摘要
目的:探讨凋亡在感染性脑损伤的发生发展以及caspase非依赖性途径在感染性脑损伤机制中的作用。方法:SD大鼠160只,随机分为NS组和LPS组各80只,LPS组颈内动脉注射LPS制作感染性脑损伤模型,NS组颈内动脉注射NS,2组均观察注射后6、12、24、48及72h5个时间点,检测各组不同时间点脑组织的EB含量,免疫组化检测脑组织NSE、GFAP蛋白及凋亡诱导因子(AIF)的表达,并应用脱氧核糖核苷酸末端转移酶介导的缺口末端标记法(TUNEL)技术检测细胞凋亡数。结果:LPS组NSE、GFAP、AIF表达及细胞凋亡数均为6h开始增加,12h表达进一步增强,24h达高峰,48-72h时渐减少,但均明显高于NS组。结论:细胞凋亡参与感染性脑损伤细胞发展过程,Caspase非依赖性途径通过AIF的表达发挥重要作用。
Objective： To explore the effect of apoptosis-inducing factor （AIF） and the caspase indeperident pathway in infectious brain injury. Methods： Models of acute infectious brain injury of rats were prepared by injecting LPS via the left internal carotid artery. One hundred and sixty rats were randomly divided into NS and LPS group, At 6 h,12 h,24 h,48 h and 72 h after acute infectious brain injury, ethidium bromide（EB） content was measured by forrnamide-method, the expression of NSE protein, GFAP protein and AIF were studied by immunohistochemistry, and apoptosis was examined by TUNEL technique. Results：The expression of NSE, GFAP, AIF and the number of apoptosis in LPS group was increased at 6 h and reached the peak at 24 h, and then decreased gradually at 48- 72 h, but still significantly higher than in NS group. Conclusion：Apoptosis plays a role in the formation and development of infectious brain injury of rats. Caspase independent pathway was involved in this process through AIF.
出处
《神经损伤与功能重建》
2008年第4期231-234,共4页
Neural Injury and Functional Reconstruction
