中华神经医学杂志
中華神經醫學雜誌
중화신경의학잡지
CHINESE JOURNAL OF NEUROMEDICINE
2014年
6期
576-580
,共5页
疏龙飞%刘家传%王金标%杨艳艳%马涛%卓健伟
疏龍飛%劉傢傳%王金標%楊豔豔%馬濤%卓健偉
소룡비%류가전%왕금표%양염염%마도%탁건위
颅脑损伤%转录因子E2相关因子2%硫氧还蛋白还原酶2%缺氧预处理
顱腦損傷%轉錄因子E2相關因子2%硫氧還蛋白還原酶2%缺氧預處理
로뇌손상%전록인자E2상관인자2%류양환단백환원매2%결양예처리
Traumatic brain injury%Nuclear factor erythroid 2-related factor 2%Thioredoxin reductases 2%Hypoxic preconditioning
目的 研究缺氧预处理对创伤性颅脑损伤大鼠脑组织抗氧化应激和神经功能的影响. 方法 SD雄性大鼠48只采用随机数字表法分为假手术组、缺氧预处理组、颅脑损伤组、缺氧预处理+颅脑损伤组,每组12只.采用低压氧舱预处理3 d(-50 kPa、3 h/d)进行缺氧预处理,用改良的Feeney's自由落体法制作颅脑损伤模型,伤后24h用改良的神经功能评分(mNSS)观察大鼠神经功能;免疫组化染色神经元核抗原(NeuN)检测神经元的存活;Western blotting和实时荧光定量PCR分别检测脑组织核转录因子NF-E2相关因子2(Nrf2)、线粒体硫氧还蛋白还原酶2(TrxR2)蛋白和mRNA的表达. 结果 与假手术组、缺氧预处理组比较,颅脑损伤组、缺氧预处理+颅脑损伤组大鼠mNSS评分增高,NeuN表达降低(0.274±0.033、0.281±0.042 vs 0.124±0.014、0.150±0.019),Nrf2、TrxR2蛋白和mRNA表达增高;与颅脑损伤组比较,缺氧预处理+颅脑损伤组大鼠mNSS评分降低,NeuN表达增高,Nrf2、TrxR2蛋白和mRNA表达增高,差异均有统计学意义(P<0.05). 结论 缺氧预处理可增加颅脑损伤后脑组织抗氧化应激的水平,并减轻神经功能缺损.
目的 研究缺氧預處理對創傷性顱腦損傷大鼠腦組織抗氧化應激和神經功能的影響. 方法 SD雄性大鼠48隻採用隨機數字錶法分為假手術組、缺氧預處理組、顱腦損傷組、缺氧預處理+顱腦損傷組,每組12隻.採用低壓氧艙預處理3 d(-50 kPa、3 h/d)進行缺氧預處理,用改良的Feeney's自由落體法製作顱腦損傷模型,傷後24h用改良的神經功能評分(mNSS)觀察大鼠神經功能;免疫組化染色神經元覈抗原(NeuN)檢測神經元的存活;Western blotting和實時熒光定量PCR分彆檢測腦組織覈轉錄因子NF-E2相關因子2(Nrf2)、線粒體硫氧還蛋白還原酶2(TrxR2)蛋白和mRNA的錶達. 結果 與假手術組、缺氧預處理組比較,顱腦損傷組、缺氧預處理+顱腦損傷組大鼠mNSS評分增高,NeuN錶達降低(0.274±0.033、0.281±0.042 vs 0.124±0.014、0.150±0.019),Nrf2、TrxR2蛋白和mRNA錶達增高;與顱腦損傷組比較,缺氧預處理+顱腦損傷組大鼠mNSS評分降低,NeuN錶達增高,Nrf2、TrxR2蛋白和mRNA錶達增高,差異均有統計學意義(P<0.05). 結論 缺氧預處理可增加顱腦損傷後腦組織抗氧化應激的水平,併減輕神經功能缺損.
목적 연구결양예처리대창상성로뇌손상대서뇌조직항양화응격화신경공능적영향. 방법 SD웅성대서48지채용수궤수자표법분위가수술조、결양예처리조、로뇌손상조、결양예처리+로뇌손상조,매조12지.채용저압양창예처리3 d(-50 kPa、3 h/d)진행결양예처리,용개량적Feeney's자유락체법제작로뇌손상모형,상후24h용개량적신경공능평분(mNSS)관찰대서신경공능;면역조화염색신경원핵항원(NeuN)검측신경원적존활;Western blotting화실시형광정량PCR분별검측뇌조직핵전록인자NF-E2상관인자2(Nrf2)、선립체류양환단백환원매2(TrxR2)단백화mRNA적표체. 결과 여가수술조、결양예처리조비교,로뇌손상조、결양예처리+로뇌손상조대서mNSS평분증고,NeuN표체강저(0.274±0.033、0.281±0.042 vs 0.124±0.014、0.150±0.019),Nrf2、TrxR2단백화mRNA표체증고;여로뇌손상조비교,결양예처리+로뇌손상조대서mNSS평분강저,NeuN표체증고,Nrf2、TrxR2단백화mRNA표체증고,차이균유통계학의의(P<0.05). 결론 결양예처리가증가로뇌손상후뇌조직항양화응격적수평,병감경신경공능결손.
Objective To research the influence of hypoxic preconditioning in anti-oxidative ability of brain tissues and neurological functions in rats after traumatic brain injury.Methods Forty eight adult male Sprague Dawley rats were randomly divided into sham-operated group,hypoxic preconditioning group (HPC),traumatic brain injury group (TBI) and hypoxic preconditioning+traumatic brain injury group (HPCT,n=12).The HPC rat models were made by hypobaric chamber for 3 d (50 kPa,3 h/d) and TBI were induced by Feeney's improved equipment.All rats were killed 24 h after injury,and the neurological functions of each group were evaluated by modified neurologieal severity scale (mNSS);the neuronal survival around contusion area was detected by NeuN immunohistochemical staining,and the protein and mRNA expressions of nuclear transcription factor-related factor 2 (Nrf2) and thioredoxin reductases 2 (TrxR2) in the brain tissues were detected by Western blotting and real-time quantitative PCR.Results The mNSS scores in the TBI and HPCT groups were significantly higher as compared with those in the sham-operated and HPC groups (P<0.05),but those in the HPCT group was significantly lower than those in the TBI group (P<0.05).The neuronal survival in the TBI and HPCT groups was decreased as compared with that in the sham-operated and HPC groups (NeuN expressions:0.274±0.033,0.281±0.042 vs 0.124±0.014,0.150±0.019),with significant difference (P<0.05),while that in the HPCT group was statistically increased as compared with that in the TBI group (P<0.05).The expressions of Nrf2 and TrxR2 in the brain tissues of TBI and HPCT groups were significantly increased as compared with those in the sham-operated and HPC groups (P<0.05),and those in the HPCT group was significantly up-regulated as compared with those in the TBI group (P<0.05).Conclusion HPC can increase the anti-oxidative ability and relieve the neurological functions missing after TBI.