小鼠开放性脑损伤后MAP-2、SDF-1、SSeCKS的表达与脑损伤经过时间的实验性研究
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摘要
目的:观察小鼠开放性脑损伤后不同时相内MAP-2、SDF-1和SSeCKS蛋白表达的关系,探讨其脑损伤后神经元和神经胶质细胞随脑损伤时间的变化规律,对其在脑损伤时间推断中的作用做出评价。方法:选取健康昆明小鼠55只,随即分成对照组(n=5)、假损伤组(n=5)、死后损伤组(n=5)和损伤组(n=40)。而损伤组在1h、3h、6h、12h、1d、3d、7d和14d等时相点各5只。通过建立小鼠开放性脑损伤模型,运用光学显微镜观察脑组织形态学的改变,利用免疫组织化学染色法(SP法)对对照组及伤后不同时间组内脑细胞中的MAP-2、SDF-1和SSeCKS蛋白进行检测,并作统计学分析。结果:三种蛋白的死后损伤组与生前损伤组相比较均有统计学意义(P<0.05)。伤后1h,MAP-2的表达下调,与正常对照组比较有统计学意义(P<0.05),脑组织损伤3d时达最低峰,14d基本达正常水平,但仍低于对照组。脑损伤后SDF-1表达上调,随着损伤时间的延长,到伤后6h,与正常对照组比较有统计学意义(P<0.05),呈持续升高状态,14d仍高于正常对照组。伤后1h,SSeCKS的表达下调,与正常对照组比较有统计学意义(P<0.05),脑组织损伤3d时达最低峰,14d基本达正常水平,但仍低于对照组。结论:1)检测MAP-2、SDF-1与SSeCKS蛋白的表达可用于生前伤和死后脑损伤的鉴别。2)小鼠开放性脑损伤后,MAP-2、SDF-1和SSeCKS的表达呈一定的时序性变化规律,可作为推断脑损伤时间的参考指标之一。
Objective: To observe the correlated expression of MAP-2、SDF-1and SSeCKS afer doing experiment which related tocranio-cerebral wound with mices, as well as to research the changes between neurons and glial cells when brain is injury, after that evaluate what role is played in brain contusion. Methods: Fifty-five healthy Kunming mices were randomly divided into 5 groups, inclouding normal control group(n=5), pseudo damage group(n=5), postmortem injury group(n=5) and brain injury(n=45)[it included 5 mices in every phase(1h, 3h, 6h, 12h, 1d, 3d, 7d, 14d)]. Through establishing model ofcranio-cerebral wound in mices, immunohistochemical method(SP) was applied to detect the expression of MAP-2、SDF-1and SSeCKS in control group with different time after injury. And the morphological changes of the mice brain were obserbed by light microscope. The immunostaining results were meassured with statistics analysis. Results: There was statistical significance on antemortem brain injury group and postmortem brain injury group(P<0.05). At 1h after injury, The expression of MAP-2 decreased, MAP-2–positive compared with the nomal group were different(P<0.05), and its marked downregulation was noted at 3 days, and then the expression became increased but it remained below the control level till 14 days after injury; The express of SDF-1 increase following the time of brain injury. At 6h after injury, SDF-1–positive compared with the nomal grou were different(P<0.05), and the expression remained above the control level till 14 days. At 1h after injury, The expression of SSeCKS decreased, SSeCKS–positive compared with the nomal group were different(P<0.05), and its marked downregulation was noted at 3 days, and then the expression became increased but it remained below the control level till 14 days after injury. Conclusion:1)It can be used to authenticate antemortem and postmortem brain injury by checking out the expression of MAP-2, SDF-1 and SSeCKS. 2)cranio-cerebral wound induced expression of MAP-2, SDF-1 and SSeCKS, The regular changes pattern of MAP-2, SDF-1 and SSeCKS level in time seems to be of value in estimating the age of brain injury.
Objective: To observe the correlated expression of MAP-2、SDF-1and SSeCKS afer doing experiment which related tocranio-cerebral wound with mices, as well as to research the changes between neurons and glial cells when brain is injury, after that evaluate what role is played in brain contusion. Methods: Fifty-five healthy Kunming mices were randomly divided into 5 groups, inclouding normal control group(n=5), pseudo damage group(n=5), postmortem injury group(n=5) and brain injury(n=45)[it included 5 mices in every phase(1h, 3h, 6h, 12h, 1d, 3d, 7d, 14d)]. Through establishing model ofcranio-cerebral wound in mices, immunohistochemical method(SP) was applied to detect the expression of MAP-2、SDF-1and SSeCKS in control group with different time after injury. And the morphological changes of the mice brain were obserbed by light microscope. The immunostaining results were meassured with statistics analysis. Results: There was statistical significance on antemortem brain injury group and postmortem brain injury group(P<0.05). At 1h after injury, The expression of MAP-2 decreased, MAP-2–positive compared with the nomal group were different(P<0.05), and its marked downregulation was noted at 3 days, and then the expression became increased but it remained below the control level till 14 days after injury; The express of SDF-1 increase following the time of brain injury. At 6h after injury, SDF-1–positive compared with the nomal grou were different(P<0.05), and the expression remained above the control level till 14 days. At 1h after injury, The expression of SSeCKS decreased, SSeCKS–positive compared with the nomal group were different(P<0.05), and its marked downregulation was noted at 3 days, and then the expression became increased but it remained below the control level till 14 days after injury. Conclusion:1)It can be used to authenticate antemortem and postmortem brain injury by checking out the expression of MAP-2, SDF-1 and SSeCKS. 2)cranio-cerebral wound induced expression of MAP-2, SDF-1 and SSeCKS, The regular changes pattern of MAP-2, SDF-1 and SSeCKS level in time seems to be of value in estimating the age of brain injury.
引文
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[6]Lin X, Nelson PJ, Frankfort B, et al. Isolation and characterization of a novel mitogenic regulatory gene, 322, which is transcriptionally suppressed in cells transformed by src and ras[J]. Mol Cell Biol, 1995, 15(5):2754-2762.
[7]Lin X, Tombler E, Nelson PJ. A novel src-and ras-suppressed protein kinase C substrate associated with cytoskeletal architecture[J]. J Biol Chem, 1996, 271(45): 28430-28436.
[8]Kitamura H, Okita K, Fujikura D, et al. Induction of src-suppressed Ckinase substrate(SSeCKS) in vascular endothelial cells by bacterial lipopolysAccharide[J]. J Histochem Cytochem, 2002, 50(2):245-255.
[9]吴旭,汪德文,张国华,等.实验室性脑挫伤GFAP, PCNA免疫组织化学研究[J].医学杂志, 1999, 15(2):65-66.
[10]陈龙,陈忆九,刘国宁.大鼠脑损伤后FN表达与脑损伤时程关系的研究[J].法医学杂志, 2001, 17(1):1-3.
[11]杨恬,细胞生物学[M],第1版,北京,人民卫生出版社, 2005, 192-193.
[12]MaccioniRB, CambiazoV. Role of microtubule-associated proteins in the control ofmicrotubule assembly. PhysiolRev. 1995, 75(4): 835.
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[16]Hatakeyama T, Matsumoto M, Brengman JM, etal. Immunohistochemicalinvestiga- tion of ischemic and postischemic damage after bilateral carotid occlusion in gerbils[J]. Stroke, 1988, 19(12):1526-1534.
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