脑溢安颗粒对脑出血大鼠脑内细胞间粘附分子-1表达和中性白细胞浸润及神经细胞损伤的影响

Effect of Naoyi’an Granule on Intercellular Adhesion Molecule-1 Expression, Neutrophil Infiltration and Neu-ronal Injury in Rats’s Brain with Cerebral Hemorrhage

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中文关键词: 脑溢安颗粒脑出血细胞间粘附分子-1 中性白细胞神经细胞

英文关键词:Naoyi’an Granule intracerebral hemorrhage intercellular adhesion molecule-1 neutrophil neuron

基金项目:国家科技部新药研究基金(No.96-901-05-225);国家中医药管理局科研基金(No.2000-J-B-03)

作者	单位
何纲	深圳市人民医院
金益强	中南大学湘雅医院中西医结合研究所
黎杏群	中南大学湘雅医院中西医结合研究所

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中文摘要:

目的:探讨脑溢安颗粒(简称脑溢安)对脑出血后脑内炎症损伤的影响。方法:采用胶原酶诱导的大鼠脑出血模型,分组处理,并用逆转录-聚合酶链式反应(RT-PCR)、免疫组织化学和组织学方法检测术后不同时间各组出血侧脑内细胞间粘附分子-1(ICAM-1)mRNA表达、脑微血管内皮细胞上ICAM-1蛋白表达、中性白细胞浸润和神经细胞损伤情况。结果:正常组和假手术组大鼠术侧脑内检测到低水平ICAM-1mRNA表达及少量ICAM-1阳性微血管,未见中性白细胞浸润和受损神经细胞。模型组大鼠出血侧脑内ICAM-1mRNA表达在术后4h显著升高,24h达到高峰,96h仍保持较高水平,168h恢复正常水平;ICAM-1阳性微血管数在术后4h显著增多,48h达到峰值,持续至168h;中性白细胞浸润和神经细胞损伤在术后4h也明显增多,均于48h达到高峰,之后逐渐下降。脑溢安组大鼠出血侧脑内ICAM-1mRNA表达水平和I-CAM-1阳性微血管数显著降低,中性白细胞浸润,神经细胞损伤明显减轻。结论:脑溢安具有抗脑出血后脑内炎症损伤作用,其作用机制可能与抑制ICAM-1介导的中性白细胞浸润有关。

英文摘要:

Objective:To explore the mechanism of Naoyi’an Granule (NYAG) in alleviating inflammatory injury of brain after intracerebral hemorrhage (ICH). Methods: The intercellular adhesion molecule-1 (ICAM-1) mRNA expression, ICAM-1 protein expression in cerebral microvessel endothelium, neutrophil infiltration and neuronal injury in hemorrhagic hemisphere in collagenase induced ICH model rats were determined at various times after modeling by using reverse transcription and polymerase chain reaction (RT-PCR), immunohistochemistry and histological examination. Results: A low level of ICAM-1 mRNA expression and few ICAM-1 positive microves-sels were detected in the hemisphere of rats in the sham operation group and the normal control group, no neutrophil infiltration and neuronal injury was found. In the model group, levels of ICAM-1 mRNA expression in brain significantly increased 4 hrs after modeling, it reached the peak at 24 hrs, remained in a high level at 96 hrs and recovered to normal at 168 hrs after operation; ICAM-1 positive microvessles increased remarkably at 4 hrs, reached the peak at 48 hrs and sustained to 168 hrs after modeling; the neutrophil infiltration and neuronal injury also showed obvious increase at 4 hrs, reached peak at 48 hrs after modeling, and declined thereafter. In the hemorrhagic hemisphere of NYAG treated group, the above-mentioned indexes were significantly lower than those in the model group. Conclusion: NYAG has protective effects against inflammatory injury in the brain after ICH, the mechanism of the effects may be associated with the inhibition of ICAM-1 mediated neutrophil infiltration.

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