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SCI大鼠脊髓前角细胞自噬相关蛋白Beclin-1表达的变化 被引量:1

CHANGES OF AUTOPHAGY RELATED PROTEIN BECLIN-1 EXPRESSION IN ANTERIOR HORN CELLS OF SPINAL CORD INJURY RATS
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摘要 目的:观察脊髓全横断损伤对脊髓前角细胞Beclin-1表达的影响。方法:雄性Wistar大鼠随机分为模型组和假手术组,建立大鼠第2腰髓全横断损伤模型,分别于损伤后6h、1d、3d、7d、14d、21d取3-4腰髓,采用免疫荧光染色法观察大鼠脊髓前角细胞自噬相关蛋白Beclin-1的表达情况。结果:与假手术组相比,模型组损伤后各时间点大鼠脊髓前角Beclin-1免疫阳性细胞数明显升高(P<0.01,P<0.05)。脊髓损伤后3d脊髓前角细胞Beclin-1免疫阳性细胞数达到高峰,21d最低。结论:Beclin-1可能参与了神经元自噬状态的改变。 Objective: To observe the effects of complete transection of spinal cord on Beclin-1 expression in anterior hom cells of rats' spinal cord. Methods: Male Wistar rats were randomly divided into model group and shamoperation group. The spinal cord injury (SCI) rat's model were made by completely Wansecting the 2^nd lumbar spinal cord. Immunofluorescent staining was used to detect the Beclin-1 protein expression in anterior horn cells of the 3^rd-4^th lumbar spinal cord 6h, 1d, 3d, 7d, 14d and 21d after injury respectively. Results: Compared with rats in sham-operation group, the Beclin- 1 positive cells in anterior hom of spinal cord of rats in model group at each time point increased obviously (P〈 0.01, P〈 0.05). The Beclin-1 positive cells in anterior hom of spinal cord reached the peak 3 days after injury, and reached the lowest 21 days after injury. Conclusions: Beclin- 1 may be involved in the changes of neuron autophagy.
机构地区 承德医学院
出处 《承德医学院学报》 2016年第2期102-104,共3页 Journal of Chengde Medical University
基金 河北省卫生厅重点课题(20150016) 河北省中医药管理局课题(2015153)
关键词 脊髓损伤 自噬 BECLIN-1 Spinal cord injury Autophagy Beclin-1
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  • 1HOU Wei-kai,XU Yu-xin,YU Ting,ZHANG Li,ZHANG Wen-wen,FU Chun-li,SUN Yu,WU Qing,CHEN Li.Adipocytokines and breast cancer risk[J].Chinese Medical Journal,2007(18):1592-1596. 被引量:11
  • 2Hall ED, SpringerJ E. Neuroprotection and acute spinal cord injury: a reappraisal[J]. NeuroRx, 2004, 1 ( 1 ) : 80 - 100.
  • 3RowlandJ W, Hawryluk G W, Kwon B, et al. Current status of acute spinal cord injury pathophysiology and emerging therapies: promise on the horizon[J]. Neurosurg Focus, 2008, 25 (5): E2.
  • 4Levine B, Kroemer G. Autophagy in the pathogenesis of disease[J]. Cell,2008,132(1):27-42.
  • 5ZhangJ, Ney P A. Role of BNlP3 and NIX in cell death, autophagy, and mitophagy[J]. Cell Death Differ, 2009,16(7): 939 -946.
  • 6Kanno H, Ozawa H, Sekiguchi A, et al. Induction of autophagy and autophagic cell death in damaged neural tissue after acute spinal cord injury in mice[J]. Spine (Phila Pa 1976),2011,36(22): E1427- E1434.
  • 7Chen H C, Fong T H, lee A W, et aI. Autophagy is activated in injured neurons and inhibited by methylprednisolone after experimental spinal cord injury[J]. Spine (Phila Pa 1976),2012,37(6): 470 -475.
  • 8Meijer AJ, Codogno P. Signalling and autophagy regulation in health, aging and disease[J]. Mol Aspects Med, 2006, 27 ( 5/6 ): 411 - 425.
  • 9Scherz-Shouval R, Shvets E, Fass E, et al. Reactive oxygen species are essential for autophagy and specifically regulate the activity of Atg4[J]. EMBOJ, 2007,26(7) : 1749 -1760.
  • 10Zhang Z , Yang X, Zhang S, et al. BNIP3 upregulation and EndoG translocation in delayed neuronal death in stroke and in hypoxia[J] . Stroke, 2007,38(5): 1606 -1613.

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