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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 observe the effects of baicalin on the expression of GABA1 and GABAAR in hemorrhagic rat brain and to explore the protective mechanism of baicalin on brain injury in rats . Methods: The model of intracerebral hemorrhage was induced by collagenase and heparin sodium and randomly divided into sham-operation group, control group and administration group. The rats were given intragastric administration of saline and baicalin respectively. At 12 h, 24 h, 72 h and 7 d after administration, the lesioned lateral brain tissues of rats in each group were removed and frozen sections were made for immunohistochemical staining. The number of GAT-1 and GABAAR positive neurons and the average optical density . Results: After intracerebral hemorrhage, the expression of GAT-1 was up-regulated. The expression of GABAAR was up-regulated 12 h after hemorrhage and began to decline 24 h later. The expression of GAT-1 and GABAAR returned to the level of no significant difference compared with sham-operated group on d 7. Compared with the model group, the number of GAT-1 positive neurons in the administration group decreased significantly, and the number of GABAAR positive neurons increased significantly. The average optical density value positively correlated with the number of positive neurons. CONCLUSION: GAT-1 and GABAAR are involved in the pathophysiological process of neuronal injury after intracerebral hemorrhage. Baicalin may rescue damaged neurons by inhibiting the expression of GAT-1 and increasing the expression of GABAAR.