脑脊髓损伤大鼠局部Th1/Th2细胞相关因子的表达及意义  

Expressions and implications of Th1/Th2 cytokines in injured rat brain and spinal cord

作　　者：许燕[1] 李雅贞[1] 张志坚[1] 孙湘兰[2] 龚爱华[1] 丁红群[1] 卢俊浩[1] 袁泉[1] 许化溪[1] 

机构地区：[1]江苏大学基础医学与医学技术学院 [2]江苏大学科学研究院,江苏镇江212013

出　　处：《细胞与分子免疫学杂志》2013年第9期919-922,926,共5页Chinese Journal of Cellular and Molecular Immunology

基　　金：国家自然科学基金(31270947;31170849)

摘　　要：目的分析大鼠急性脑脊髓性损伤后脑脊髓中Th1和Th2细胞相关因子的表达水平,探讨其在持续性二次损伤中可能的作用。方法制备SD大鼠急性脑脊髓性损伤模型,随机分为损伤组和脂多糖(LPS)处理组,各组又分别对脑和脊髓进行实验处理。用荧光定量PCR分别检测不同组别大鼠脑脊髓中Th1和Th2细胞相关因子,并进行相关性分析。结果与对照组相比,损伤和LPS处理的脑组织Th1细胞相关的细胞因子IFN-γ表达明显增高(P<0.05),而T-bet的表达并无明显改变;在损伤和LPS处理的脊髓中,IFN-γ和转录因子T-bet、HLX的表达均显著升高(P<0.05)。无论是脊髓损伤组还是LPS处理组,细胞因子IL-4和转录因子GATA3均与对照组无异,呈低表达状态。结论脑脊髓损伤后呈现不同程度的Th1细胞相关因子上调,尤以可溶性的细胞因子IFN-γ为显著,脊髓损伤时出现T-bet与HLX表达上调。Objective To detect the expression levels of Thl/Th2 cytokines in the acute injury of brain and spinal cord in rats, and explore their possible roles in sustained secondary injury. Methods The acute brain and spinal cord injury models in SD rats were established and randomly divided into injury group and lipopolysaccharide （LPS） treatment group, and each group was experimentally intervened in the brain and spinal cord, respectively. The mRNA of Thl/Th2 cytokines were deter- mined by quantitative real-time PCR （qRT-PCR） and analyzed in correlation. Results Compared with the control group, in injury and LPS treatment groups, the level of IFN-y （as a Thl associated cytokine） in brain tissue significantly increased （P 〈0.05）, while the expression of T-bet did not significantly change; in spinal cord, the levels of IFN-γ and transcription factors T-bet, HLX rose significantly （P 〈 0.05 ）. The cytokine IL-4 and transcription factor GATA3 in both injury and LPS treatment groups were as low as those in the control group. Conclusion The expressions of Th1 associated cytokines, especially soluble cytokine IFN-γ, increased in brain and spinal cord injury. The up-regulated T-bet and HLX expressions were only observed in spinal injury.

关 键 词：脑脊髓损伤 TH1 TH2 细胞因子 转录因子 基因表达 

分 类 号：R392.11[医药卫生—免疫学] R651.15[医药卫生—基础医学]