摘要
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-kB（NF-kB）表达及核转位的变化。方法以SRC1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-kB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-a、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-kB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-kB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-a、IL-1β、IL-6均升高，但SRC1基因敲除小鼠升高更为显著。结论SRC1蛋白对严重烧伤具应激性保护作用，缺失SRC1蛋白使NF—kB功能增强更显著，致炎性细胞因子TNF-a、IL-1β、IL-6更大量产生，使整体伤情征象更重。
Objective To study the effect of SRC 1 deficiency on the expression and nuclear translocation of NF-kB in mice after burn injury . Methods SRC-1 knock out mice and wild mice were divided into expriment group and control group according to their genotype. The difference of expression of NF-kB in total hepatic protein extract was investigated before burn, lh after burn, 6h after burn and 12h after burn. The difference of translocation of NF-kB into nuclear was also measured in hepatic nuclear eatract. At the same time, the serum samples were acquired before burn, l h after burn as well as 6h after burn. The levels of cytokines TNF α,IL- 1β as well as IL-6 in serum samples were measured. Results The level of NF-kB expression in total hepatic protein extract increased in SRC-1 knock-out mice,and declined in wild mice after burn injury . the nuclear translocation of NF-kB were all increased in two groups after burn,but the quantity of NF-kB in nuclear extract was more higher in SRC-1 knock out mice than that in wild mice. The level of serum TNF-α,IL-1β as well as IL-6 all increased in two groups. But much higher level of proinflammtory cytokine were observered in SRC-1 knock-out mice as compared with wild mice. Conelusion SRC-1 protein can protect body from burn stress,The abscent of SRC 1 enhanced the function of NF-kB after burn injury. As a result,more pro-inflammatory cytokines were scrected during burn injury and more severe symptoms were observed in SRC-1 knock-out mice after burn injury.
出处
《重庆医学》
CAS
CSCD
2008年第17期1897-1899,共3页
Chongqing medicine
基金
国家重点基础研究发展规划资助项目("973"项目)
No.G1999054201
海外青年学者合作研究基金资助项目(30328025)
