| 黄冬冬 刘冬梅 孙汝智 吴晓华 崔福江 刘明清 李清君.大蒜素对全脑缺血再灌注大鼠脑保护机制的研究[J].,2015,15(35):6848-6851 |
| 大蒜素对全脑缺血再灌注大鼠脑保护机制的研究 |
| Cerebral Protection Mechanismof Allicin on Cerebral Ischemia Reperfusionin Rats |
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| DOI： |
| 中文关键词: 全脑缺血再灌注 大蒜素 ICAM-1 炎症反应 |
| 英文关键词: Total brain ischemia Allicin ICAM-1 Inflammatory reaction |
| 基金项目:沧州市科学技术研究与发展指导计划项目（131302111） |
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| 中文摘要: |
| 目的：通过大蒜素预处理，观察全脑缺血再灌注大鼠海马区ICAM-1 的表达，从而探讨大蒜素的脑保护机制。方法：雄性
Wistar 大鼠30 只，随机分为5 组：假手术组、缺血再灌注组、缺血再灌注+ 大蒜素10、20、30 mg/kg 组。采用四血管闭塞法制备大
鼠全脑缺血再灌注模型，于再灌注24 h 取出海马，硫堇染色观察海马组织的形态学改变，免疫组织化学染色测定海马CA1 区
ICAM-1 免疫反应阳性细胞面积和积分光密度值。结果：通过给予大鼠全脑缺血8 min 再灌注24 h处理，海马CA1 区组织形态学
改变显著，神经元密度明显降低；ICAM-1的表达显著增加。静脉给予大蒜素可使缺血再灌注海马组织形态学改变明显改善，存活
神经元数目增加，ICAM-1 表达显著较少。结论：大蒜素可以通过减少ICAM-1 的表达抑制全脑缺血再灌注后的炎症损失从而发
挥脑保护作用。 |
| 英文摘要: |
| Objective:Through the observation of allicin preconditioning, observing the expression on cerebral ischemia-reperfusion
in ICAM-1 area of hippocampus in rats, to study the mechanismof cerebral protection of allicin.Methods:30 male Wistar rats, were
randomly divided into 5 groups: sham operation group, ischemia reperfusion group, ischemia reperfusion+garlicin 10, 20, 30 mg/kg
group. By four vessel occlusion methods for the preparation of rats with global cerebral ischemia reperfusion model in 24 h after reperfusion,
removing the hippocampus, thionine staining to observe morphological changes of hippocampal tissue, Immunohistochemical staining
was measured hippocampal CA1 area of ICAM-1 immunoreactivity and integral optical density of positive cells.Results:By giving
complete cerebral ischemia 8min reperfusion in rats 24h, morphology of hippocampal CA1 area organization changed significantly, neuron
density decreased significantly; the expression of ICAM-1 increased significantly. Intravenous administration of allicin can make ischemia
and morphology of hippocampal tissue perfusion changes significantly improved, the number of survival neurons increased, the
expression of ICAM-1 was significantly less.Conclusion:Allicin can reduce ICAM-1 by inhibiting the expression and play a role in brain
protection after cerebral ischemia - reperfusion inflammation loss. |
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