CAJ | 학술논문

目的：探讨中度颅脑液压损伤(TBI)大鼠模型生化指标脂质氧化终产物丙二醛(MDA)及抗氧化剂谷胱甘肽(GSH)含量相关指标的变化，并探讨其与继发性脑损伤间的关系。方法将雄性Sprague-Dawley大鼠48只按随机数字表法分成中度颅脑损伤(mTBI)组和假手术(Sham-TBI)组，每组24只。以液压中度TBI指标致伤mTBI组，并于伤后6 h、24 h处死大鼠，通过ELISA免疫酶技术测定抗氧化剂GSH和脂质氧化产物MDA在2组的不同表达，评价大鼠颅脑创伤后的氧化应激损伤。应用SPSS 19.0统计软件，对两组的GSH和MDA浓度比较采用独立样本t检验。结果 mTBI组脑组织见挫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组中的MDA浓度较Sham-TBI组显著升高[6 h时分别为(8.34±2.03)μg/g和(3.92±1.20)μg/g，t=6.493，P=0.000]，随伤后时间的延长，MDA的浓度显著升高[24 h时分别为(12.74±2.44)μg/g和(3.96±1.18)μg/g，t=11.222， P=0.000]；而TBI后mTBI组GSH浓度显著低于Sham-TBI组[6 h时分别为(2.65±0.63)μg/g和(4.90±0.56)μg/g，t=9.247，P=0.000]，随伤后时间的延长，GSH的浓度显著降低[24 h时分别为(2.20±0.62)μg/g和(4.88±0.55)μg/g；t=11.202，P=0.000]。结论液压TBI模型致伤能量能够测量，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呈正相关，外伤后早期阻断氧化应激过程可能起到脑保护作用。
목적：탐토중도로뇌액압손상(TBI)대서모형생화지표지질양화종산물병이철(MDA)급항양화제곡광감태(GSH)함량상관지표적변화，병탐토기여계발성뇌손상간적관계。방법장웅성Sprague-Dawley대서48지안수궤수자표법분성중도로뇌손상(mTBI)조화가수술(Sham-TBI)조，매조24지。이액압중도TBI지표치상mTBI조，병우상후6 h、24 h처사대서，통과ELISA면역매기술측정항양화제GSH화지질양화산물MDA재2조적불동표체，평개대서로뇌창상후적양화응격손상。응용SPSS 19.0통계연건，대량조적GSH화MDA농도비교채용독립양본t검험。결과 mTBI조뇌조직견좌상조급주망막하강출혈，HE염색후가견신경원손상핵고축，세포배사정공포상，이Sham-TBI조미견신경원손상표현。TBI후mTBI조중적MDA농도교Sham-TBI조현저승고[6 h시분별위(8.34±2.03)μg/g화(3.92±1.20)μg/g，t=6.493，P=0.000]，수상후시간적연장，MDA적농도현저승고[24 h시분별위(12.74±2.44)μg/g화(3.96±1.18)μg/g，t=11.222， P=0.000]；이TBI후mTBI조GSH농도현저저우Sham-TBI조[6 h시분별위(2.65±0.63)μg/g화(4.90±0.56)μg/g，t=9.247，P=0.000]，수상후시간적연장，GSH적농도현저강저[24 h시분별위(2.20±0.62)μg/g화(4.88±0.55)μg/g；t=11.202，P=0.000]。결론액압TBI모형치상능량능구측량，중도폐합성로뇌외상가도치뇌조직병이학개변화양화응격손상，차양화응격손상지표여뇌손상시간정정상관，외상후조기조단양화응격과정가능기도뇌보호작용。
Objective To study the change of biochemical index of malondialdehyde (MDA) and glutathione (GSH) of moderate traumatic brain injury (TBI) rats model, which are the end products of lipid oxidation and antioxidant, respectively. To explore the relationship between these two chemicals and secondary brain injury. Methods 48 adult male Sprague-Dawley rats were randomly assigned to 2 groups : moderate-TBI (mTBI, n=24) group and sham-TBI (sham, n=24) group. Hydraulic moderate TBI index was induced to mTBI group. The rats were killed 6 h and 24 h after injured respectively, the levels of MDA and GSH were examined by ELISA enzymictechnology to analyze the different expression among 2 groups and to evaluate the oxidative stress injury of the rats after traumatic brain injury. The data was analyzed by SPSS 19.0 statistical analysis software, the concentration of GSH and MDA among 2 groups was tested by independent-samples t Test. 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. However, no similar injury could be found in sham group. The concentration of MDA in mTBI group was significantly higher than that in sham group (in 6 h, level of mTBI 8.34 ± 2.03μg/g, level of sham 3.92 ± 1.20μg/g, t=6.493, P=0.000), and the concentration displayed a significant upregulated trend as time went by post TBI (in 24 h, level of mTBI 12.74 ± 2.44μg/g, level of sham 3.96 ± 1.18μg/g, t=11.222, P=0.000). The concentration of GSH in mTBI group was significantly lower than that in sham group (in 6 h, level of mTBI 2.65 ± 0.63μg/g, level of sham 4.90 ± 0.56μg/g, t=9.247, P=0.000), and the concentration displayed a significant downtrend as time went by post TBI (in 24 h, level of mTBI 2.20 ± 0.62μg/g, level of sham 4.88 ± 0.55μg/g, t=11.202, P=0.000). Conclusions The injury level of hydraulic TBI model can be evaluated, moderate closed brain trauma resulted in brain tissue pathological changes and oxidative stress injury. The index of oxidative stress was correlated with the injury period. Blockage of the process of the oxidative stress in the early stage post TBI may play an important role in neuroprotective effect.