To investigate the action mechanism of cortex NF-kB activation and the miR-146a transcription regulation mode in the inflammatory reaction process after mild traumatic brain injury(TBI) in rats. Methods The 60 healthy male SD rats were selected and randomly divided into the control group(n=10) and the mild traumatic brain injury(TBI) group(n = 50). The mild TBI group was sub divided into five subgroups according to different time points: 1,3 ,6 ,12 ,24 h after brain injury. 10% chlo-ralic hydrasCO. 3 mL/100 g) was intraperitoneally injected. The Marmarou s method was adopted to induce rat mild TBI by dropping the copper rod, weighed 4 50 g and 18 mm in diameter,from 1 M height. The control group was only given corresponding anesthesia, scalp incision and suture. The changes of cortex NF-kB and miR-14 6a were compared between the two groups using real-time quantitative PCR and Western blot methods. Results At 1,3,6,12,24 h after TBI,miR-146a expression was significantly up-regulated by 1. 21 + 0. 15,1. 73 + 0. 29,2. 36 + 0. 24,3. 60 + 0. 37,1. 97 + 0. 26 fold compared with the control group, which reached to the expression peak at 6 - 12 h after TBI, its transcription level was down-regulated at 24 h. The activation and nuclear translocation of NF-kB was basically similar to the expression pattern of miR-146a. Conclusion The expression of miR-146a in mild TBI is significantly up-regulated, NF-kB enhances the transcription level of miR-146a by upstream control components. NF-kB-miR-14 6a pathway may play an important role in promoting the inflammatory reaction process after TBI.%目的 探讨轻型脑创伤后大鼠皮质区核因子κB(NF-κB)活化及其microRNA(miRNA)-146a转录调控模式在炎症反应过程中的作用机制.方法 选择健康雄性SD大鼠60只,随机分为对照组(n=10)、轻型脑创伤组(n=50).轻型脑创伤组分为创伤后1、3、6、12和24 h 5个时间点,10%水合氯醛(0.3 mL/100 g)腹腔内注射,采用Marmarou′s方法,用质量450 g、直径18 mm的铜棒由1.0 m高度自由落下,造成大鼠轻型脑创伤.对照组仅给予相应麻醉、头皮切开及缝合处理.采用实时定量PCR及Western blot方法比较两组大鼠脑皮质NF-κB和miR-146a表达水平的变化.结果 脑创伤1、3、6、12、24 h后miR-146a表达水平显著上调,分别为对照组的1.21±0.15,1.73±0.29,2.36±0.24,3.60±0.37,1.97±0.26倍.伤后6～12 h为表达高峰,24 h其转录水平有所下调.NF-κB的活化与核转位与miR-146a的表达模式基本一致.结论 轻型脑创伤后皮质区miR-146a表达水平显著上调,NF-κB通过miR-146a上游调控元件增强了miR-146a的转录水平,NF-κB-miR-146a途径可能在促进脑创伤后炎症反应过程中发挥重要作用.
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