,上调bcl-2基因表达可能是其作用机制之一。
[ Objective ] To observe the effect of ligustrazine （Lig） on cell apoptosis and expression of bcl-2 and p53 in rats hippocampal neurons after anoxia, and to explore its protective mechanism. [ Methods ] Primary culture technique of rat hippocampal neurons was used to establish the model of anoxia. At the 14^th day of the culturing, the cultured cells were divided into model group, and high-, middle- and low-dosage ligustrazine （800, 200 and 50 μg/mL respectively） groups, which were exposed to anoxia environment for continuous 1.5 hours. Flow cytometer was used for the quantitative analysis of apoptosis rate of neurons, and in-situ hybridization was used to detect the bcl-2 and p53 mRNA expression of hippocampal neurons. [ Results] In middle-dosage ligustrazine group after exposure to anoxia environment for 1.5 hours, the apoptosis rate and the bcl-2 and p53 mRNA expression of hippocampal neurons differed from those in other groups （ P 〈 0.05 ）. [ Conclusion ] The existence of hippocampal neurons apoptosis under the culturing condition of serum free and anoxia illustrates that apoptosis is one of the pathways of neurons impairment after cerebral ischemia. Proper dosage of ligustrazine can suppress neurons apoptosis, and perhaps up-regulation of bcl-2 mRNA expression and inbibition of p53 mRNA expression is one of its nerve protective mechanisms.
出处
《广州中医药大学学报》
CAS
2007年第6期490-493,共4页
Journal of Guangzhou University of Traditional Chinese Medicine
基金
国家中医药管理局资助项目(编号:AKI98031)
