CAJ | 학술논문

目的探讨高压氧对颅脑外伤的治疗作用及与脑组织中NF-κB(P50)表达之间的关系. 方法 120只SD大鼠按随机数字表法分为假手术组(仅开颅钻孔,不行打击)、外伤对照组(Feeney自由落体损伤模型制作法制造中度大鼠脑外伤模型,但不接受氧治疗)、常压氧治疗组(脑外伤模型制作成功后立即接受正常压力下纯氧吸入治疗)、高压氧治疗组(脑外伤模型制作成功后立即接受0.2 MPa压力下高压氧治疗),并于伤后6h、1 d、3 d、5 d、7 d五个时相点断头法取脑组织(每时相点6只),光镜下观察脑组织损伤水肿的病理变化以及采用免疫组化方法检测NF-κB(P50)在脑组织中的表达情况. 结果高压氧干预使相同时相点高压氧治疗组大鼠脑水肿情况及损伤程度较外伤对照组明显减轻,而常压氧干预作用则不明显.假手术组各时相点仅见微量的NF-κB(P50)阳性表达或不表达,其他各组脑损伤后6 h即发现损伤脑组织内NF-κB(P50)阳性表达上调,且持续呈增高趋势,伤后5 d时达到最高值.高压氧治疗组与外伤对照组及常压氧治疗组相比在相同时相点NF-κB(P50)表达均有增强,差异有统计学意义(P<0.05). 结论高压氧治疗对损伤神经细胞具有保护、修复的治疗作用,增加NF-κB(P50)在脑组织细胞中的表达可能是其神经保护途径之一.
목적 탐토고압양대로뇌외상적치료작용급여뇌조직중NF-κB(P50)표체지간적관계. 방법 120지SD대서안수궤수자표법분위가수술조(부개로찬공,불행타격)、외상대조조(Feeney자유락체손상모형제작법제조중도대서뇌외상모형,단불접수양치료)、상압양치료조(뇌외상모형제작성공후립즉접수정상압력하순양흡입치료)、고압양치료조(뇌외상모형제작성공후립즉접수0.2 MPa압력하고압양치료),병우상후6h、1 d、3 d、5 d、7 d오개시상점단두법취뇌조직(매시상점6지),광경하관찰뇌조직손상수종적병리변화이급채용면역조화방법검측NF-κB(P50)재뇌조직중적표체정황. 결과 고압양간예사상동시상점고압양치료조대서뇌수종정황급손상정도교외상대조조명현감경,이상압양간예작용칙불명현.가수술조각시상점부견미량적NF-κB(P50)양성표체혹불표체,기타각조뇌손상후6 h즉발현손상뇌조직내NF-κB(P50)양성표체상조,차지속정증고추세,상후5 d시체도최고치.고압양치료조여외상대조조급상압양치료조상비재상동시상점NF-κB(P50)표체균유증강,차이유통계학의의(P<0.05). 결론 고압양치료대손상신경세포구유보호、수복적치료작용,증가NF-κB(P50)재뇌조직세포중적표체가능시기신경보호도경지일.
Objective To investigate the relation between the therapeutic effect of hyperbaric oxygen treatment and nuclear factor-κB (NF-κB) (P50) expression in the brain tissue in mice with traumatic brain injury (TBI). Methods A total of 120 SD rats were randomly divided into sham-operated, TBI model, normobaric oxygen and hyperbaric oxygen (0.2 MPa) groups, and in the latter 3 groups, TBI was induced using Feeney's method. At 6 h and 1, 3, 5, and 7 d following TBI (6 rats at each time point), the rats were sacrificed to observe the pathological changes in the brain tissues under light microscope and detect the expression of NF-κB (P50) using immunohistochemistry. Results The rats in hyperbaric oxygen group showed lessened brain edema as compared with those in TBI model and normobaric oxygen groups. Only trace amount of NF-κB (P50) expression was observed in the sham-operated group, while in the 3 groups with TBI, NF-κB (P50) expression began to increase as early as 6 h after TBI and kept increasing till reaching the peak level at 5 days. At each of the time points for observation, the expression ofNF-κB (PS0) in hyperbaric oxygen group was significantly higher than those in TBI and normobaric oxygen groups (P<0.05). Conclusion Hyperbaric oxygen treatment offers protection of the injured neural cells and promotes their repair in rats following TBI. Increased NF-κB (P50) expression in the brain tissue may serve as one of the pathways mediating the neuroprotective effect of hyperbaric oxygen treatment.