期刊文献+

bcl-2、Bax基因在面神经损伤后面神经元的表达及对神经元凋亡的调节 被引量:2

Expression of bcl-2 and Bax Genes in Facial Neurons and Their Regulation of Neuron Apoptosis Following Facial Neurotmesis in Rats
下载PDF
导出
摘要 目的 :探讨切断面神经干后面神经元bcl_2、Bax基因表达变化与面神经元细胞凋亡的关系。方法 :将 6 0只成年Wistar大白鼠左侧面神经干切断作为实验组 ,右侧面神经干未切断作为对照组。应用ABC免疫组化染色方法和原位末端标记法 (TUNEL)观察术后 3、7、15、2 1、30、6 0d实验组与对照组面神经元内bcl_2、Bax基因的表达及面神经元凋亡的情况。结果 :切断面神经干后 3d ,bcl_2、Bax基因表达开始增多 ,2 1d达高峰 (P <0 0 1) ,bcl_2 /Bax比值达最低 (P <0 0 1) ;切断面神经干后 3d ,实验组面神经元凋亡较对照组增多 ,2 1d达凋亡高峰 (P <0 0 1)。结论 :bcl_2。 Objective: The aim of this study is to investigate the relationship between the expression changes of bcl_2 and Bax genes and their functions in facial neuronal apoptosis after amputating the facial nerve.Methods: Rats were randomized into two groups, including the experimental and the control group. The changes of expression of bcl_2 and Bax genes in the facial neurons and facial neuronal apoptosis were observed after the facial nerve amputation using the methods of ABC immunohistochemical staining and TUNEL.Results: The expression of bcl_2 and Bax genes and the apoptosis of facial neurons were significantly higher in the experimental group than those of the control group from the 3rd to 21st day after amputation, but the bcl_2/Bax significantly decreased compared with that of the control group.Conclusion: This indicated that bcl_2 and Bax might play an important regulation role in the process of facial neurons apoptosis following facial nerve amputation.\;
出处 《华西口腔医学杂志》 CAS CSCD 北大核心 2001年第6期360-362,共3页 West China Journal of Stomatology
关键词 BCL-2 BAX 细胞凋亡 面神经元 轴突切断 基因调控 大鼠 面神经损伤 bcl_2\ \ Bax\ \ apoptosis\ \ facial neurons\ \ neurotmesis\ \ rats
  • 相关文献

参考文献4

  • 1王亦德.创伤早期处理[M].北京:人民卫生出版社,1994.731-733.
  • 2Mu X,Ann Neurol,1996年,40卷,3期,379页
  • 3Yin X M,Nature,1994年,369卷,2期,321页
  • 4王亦德,创伤早期处理,1994年,731页

同被引文献37

  • 1Natsume A, Wolfe D, Hu J, et al. Enhanced functional recovery after proximal nerve root injury by vector-mediated gene transfer. Exp Neurol, 2003 ,184(2):878-886
  • 2Schreiber M, Kolbus A, Piu F, et al. Control of cell cycle progression by c-Jun is P53 dependent. Genes Dev, 1999 ,13(5):607-619
  • 3Sheikh MS, Chen YQ, Smith ML, et al. Role of P21 Waf1/Cip1/Sdi1 in cell death and DNA repair as studied using a tetracycline-inducible system in P53-deficient cells. Oncogene, 1997, 14(15):1 875-1 882
  • 4Bunz F, Dutriaux A, Lengauer C, et al. Requirement for P53 and P21 to sustain G2 arrest after DNA damage. Science,1998, 282(5393):1 497-1 501
  • 5Corbet SW, Clarke AR, Gledhill S,et al. P53-dependent and -independent links between DNA-damage, apoptosis and mutation frequency in ES cells. Oncogene, 1999, 18(8):1 537-1 544
  • 6Granville DJ, Carthy CM, Hunt DW, et al. Apoptosis: molecular aspects of cell death and disease. Lab Invest, 1998, 78(8):893-913
  • 7Sakamoto T, Kawazoe Y, Shen JS, et al. Adenoviral gene transfer of GDNF, BDNF and TGF beta 2, but not CNTF, cardiotrophin-1 or IGF1, protects injured adult motoneurons after facial nerve avulsion. Neurosci Res, 2003, 72(1):54-64
  • 8Dai CF, Kanoh N, Li KY, et al. Study on facial motoneuronal death after proximal or distal facial nerve transection. Am J Otol,2000,21(1):115-118
  • 9Kanno T, Sato EE, Muranaka S,et al. Oxidative stress underlies the mechanism forCa2+-induced permeability transition of mitochondria. Free Radic Res, 2004, 38(1):27-35
  • 10Cai J, Yang J, Jones DP. Mitochondrial control of apoptosis: the role of cytochrome c. Biochim Biophys Acta,1998, 1366(1-2):139-149

引证文献2

二级引证文献8

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