CAJ | 학술논문

目的：探讨缺氧预处理（ HPC）对颅脑损伤大鼠NF-κB表达及神经元活性的影响。方法将雄性SD大鼠，随机分为对照组（ Con 组）、缺氧预处理组（ HPC 组）、外伤组（ TBI 组）、缺氧预处理＋外伤组（ HPCT组）。采用RT-qPCR、Western blotting测定挫伤区NF-κB mRNA和蛋白表达，免疫组化NeuN染色法测定神经元活性变化情况。结果 TBI组和HPCT组NF-κB mRNA 3 h-1 d明显升高，NF-κB蛋白3 h-7 d明显升高，NeuN 3 h-14 d明显降低（P＜0．05）。 HPCT组NF-κB mRNA 3 h-1 d及NF-κB蛋白3 h-7 d均低于TBI组，而NeuN表达3 h-7 d高于TBI组（P＜0．05）。结论缺氧预处理在一定时间窗内抑制NF-κB表达可能对神经元起保护作用。
목적：탐토결양예처리（ HPC）대로뇌손상대서NF-κB표체급신경원활성적영향。방법장웅성SD대서，수궤분위대조조（ Con 조）、결양예처리조（ HPC 조）、외상조（ TBI 조）、결양예처리＋외상조（ HPCT조）。채용RT-qPCR、Western blotting측정좌상구NF-κB mRNA화단백표체，면역조화NeuN염색법측정신경원활성변화정황。결과 TBI조화HPCT조NF-κB mRNA 3 h-1 d명현승고，NF-κB단백3 h-7 d명현승고，NeuN 3 h-14 d명현강저（P＜0．05）。 HPCT조NF-κB mRNA 3 h-1 d급NF-κB단백3 h-7 d균저우TBI조，이NeuN표체3 h-7 d고우TBI조（P＜0．05）。결론결양예처리재일정시간창내억제NF-κB표체가능대신경원기보호작용。
Objective To explore the effect of hypoxic preconditioning on neuronal activity in traumatic brain injury rats, and to research the influence of nuclear factor-κB (NF-κB) on neuronal activity.Methods Male rats were randomly divided into control group ( Con ), hypoxic preconditioning group (HPC), traumatic brain injury group (TBI) and traumatic brain injury after hypoxic preconditioning group ( HPCT ) .RT-qPCR and Western blotting were used to detect the expression of NF-κB, Immunohistochemistry was used to measure the average optical density of NeuN-positive.Results In the TBI and HPC groups, the mRNA levels of NF-κB at 3 h, 6 h, 12 h, 1 d and the expression of NF-κB at 3 h, 6 h, 12 h, 1 d, 3 d, 7 d were all significantly increased ( P<0 .05 ) .The expression of NeuN in TBI and HPC groups were significantly decreased during the period from 3 h to 14 d(P<0.05).In the HPCT group, the mRNA levels of NF-κB at 3 h, 6 h, 12 h, 1 d and the expression of NF-κB at 3 h, 6 h, 12 h, 1 d, 3 d, 7 d were lower than TBI group , however , the expression of NeuN were higher than TBI group at the same period with NF-κB(P<0.05).Conclusion Hypoxic preconditioning could protect neurons via inhibiting the expression of NF-κB in rats crotex after traumatic brain injury within a certain time window .