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复方丹参对大鼠脑缺血再灌注后大脑皮层神经细胞凋亡和Bcl-2 mRNA表达的影响 被引量:7

EFFECT OF SALVIA MILTEORRHIZA ON NEURONAL APOPTOSIS AND EXPRESSION OF BCL-2 mRNA IN THE CEREBRAL CORTEX AFTER BRAIN ISCHEMIA-REPERFUSION INJURY IN RATS
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摘要 为了探讨中药复方丹参对大鼠局灶性脑缺血再灌注后大脑皮层神经细胞凋亡及Bcl-2mRNA表达的影响和保护作用,本研究采用大脑中动脉内栓线阻断法(MCAO)造成局灶性脑缺血再灌注模型,应用原位末端标记(TUNEL)和原位杂交技术检测大鼠大脑皮层神经细胞凋亡和神经细胞Bcl-2mRNA的表达,并进行图像分析。结果显示:缺血再灌注组凋亡神经细胞主要位于缺血侧大脑皮层缺血边缘区(半暗区);缺血侧大脑皮层缺血边缘区神经细胞Bcl-2mRNA的表达在缺血再灌注2h后升高,随着缺血再灌注时间的延长逐渐增强;复方丹参保护组神经细胞Bcl-2mRNA的表达明显强于缺血再灌组(P<0.01),凋亡神经细胞数明显低于缺血再灌组(P<0.01)。上述结果说明复方丹参可通过上调神经细胞Bcl-2mRNA的表达,抑制神经细胞凋亡,减轻缺血再灌注对大鼠大脑皮层神经细胞的损伤。 To explore the neuronal apoptosis and gene expression of Bcl-2 mRNA in the cerebral cortex after focal brain ischemic reperfusion injury in rat and the protective effect of salvia milteorrhiza(SM), the method of reversible middle cerebral artery occlusion(MCAO) without craniotomy was used to establish model of focal brain ischemic reperfusion injury in rats. The apoptosis of neurons were observed with the terminal deoxynucleotidyl tranferase mediated Dutp-flourescein nik end-labeling (TUNEL) assay and the expression of Bcl-2 mRNA was determined by in situ hybridization and image analysis. The results showed that TUNEL-positive cell were mainly located in ischemic penumbra of the ischemia-reperfusion group, the expression of Bcl-2 mRNA began to increase 2 hours after reperfusion in isehemic penumbra and increase gradually was more obvious following the ischemic reperfusion time-proloned. The expression of Bcl-2 mRNA increased significantly and the number of the neuronal apoptosis dereased obviously in the SM group compared with the ischemia-reperfusion group ( P 〈0.01 ) . The present results indicate that SM can increased the expression of Bcl-2 mRNA, decreased neuronal apoptosis and attenuated the neuronal injury in cerebral cortex caused by ischemic reperfusion.
出处 《神经解剖学杂志》 CAS CSCD 北大核心 2006年第6期661-664,共4页 Chinese Journal of Neuroanatomy
关键词 脑缺血再灌注 凋亡 BCL-2 复方丹参 大脑皮层 大鼠 brain ischemia-reperfusion, bcl-2 mRNA, apoptosis, salvia milteorrhiza, cerebral cortex, rat
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