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大鼠额叶创伤后早期神经元型一氧化氮合酶的表达变化

Expression of Neuronal Nitric Oxide Synthase in the Early Stage After Frontal Cortex Injury in Rats
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摘要 目的观察大鼠额叶创伤后不同时间点创伤区及周边皮质神经元型一氧化氮合酶(nNOS)的表达变化。方法采用成年健康SD大鼠(76只)脑额叶锐器损伤模型,随机分成空白对照组、假手术组和脑损伤组3组。于伤后0、1、3、6、12、24h等6个时间点分别采用尼氏染色法、免疫荧光组织化学方法、Western blot法来观察创伤区及周边皮质神经元的病理变化、nNOS阳性细胞和nNOS蛋白的表达变化。结果尼氏染色显示创伤区及周边皮质神经元数目减少,胞浆染色加深,尼氏小体减少,神经元突起不明显甚至消失。免疫荧光组织化学、Western blot免疫印迹显示,空白对照组及假手术组额叶皮质中偶见nNOS阳性细胞,nNOS蛋白表达量较低;伤后1h创伤区及周边nNOS阳性细胞表达开始增多,nNOS蛋白表达开始升高,6h达高峰,12h开始下降。结论大鼠额叶创伤后早期创伤区及周边皮质有nNOS的时程表达变化。 Objective To observe the expression of neuronal nitric oxide synthase (nNOS) during 0, 1,3,6,12,24 h after frontal cortex injury in rats. Methods Seventy-six adult SD rats were randomly divided into three groups: the control group, sham group and brain injury group. The pathological changes in the early stage in the damaged area were observed by using Nissl staining; the expression of nNOS protein and its cells with positive reaction were examined with Western blot and inununofluorescencehistochemistry respectively. Results Nissl staining results showed that the number of neurons decreased, the staining of cytoplasm darkened, nissl bodies decreased and the processes of neurons were not prominent or diminished in the injury frontal cortex. Immunofluorescence-histochemistry and Western blot showed that nNOS were low in the frontal cortex in the control group or sham group, increased gradually from 1 h after frontal cortex injury, reached its peak 6 h, after that and then decreased gradually from 12 h. Conclusion Time-course expression changes of nNOS in the damaged area existes in the early stage after frontal cortex injury in rats.
出处 《苏州大学学报(医学版)》 CAS 北大核心 2009年第1期33-35,F0003,共4页 Suzhou University Journal of Medical Science
基金 江苏省高校自然科学基金指导计划资助项目(05KJD180165)
关键词 额叶创伤 神经元型一氧化氮合酶 免疫印迹 免疫荧光组织化学 大鼠 frontal cortex injury neuronal nitric oxide synthase Western blot immunofluorescence-histochemistry rat
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  • 1陈建业,王晓明,刘戟,陈璟歆,王若菡,彭文珍,程汉华,陈俊杰.人脑髓鞘碱性蛋白对H_2O_2诱导人肺癌细胞YTLMC-90凋亡的抑制作用[J].癌症,2006,25(2):170-174. 被引量:9
  • 2贾军,边富杰.亚低温对急性脑损伤后大鼠脑组织一氧化氮合酶活性的影响[J].实用诊断与治疗杂志,2006,20(5):353-354. 被引量:1
  • 3Conti AC, Raghupathi R, John Q, et al. Experimantal brain injury induces regionally distinct apoptosis during the acute and delayed posttraumatic period[ J]. J Neurosci, 1998,18(15) :5663-5672.
  • 4Xu Y, Tao Y. Involvement of the NMDA receptor/nitric oxide signal pathway in platelet-activating factor-induced neurotoxicity [ J ].Neuroreport, 2004,15 (2): 263-266.
  • 5Cherian L, Hlatky R, Robertson CS, et al. Nitric oxide in traumatic brain injury[J]. Brain Pathol,2004,14(2): 195-201.
  • 6Rink A, Fung M, Trojanowski JQ, et al. Evidence of apoptosis cell death after experimental traumatic brain injury in the rat[J]. AM J Pathol,1995,147(6): 1575-1583.
  • 7Newcomb JK, Zhao X, Pike BR, et al. Temporal profile of apoptosis-like changes in neurons and astrocytes following controlled cortical impact injury in the rat[ J]. Exp Neurol, 1999,158( 1 ) :76-88.
  • 8Ng I, Yeo TT, Tang WY, et al. Apoptosis occurs after cerebral contusions in humans [ J ]. Neurosurgery, 2000,46 (4): 949-956.
  • 9Shaw K, Mackinnom MA, Raghupathi R, et al. TUNEL-positive staining in white ad grey matter after fatal head injury in man [ J ]. Clin Neuropathol, 2001,20 (3): 106-112.
  • 10Clark RS, Cheng J, Watkins SL, et al. Apoptosis-suppressor gene Bcl-2expression after tranmatic brain injury in rats [ J]. J Neurosci, 1997,17(23) :9172-9182.

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