大鼠二次脑损伤后脑组织SOD及MDA的变化研究
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摘要
目的:观察大鼠二次脑损伤后脑组织SOD及MDA的变化,进一步探讨过氧化反应在二次脑损伤机制中的作用。方法:90只雄性SD大鼠随机分为正常对照组(A组)、弥漫性脑损伤组(B组)和二次脑损伤组(C组),建模成功后,分别于伤后1 h、3 h、6h、12 h、24 h、48 h处死动物,取额叶组织匀浆,分别测定大鼠脑内SOD及MDA的含量。结果:伤后1h开始,B、C组中SOD含量呈现先上升后下降的趋势,并随时间呈持续下降趋势直至伤后24 h,C组较B组下降程度更加明显(P<0.05);伤后3 h,B、C组中SOD含量均增高,B组增高程度和速率均高于C组(P<0.05)。伤后1 h开始,B、C组MDA含量呈升高趋势,并于24小时达峰值,C组升高趋势较B组更显著,伤后6 h、24 h、48 h,C组与B组之间相比统计学差异显著(P<0.05)。结论:创伤性脑损伤及二次脑损伤后,脑组织内过氧化反应明显加重,SOD及MDA均出现明显变化,二次脑损伤的过氧化反应较脑损伤组更加严重且持续时间更长,且MDA较SOD的变化具有滞后性。
Objective: Testing the changes of superoxide dismutase(SOD) and malondialdehyde(MDA) in rats with diffuse brain injury(DBI) or secondary brain insult(SBI), to analyze the effects and significance of peroxidation in development of rats SBI. Methods:90 male SD rats were randomly divided into normal control group(group A), DBI group(group B) and SBI group(group C). After the success of the modeling, the rats were put to death, and the frontal tissue homogenate were taken after injury 1 h, 3 h, 6 h, 12 h, 24 h, and48 h respectively, to determine the content of SOD and MDA. Results: From the first 1 h after injury, SOD content in B and C groups presents the downward trend after rising first, and the declining trend over time until 24 h after injury, the degree of decline in group C is more obvious compared with that in group B(P< 0.05); 3 h after injury, SOD content in B and C groups were higher, the higher degree and the rate of B group were higher than in group C(P<0.05). From the first 1 h after injury, MDA content in groups B and showed a trend of increase, and in 24 hours to spike, group C increased more significantly than group B, at 6 h, 24 h, and 48 h after injury, the differences between Group B and Group C were statistically significant(P<0.05). Conclusion: After DBI or SBI in rats, peroxidation increase obviously, SOD and MDA change ap- parently, peroxidation in SBI is more serious than that in DBI and last longer, and the changes of MDA are later than those of SOD.
Objective: Testing the changes of superoxide dismutase(SOD) and malondialdehyde(MDA) in rats with diffuse brain injury(DBI) or secondary brain insult(SBI), to analyze the effects and significance of peroxidation in development of rats SBI. Methods:90 male SD rats were randomly divided into normal control group(group A), DBI group(group B) and SBI group(group C). After the success of the modeling, the rats were put to death, and the frontal tissue homogenate were taken after injury 1 h, 3 h, 6 h, 12 h, 24 h, and48 h respectively, to determine the content of SOD and MDA. Results: From the first 1 h after injury, SOD content in B and C groups presents the downward trend after rising first, and the declining trend over time until 24 h after injury, the degree of decline in group C is more obvious compared with that in group B(P< 0.05); 3 h after injury, SOD content in B and C groups were higher, the higher degree and the rate of B group were higher than in group C(P<0.05). From the first 1 h after injury, MDA content in groups B and showed a trend of increase, and in 24 hours to spike, group C increased more significantly than group B, at 6 h, 24 h, and 48 h after injury, the differences between Group B and Group C were statistically significant(P<0.05). Conclusion: After DBI or SBI in rats, peroxidation increase obviously, SOD and MDA change ap- parently, peroxidation in SBI is more serious than that in DBI and last longer, and the changes of MDA are later than those of SOD.
引文
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[18]荆俊杰,王守森,杨庆武,等.纳洛酮对弥漫性脑损伤合并二次脑损伤大鼠c-fos表达和β-内啡肽水平的影响[J].解放军医学杂志,2012,37(9):26-29Jing Jun-jie,Wang Shou-sen,Yang Qing-wu,et al.Effect of naloxone hydrochloride on c-fos protein expression in brain and plasma beta-endorphin level in rats with diffuse brain injury and secondary brain insult[J].Med J Chin PLA,2012,37(9):26-29
[2]Mustafa AG,Alshboul OA.Pathophysiology of traumatic brain injury[J].Neurosciences,2013,18(3):222-234
[3]白红民,费舟,章翔,等.大鼠二次脑损伤模型的建立[J].中华创伤杂志,2002,18(4):214-217Bai Hong-min,Fei Zhou,Zhang Xiang,et al.Rat model of diffuse brain injury with secondary brain insult[J].Chin J Trauma,2002,18(4):214-217
[4]费舟,晁晓东.加强二次脑损伤因素的循证医学研究[J].解放军医学杂志,2012,37(2):90-93Fei Zhou,Chao Xiao-dong.Evidengce-based medical study to enhence secongdary brain injury factors[J].Med J Chin PLA,2012,37(2):90-93
[5]费舟,章翔.二次脑损伤[J].中华神经外科疾病研究杂志,2006,5(5):471-473Fei Zhou,Zhang Xiang.Secondary brain insult[J].Chin J Neurosurg Dis Res,2006,5(5):471-473
[6]Feng JF,Zhao X,Gurkof GG,et al.Post-traumatic hypoxia exacerbates neuron cell death in the hippocampus[J].J Neurotrauma,2012,29:l167-1179
[7]费舟,章翔,王晓峰,等.二次脑损伤神经细胞内游离Ca2+、脑组织丙二醛与血液流变性的改变[J].中国危重病急救医学,2000,12(8):505-508Fei Zhou,Zhang Xiang,Wang Xiao-feng,et al.Changes in neuronal Ca,malondialdehyde in brain tissue and hemorrheology after secondary brain insults[J].Chinese Critical Care Medicine,2000,12(8):505-508
[8]费舟,章翔,白红民,等.缺血性二次脑损伤大鼠脑皮层第Ⅲ组m Glurs改变及意义[J].第四军医大学学报,2002,23(23):2117-2120Fei Zhou,Zhang Xiang,Bai Hong-min,et al.Changes and efects of groupⅢmetabotropic glutamate receptors in the cerebral cortex of rats with diffuse brain injuries coupled with ischemic secondary brain insults[J].J Fourth Mil Med Univ,2002,23(23):2117-2120
[9]李宾,宋振全,梁国标,等.8-OH-DPAT对弥漫性脑损伤及合并二次脑损伤大鼠神经元凋亡的影响[J].创伤外科杂志,2013,15(4):310-314Li bin,Song Zhen-quan,Liang Guo-biao,et al.Neural apoptosis effect of 8-o H-DPAT on difuse brain injury and secondary brain injury in rats[J].J Trauma Sur,2013,15(4):310-314
[10]Shultz SR,Bao F,Weaver LC,et al.Treatment with an anti-CD11d integrin antibody reduces neuroinflammation and improves outcome in a rat model of repeated concussion[J].J Neuroinflammation,2013,10(26):1-15
[11]Ismailoglu O,Atilla P,Palaoglu S,et al.The therapeutic effects of melatonin and nimodipine in rats after cerebral cortical injury[J].Turk Neurosurg,2012,22(6):740-746
[12]Hall ED,Vaishnav RA,Mustafa AG.Antioxidant therapies for traumatic brain injury[J].Neurotherapeutics,2010,7(1):51-61
[13]Toklu HZ,Hakan T,Biber N,et al.The protective effect of alpha lipoic acid against traumatic brain injury in rats[J].Free Radic Res,2009,43:658-667
[14]Xiong Y,Shie FS,Zhang J,et al.Prevention of mitochondrial dysfunction in post-traumatic mouse brain by superoxide dismutase[J].J Neurochem,2005,95:732-744
[15]Mustafa AG,Singh IN,Wang J,et al.Mitochondrial protection after traumatic brain injury by scavenging lipid peroxyl radicals[J].J Neurochem,2010,114(1):271-280
[16]Hsiang JN,Wang JY,Ip SM,et al.The time course and regional variations of lipid peroxidafion after diffuse brain injury in rats[J].Acta neurchirol Wien,1997,139(5):464-468
[17]荆俊杰,王守森,杨庆武,等.大鼠二次脑损伤后脑内c-fos基因表达和血浆β-内啡肽的变化及意义[J].中国临床神经外科杂志,2007,12(1):34-38Jing Jun-jie,Wang Shou-sen,Yang Qing-wu,et al.Expression of c-fos gene and changes in plasma level ofβ-endorphin after secondarybrain insults and their significance in rats[J].Chin J Clin Neurosurg,2007,12(1):34-38
[18]荆俊杰,王守森,杨庆武,等.纳洛酮对弥漫性脑损伤合并二次脑损伤大鼠c-fos表达和β-内啡肽水平的影响[J].解放军医学杂志,2012,37(9):26-29Jing Jun-jie,Wang Shou-sen,Yang Qing-wu,et al.Effect of naloxone hydrochloride on c-fos protein expression in brain and plasma beta-endorphin level in rats with diffuse brain injury and secondary brain insult[J].Med J Chin PLA,2012,37(9):26-29