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目的研究类固醇受体辅活化子-1(SRC-1)基因敲除小鼠严重烧伤早期肝脏核因子-κB(NF-κB)表达及核转位的变化。方法以SRC-1基因敲除小鼠为实验组,以野生型小鼠为对照组,以小鼠15%~20%TBSAⅢ度烧伤为实验模型,观察两组在严重烧伤前及烧伤后1、6、12h肝脏总蛋白NF-κB表达及伤后核转位的变化,同时提取致伤前、致伤后1、6h血清标本,观察炎性细胞因子TNF-α、IL-1β、IL-6的变化。结果与野生型小鼠相比,SRC-1基因敲除小鼠严重烧伤后肝脏总蛋白NF-κB水平有所增加,而野生型小鼠有所下降。从核转位的情况来看,SRC-1基因敲除小鼠致伤后NF-κB的入核能力明显强于野生型小鼠,6h差别最大。两组致伤后炎性细胞因子TNF-α、IL-1β、IL-6均升高,但SRC-1基因敲除小鼠升高更为显著。结论SRC-1蛋白对严重烧伤具应激性保护作用,缺失SRC-1蛋白使NF-κB功能增强更显著,致炎性细胞因子TNF-α、IL-1β、IL-6更大量产生,使整体伤情征象更重。
Objective To investigate the expression of nuclear factor-κB (NF-κB) and nuclear translocation in the early stage of severe burn in steroid receptor co-activator-1 (SRC-1) knockout mice. Methods SRC-1 knockout mice were used as experimental group, wild type mice as control group, 15% -20% TBSA Ⅲ degree burn mice as experimental model, The expression of NF-κB and the nuclear translocation after 6 and 12 h of liver injury were detected. Serum samples were collected before wounding and at 1,6 h after injury. The levels of inflammatory cytokines TNF-α, IL-1β and IL-6 The change. Results Compared with the wild-type mice, the levels of NF-κB in the liver were significantly increased in the SRC-1 knockout mice and the levels in the wild-type mice were decreased. From the nuclear translocation situation, SRC-1 knockout mice NF-κB induced nuclear injury was significantly stronger than wild-type mice, 6h the difference between the maximum. The inflammatory cytokines TNF-α, IL-1β and IL-6 were increased in both groups, but the SRC-1 knockout mice increased more significantly. CONCLUSIONS: SRC-1 protein has a protective effect on severe burn injury. The lack of SRC-1 protein enhances the function of NF-κB more significantly and produces a greater amount of inflammatory cytokines TNF-α, IL-1β and IL-6 The overall injury signs heavier.