浙江创伤外科
浙江創傷外科
절강창상외과
ZHEJIANG JOURNAL OF TRAUMATIC SURGERY
2014年
6期
899-901,902
,共4页
杨帆%王永青%彭余江%邵波%朱良才%段红宇%何玺君%李慧勇%杨鹏翔%陈慧慧
楊帆%王永青%彭餘江%邵波%硃良纔%段紅宇%何璽君%李慧勇%楊鵬翔%陳慧慧
양범%왕영청%팽여강%소파%주량재%단홍우%하새군%리혜용%양붕상%진혜혜
颅脑损伤%继发性脑损伤%NF-κB%氧化应激%细胞凋亡
顱腦損傷%繼髮性腦損傷%NF-κB%氧化應激%細胞凋亡
로뇌손상%계발성뇌손상%NF-κB%양화응격%세포조망
Traumatic brain injury%Secondary brain injury%NF-κB%Oxidative stress%Apoptosis
目的：探讨NF-κB在颅脑损伤后继发氧化应激及细胞凋亡之间的关系及可能机制。方法成年健康雄性SD大鼠48只，随机分为对照组（n=6）和颅脑损伤组（n=42）。颅脑损伤组通过改良Feeney法建立颅脑损伤模型，根据伤后处死时间分为1、3、6、12及24小时、3和7天共7个亚组，每亚组各6只。每亚组随机取3只大鼠处死，取挫伤灶周围组织行脑组织超氧化物歧化酶（SOD）、丙二醛（MDA）、谷胱甘肽（GSH）测定；剩余的3只大鼠采用免疫组织化学方法检测挫伤灶周围脑组织中NF-κB的表达情况，同时采用TUNEL法观察脑挫伤灶周围细胞凋亡情况。结果颅脑损伤后1小时可见NF-κB蛋白明显表达，3~12小时表达逐渐加强，并于24小时达到高峰，3~7天表达稍减弱，但仍为高表达状态；NF-κB蛋白表达与MDA、SOD及GSH相关（r=0.731, r=-0.702, r=-0.674，P值均<0.05），与细胞凋亡水平相关（r=0.720, P<0.05）。结论颅脑损伤后NF-κB蛋白表达的变化规律参与了继发性脑损伤中氧化应激反应及细胞凋亡等病理过程，抑制氧化应激水平，控制细胞凋亡，减少或减轻继发性脑损伤。
目的：探討NF-κB在顱腦損傷後繼髮氧化應激及細胞凋亡之間的關繫及可能機製。方法成年健康雄性SD大鼠48隻，隨機分為對照組（n=6）和顱腦損傷組（n=42）。顱腦損傷組通過改良Feeney法建立顱腦損傷模型，根據傷後處死時間分為1、3、6、12及24小時、3和7天共7箇亞組，每亞組各6隻。每亞組隨機取3隻大鼠處死，取挫傷竈週圍組織行腦組織超氧化物歧化酶（SOD）、丙二醛（MDA）、穀胱甘肽（GSH）測定；剩餘的3隻大鼠採用免疫組織化學方法檢測挫傷竈週圍腦組織中NF-κB的錶達情況，同時採用TUNEL法觀察腦挫傷竈週圍細胞凋亡情況。結果顱腦損傷後1小時可見NF-κB蛋白明顯錶達，3~12小時錶達逐漸加彊，併于24小時達到高峰，3~7天錶達稍減弱，但仍為高錶達狀態；NF-κB蛋白錶達與MDA、SOD及GSH相關（r=0.731, r=-0.702, r=-0.674，P值均<0.05），與細胞凋亡水平相關（r=0.720, P<0.05）。結論顱腦損傷後NF-κB蛋白錶達的變化規律參與瞭繼髮性腦損傷中氧化應激反應及細胞凋亡等病理過程，抑製氧化應激水平，控製細胞凋亡，減少或減輕繼髮性腦損傷。
목적：탐토NF-κB재로뇌손상후계발양화응격급세포조망지간적관계급가능궤제。방법성년건강웅성SD대서48지，수궤분위대조조（n=6）화로뇌손상조（n=42）。로뇌손상조통과개량Feeney법건립로뇌손상모형，근거상후처사시간분위1、3、6、12급24소시、3화7천공7개아조，매아조각6지。매아조수궤취3지대서처사，취좌상조주위조직행뇌조직초양화물기화매（SOD）、병이철（MDA）、곡광감태（GSH）측정；잉여적3지대서채용면역조직화학방법검측좌상조주위뇌조직중NF-κB적표체정황，동시채용TUNEL법관찰뇌좌상조주위세포조망정황。결과로뇌손상후1소시가견NF-κB단백명현표체，3~12소시표체축점가강，병우24소시체도고봉，3~7천표체초감약，단잉위고표체상태；NF-κB단백표체여MDA、SOD급GSH상관（r=0.731, r=-0.702, r=-0.674，P치균<0.05），여세포조망수평상관（r=0.720, P<0.05）。결론로뇌손상후NF-κB단백표체적변화규률삼여료계발성뇌손상중양화응격반응급세포조망등병리과정，억제양화응격수평，공제세포조망，감소혹감경계발성뇌손상。
Objective To explore the relationship between NF-κB, the level of oxidative stress and apoptosis after secondary brain injury, as well as its potential mechanisms. Methods 48 adult and healthy male rats were divided into 2 groups randomly:the control group(n=6) and TBI group (n=42). TBI was induced using improved Feeney method. The TBI group was divided into 7 subgroups according sacrificed time, 1 h, 3 h, 6 h, 12 h, 24 h, 3 d, and 7 d after injury, each 6 rats. Each subgroup were randomly selected 3 rats after being killed, measure the water content, the su-peroxide dismutase (SOD), malondialdehyde (MDA) and glutathione (GSH) of brain tissue. Specimens were taken from the left three rats in the sub-group, NF-κB of brain tissue around the contusion was measured by using immunohistochemical method, cell apoptosis was observed using TUNEL method. Results Results NF-κB was expressed obviously around the lesion in 1h group, and strongly expressed in 3-12h, and reached a peak in 24h after the injury, while reduced in 3-7d, but still in high level. NF-κB expression strongly correlated with the degree of cerebral edema (r=0.651, P<0.05), strongly correlated with the level of MDA, SOD and GSH (r=0.731, r=-0.702, r=-0.674, P<0.05, P<0.05, P<0.05), and with the level of brain tissue apoptosis (r=0.720, P<0.05). Conclusion Expression of NF-κB protein after brain injury were involved in a series of pathological process of secondary brain injury, such as oxidative stress, apoptosis, which can inhibit oxidative stress levels, control apoptosis, prevent the development of vaso-genic cerebral edema, and reduce or mitigate secondary brain injury.
