摘要
目的研究大鼠实验性脑出血后脑组织TLR2、NF-B/p65及caspase-3在各时间点表达的变化规律,并初步探讨实验性脑出血后三者的动态变化与细胞凋亡的关系,从而探讨TLR2信号通路在实验性脑出血后继发损伤(主要指凋亡)中的作用。方法将大鼠随机分为脑出血组、假手术组和正常对照组,应用立体定向技术,将自体不凝血注入大鼠尾状核制备脑出血模型,分别在不同时间点断头取脑,连续冠状切片作TUNEL染色和免疫组化染色。结果 TLR2、NF-B/p65及caspase-3均在实验性脑出血后6h开始增多,1d其表达继续上升,3d达高峰,此后开始下降,持续到7d仍高于对照组(P<0.05),并且与TUNEL阳性细胞的表达变化趋势相一致。结论 TLR2介导的NF-κB信号途径可能参与实验性脑岀血后的炎症反应,并可能通过caspase-3介导神经元损伤和凋亡。
Objective To study the dynamic change of the expression of TLR2, NF-B/p65 and caspase-3 in rat brain after experimental intracerebral hemorrhage （ICH）,investigate the relationship between the three proteins and apoptosis and discuss the role of TLR2 pathway in secondary lesion after experimental ICH.Methods The rats were randomly divided into ICH group, sham group and control group.ICH rat models were prepared with stereotaxic infusion of autologous blood into caudate nucleus.The brains of rats were removed at different times and successive coronal slices were made and then stained （TUNEL and immunohistochemistry staining）.Results TLR2,NF-B/p65 and caspase-3 all began to increase at 6h after ICH, continued to increase on 1d, reached peak on 3d and then began to decrease, but was still higher than control on 7d （P0.05）, which changed as the apoptosis did.Conclusion NF-κB pathway mediated by TLR2 may be involved in inflammation after experimental ICH and may mediate caspase-3 to cause damage and apoptosis of neurons.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2010年第6期484-488,共5页
Journal of Apoplexy and Nervous Diseases
基金
辽宁省自然科学基金项目(20052095)
辽宁省高等学校科学技术研究项目(2008844)
