中华脑科疾病与康复杂志(电子版)
中華腦科疾病與康複雜誌(電子版)
중화뇌과질병여강복잡지(전자판)
CHINESE JOURNAL OF BRAIN DI8SEASES AND REHABILITATIN(ELECTRONIC EDITION)
2014年
6期
41-44
,共4页
林恒州%张猛%黄贤键%张秋生%纪涛%何毅%李维平
林恆州%張猛%黃賢鍵%張鞦生%紀濤%何毅%李維平
림항주%장맹%황현건%장추생%기도%하의%리유평
颅脑损伤%大鼠,Sprague-Dawley%氧化性应激%丙二醛%谷胱甘肽
顱腦損傷%大鼠,Sprague-Dawley%氧化性應激%丙二醛%穀胱甘肽
로뇌손상%대서,Sprague-Dawley%양화성응격%병이철%곡광감태
Craniocerebral trauma%Rats,Sprague-Dawley%Oxidative stress%Malondialdehyde%Glutathione
目的:通过建立大鼠中度颅脑液压损伤模型,检测损伤病灶生化指标脂质氧化终产物丙二醛及抗氧化剂谷胱甘肽含量的变化,探讨其与继发性脑损伤之间的关系,为后续研究提供实验基础。方法雄性Sprague-Dawley大鼠48只,随机分成中度颅脑损伤组( mTBI组)和假手术组( sham-TBI组),各24只。以液压中度颅脑损伤指标致伤TBI组。并于伤后6 h、24 h处死大鼠,通过ELISA技术测定抗氧化剂谷胱甘肽和脂质氧化产物丙二醛在两组的不同表达,采用独立样本t检验评价大鼠颅脑创伤后的氧化应激损伤。结果 mTBI组脑组织见损伤灶及蛛网膜下腔出血,HE染色后可见神经元损伤核固缩,细胞坏死呈空泡状,而sham-TBI组未见神经元损伤表现。 TBI后mTBI组中丙二醛浓度较sham-TBI组显著升高,随伤后时间延长丙二醛浓度显著升高( t6 h =6.49,P<0.01;t24 h =11.22,P<0.01);而TBI后mTBI组谷胱甘肽浓度显著低于sham-TBI组,随伤后时间延长谷胱甘肽浓度显著降低(t6 h =9.25,P<0.01;t24 h =11.24,P<0.01)。结论液压颅脑损伤模型致伤能量能够测量,稳定性及重复性良好,伤情可能分级。中度闭合性颅脑外伤可导致脑组织病理学改变和氧化应激损伤,且氧化应激损伤指标与脑损伤时间有关,外伤后早期阻断氧化应激过程可以起到脑保护作用。
目的:通過建立大鼠中度顱腦液壓損傷模型,檢測損傷病竈生化指標脂質氧化終產物丙二醛及抗氧化劑穀胱甘肽含量的變化,探討其與繼髮性腦損傷之間的關繫,為後續研究提供實驗基礎。方法雄性Sprague-Dawley大鼠48隻,隨機分成中度顱腦損傷組( mTBI組)和假手術組( sham-TBI組),各24隻。以液壓中度顱腦損傷指標緻傷TBI組。併于傷後6 h、24 h處死大鼠,通過ELISA技術測定抗氧化劑穀胱甘肽和脂質氧化產物丙二醛在兩組的不同錶達,採用獨立樣本t檢驗評價大鼠顱腦創傷後的氧化應激損傷。結果 mTBI組腦組織見損傷竈及蛛網膜下腔齣血,HE染色後可見神經元損傷覈固縮,細胞壞死呈空泡狀,而sham-TBI組未見神經元損傷錶現。 TBI後mTBI組中丙二醛濃度較sham-TBI組顯著升高,隨傷後時間延長丙二醛濃度顯著升高( t6 h =6.49,P<0.01;t24 h =11.22,P<0.01);而TBI後mTBI組穀胱甘肽濃度顯著低于sham-TBI組,隨傷後時間延長穀胱甘肽濃度顯著降低(t6 h =9.25,P<0.01;t24 h =11.24,P<0.01)。結論液壓顱腦損傷模型緻傷能量能夠測量,穩定性及重複性良好,傷情可能分級。中度閉閤性顱腦外傷可導緻腦組織病理學改變和氧化應激損傷,且氧化應激損傷指標與腦損傷時間有關,外傷後早期阻斷氧化應激過程可以起到腦保護作用。
목적:통과건립대서중도로뇌액압손상모형,검측손상병조생화지표지질양화종산물병이철급항양화제곡광감태함량적변화,탐토기여계발성뇌손상지간적관계,위후속연구제공실험기출。방법웅성Sprague-Dawley대서48지,수궤분성중도로뇌손상조( mTBI조)화가수술조( sham-TBI조),각24지。이액압중도로뇌손상지표치상TBI조。병우상후6 h、24 h처사대서,통과ELISA기술측정항양화제곡광감태화지질양화산물병이철재량조적불동표체,채용독립양본t검험평개대서로뇌창상후적양화응격손상。결과 mTBI조뇌조직견손상조급주망막하강출혈,HE염색후가견신경원손상핵고축,세포배사정공포상,이sham-TBI조미견신경원손상표현。 TBI후mTBI조중병이철농도교sham-TBI조현저승고,수상후시간연장병이철농도현저승고( t6 h =6.49,P<0.01;t24 h =11.22,P<0.01);이TBI후mTBI조곡광감태농도현저저우sham-TBI조,수상후시간연장곡광감태농도현저강저(t6 h =9.25,P<0.01;t24 h =11.24,P<0.01)。결론액압로뇌손상모형치상능량능구측량,은정성급중복성량호,상정가능분급。중도폐합성로뇌외상가도치뇌조직병이학개변화양화응격손상,차양화응격손상지표여뇌손상시간유관,외상후조기조단양화응격과정가이기도뇌보호작용。
Objective The rat fluid percussion brain injury model was established ,as to investigate the alternate concentration of malondialdehyde and glutathione in the penumbral region of ipsilateral -injured cortex,which were the end product of lipid peroxidation and antioxidant , respectively.The relationship between these two chemicals and secondary brain injury was explored .Methods Totally 48 adult male Sprague-Dawley rats were randomly assigned to 2 groups,moderate-traumatic brain injury(mTBI,n=24)and sham-TBI(n=24).Moderate TBI was induced to mTBI group ,and sham-TBI rats were induced all surgery procedures without TBI .Malondialdehyde and glutathione levels in the penumbral region of ipsilateral -injured cortex were examined at 6 h and 24 h post-TBI by ELISA to evaluate the oxidative stress injury in the two groups and independent sample t test was used in this evaluation .Results Brain contusion and subarachnoid hemorrhage could be observed in mTBI rats .In brain sections with HE staining , nuclear pyknosis and vesicular neurons could be detected in mTBI rats .However ,no similar injury could be found in mTBI group . The concentration of malondialdehyde in mTBI group was significantly higher than that in sham -TBI group, and the concentration displayed a significant up regulated trend as time went by post -TBI( t6 h =6.49,P<0.01;t24 h =11.22 ,P<0.01 ) .The concentration of glutathione in mTBI group was significantly lower than that in sham-TBI group,and the concentration displayed a significant down-regulated trend as time went by post-TBI(t6 h =9.25,P<0.01;t24 h =11.24,P<0.01).Conclusion The severity of brain injury induced by fluid percussion could be evaluated and classified , and this injury model could be repeated in stable condition .Moderate brain injury results in brain pathological changes and oxidative stress injury .The index of oxidative stress is correlated with injury period .Blockage of the process of the oxidative stress in the early stage post-TBI may play an important role in neuroprotection .