缺血再灌注损伤大鼠脑组织及外周血炎症细胞因子分析

Analysis of inflammatory cytokines in brain tissue and peripheral blood of ischemia-reperfusion rats

目的探讨大鼠脑缺血再灌注损伤后6 h和24 h时炎症细胞因子在脑组织和血清中的变化,初步分析炎症因子在早期缺血再灌注损伤中的作用。方法构建大鼠脑中动脉闭塞模型,运用流式高通量多因子检测方法测定各因子变化。结果缺血再灌注6 h,脑组织中促炎细胞因子IL-6、IFN-γ、MIP-2、TNF-α、IL-1β均升高;抗炎细胞因子IL-10升高,差异均有统计学意义(P<0.05)。缺血再灌注24 h,促炎细胞因子IL-6、MIP-2、IL-1β升高。缺血再灌注24 h较6 h促炎细胞因子IL-6、IL-1β升高,IFN-γ、MIP-2降低,差异均有统计学意义(P<0.05)。血清中,缺血再灌注6 h和24 h促炎细胞因子IL-6、IFN-γ、MIP-2、TNF-α、IL-1β均升高。缺血再灌注24 h,抗炎细胞因子IL-10、IL-13升高。缺血再灌注24 h较6 h促炎细胞因子IL-6、MIP-2、TNF-α、IL-1β升高,IFN-γ降低;抗炎细胞因子IL-13持续升高,差异均有统计学意义(P<0.05)。结论血中炎症因子的变化可作为脑缺血再灌注的血清标志物。

Objective To investigate the changes of inflammatory cytokines in brain tissue and serum at 6 h and 24 h respectively after cerebral ischemia-reperfusion(I/R)injury in rats.To conduct a preliminary analysis of how inflammatory cytokines act in early ischemia-reperfusion injury.Methods To set up the rat middle cerebral artery occlusion(MCAO)model,and the changes of each factor were measured by multiple immunoassays for flow test.Results In I/R 6 h,the levels of pro-inflammatory cytokines including IL-6,IFN-γ,MIP-2,TNF-α and IL-1β increased in brain tissue,so does anti-inflammatory cytokines IL-10,with the differences statistically significant(P<0.05).In I/R 24 h,the pro-inflammatory cytokines including IL-6,MIP-2,IL-1β increased.Compared with I/R at 6 h,pro-inflammatory cytokines IL-6,IL-1β increased whereas IFN-γ,MIP-2 decreased in I/R 24 h,with the differences statistically significant(P<0.05).In serum,the levels of pro-inflammatory cytokines including IL-6,IFN-γ,MIP-2,TNF-α and IL-1β increased in both I/R 6 h and 24 h.In the I/R 24 h,anti-inflammatory cytokines IL-10 and IL-13 increased.Compared with I/R 6 h,pro-inflammatory cytokines IL-6,MIP-2,TNF-α,IL-1β increased and IFN-γ decreased whereas anti-inflammatory IL-13 increased continuously in I/R 24 h,with the differences statistically significant(P<0.05).Conclusion The changes of inflammatory cytokines in peripheral blood can be used as serum markers of cerebral ischemia-reperfusion.