期刊文献+

一氧化氮合酶在缺氧胎鼠组织中的表达及当归保护机制的实验研究

NOS EXPRESSION IN HYPOXIA FETAL RATS AND THE PROTECTIVE EFFECTS OF CHINESE ANGELICA ON BONE MARROW,NERVOUS TISSUE AND CARTILAGINOUS TISSUE
下载PDF
导出
摘要 目的探讨一氧化氮合酶(NitricOxideSynthase,NOS)在宫内缺氧状态下胎鼠骨髓、软骨、神经组织中的表达,以及中药当归注射液(Angelicainjection)对宫内缺氧组织的保护作用。方法孕龄19天的Wistar孕鼠随机分为对照组、缺氧组和当归组,分别给予尾静脉注射0.9%生理盐水、尾静脉注射0.9%生理盐水后建立缺氧模型及尾静脉注射25%的当归注射液后建立缺氧模型处理,行石蜡切片和免疫组化实验以及图像分析和统计分析。结果对照组组织中nNOS低表达,缺氧组和当归组中nNOS高表达;而后两组比较,当归组nNOS含量比缺氧组明显减少(P<0.05)。结论成功建立宫内胎鼠缺氧模型。nNOS激活产生适量NO对胚胎发育起着生理调节作用,其过量表达则可能是宫内缺氧时引起胚胎多种组织细胞,特别是神经组织损伤的重要机制之一。当归注射液下调nNOS表达活性,对宫内缺氧胎鼠有保护作用。 Objective: To investigate the expression of NOS and the protective effects of Chinese angelica injection on fetal rats' hypoxia tissue in uterus. Methods: 12 female pregnant Wistar rats were randomly divided into three groups:the control group(CG), the hypoxia group(HG) and angelica injection group(AG), and each group having 4 rats. The rats of AG were injected with 25% Chinese angelica injection (8ml/kg) through tail vein before they were in hypoxia state. Ten embryos of each group were made into paraffin sections. The expression of NOS was then determined by immtmohistoehemistry, and their average light - density disposed by image processing system was analyzed with statistical methods. Result: In bone marrow, nerve and cartilage tissues observed, the NOS - postive cells were young erythroblasts, nerve cells and chondroeyte, respectively. The immunohistochemical staining and the mean optical density of NOS was low in CG and high in HG and AG( P 〈 0.05). In AG, the value was significantly lower compared with that in HG( P 〈 0.05). Conclusion: The model of intra- uterine hypoxia fetal rats was established. Angelica injection might down- regulate nNOS expression to protect the hypoxia fetal rats.
出处 《泸州医学院学报》 2005年第4期294-298,共5页 Journal of Luzhou Medical College
关键词 缺氧 一氧化氮合酶 当归注射液 保护 胎鼠 Hypoxia Nitric Oxide Synthase Angelica Injection Protection Fetal Rats
  • 相关文献

参考文献11

  • 1季凤清,岳旭,孙海梅,郭艳茹,郭崇洁,赵天德.一氧化氮合酶与缺氧复氧所致神经细胞凋亡及银杏叶提取物的保护作用[J].解剖学报,2002,33(3):235-239. 被引量:12
  • 2Yick L W, Wu W So KF, et al. Time course of NOS expression and neuronal death in Clarke' s nucleus following traumatic injury in adult rat spinal cord [J]. Neurosci Lett, 1998; 241(2) : 155.
  • 3Yu WH. Regulation of nitric oxide synthase expression in motoneurons following nerve injury[J]. J Neurosci, 1997; 19(3) : 247.
  • 4Brown GC, Borutaite V. Nitric oxide, cytochrome c and mitochondria [J]. Biochem Sco Symp, 1999; 66 (1): 17.
  • 5Bjelke B, Aden U, Dahlberg V, et al. MRI evaluation and functional assessment of brain injury after hypoxic ischemia in neonatal mice [J]. Stroke. 2072; 33 (5): 1405.
  • 6Snyder SH. Nitric oxide: First in a new class of neurotransmitters [J]. Science, 1992; 257 (5069): 494.
  • 7Papapetroporlos A, Rudic hRD, Sessa WC. Molecular control of nitric oxide synthases in the cardiovascular system [J]. Cardiocasc Res, 1999; 43 (3): 509.
  • 8谢兴国,蔡文琴,张吉强,李成仁.一氧化氮合酶阳性神经元在小鼠脑内的分布[J].解剖学杂志,2002,25(1):47-50. 被引量:17
  • 9Winkler T, Sharma HS, Stallberg E, et al. Spinal cord evoked potential and edema in the pathophysiology of rat spinal cord injury. Involement of nitric oxide [J]. Amino Acids.1998; 14 (1-3): 131.
  • 10Myatt L, Brewer DI, Langdon G, et al. Attanuation of the vasoconsyictor effects of thromboxane and endotydlium by nitric oxide in the human fetalplacenta circulation [J]. Am J Obstet Gynecol, 1992; 166:224.

二级参考文献3

共引文献27

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部