摘要
目的:观察黄芩苷对出血性大鼠脑内γ氨基丁酸运载蛋白1(GAT-1)和γ氨基丁酸A受体(GABAAR)表达的影响,探讨黄芩苷对大鼠脑损伤的保护机制。方法:采用胶原酶+肝素钠法诱导脑出血模型,并随机分为假手术组、对照组和给药组,分别灌胃给予生理盐水和黄芩苷。给药后12 h,24 h,72 h和7 d取出各组大鼠损伤侧脑组织制作冰冻切片进行免疫组化染色,测定标本中GAT-1和GABAAR阳性神经元的数目以及平均光密度值。结果:脑出血后GAT-1表达上调,GABAAR表达在出血后12 h有所上调,24 h后开始下降,d 7时GAT-1和GABAAR表达恢复到与假手术组比较无显著差异的水平。与模型组比较,给药组GAT-1阳性神经元数目明显下降,GABAAR阳性神经元数目明显增多。平均光密度值与阳性神经元数目变化成正相关。结论:GAT-1和GABAAR参与脑出血后神经元损伤的病理生理过程,黄芩苷可能通过抑制GAT-1的表达、增加GABAAR的表达挽救受损神经元。
Objective： To study the effect of baicalin on the expression of GABA transporter GAT-1 and GABA receptor GABAAR in the brain after experimental intracerebral hemorrhage in rats.Methods： The intracerebral hemorrhage was induced by collagenase＋heparin sodium in rats.The rats were treated with baicalin or saline.The brain tissues were isolated,and frozen sections were prepared for immunohistochemical examination at 12,24,72 h and 7 days after intracerebral hemorrhage.The numbers of GAT-1 and GABAAR positive neurons were calculated and the average optical density was detected.Results： GAT-1 expression was up-regulated after intracerebral hemorrhage.GABAAR expression was up-regulated 12 h,but obviously decreased 24 h after intracerebral hemorrhage.On the 7th day after intracerebral hemorrhage,both expressions were not significantly different from that in sham group.Baicalin obviously decreased the number of GAT-1 positive neurons,and increased GABAAR positive neurons after intracerebral hemorrhage.The average optical density was positively correlated with the number of positive neurons.Conclusion： GAT-1 and GABAAR are involved in neuron injury after intracerebral hemorrhage in rats.Baicalin has a protective effect on brain damage after intracerebral hemorrhage through inhibiting GAT-1 expression and enhancing GABAAR expression.
出处
《中国新药杂志》
CAS
CSCD
北大核心
2010年第11期970-974,共5页
Chinese Journal of New Drugs
基金
安徽省自然科学基金(2004kj025)
安徽大学创新团队计划基金(02203109)
