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奥扎格雷钠对大鼠局灶性脑缺血血小板内皮细胞黏附分子-1、Bcl-2、Bax表达的影响 被引量:2

Effect of Sodium Ozagrel on PECAM-1,Bcl-2,Bax following focal cerebral ischemia in rats
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摘要 目的观察大鼠局灶性脑缺血后脑组织中血小板内皮细胞黏附分子-1(PECAM-1、CD31)、Bcl-2、Bax表达的改变及奥扎格雷钠对其表达的影响。方法采用线栓法制作大鼠大脑中动脉局灶性脑缺血模型,制模成功大鼠随机分为奥扎格雷钠组和生理盐水组,脑组织切片免疫组化染色检测不同时间点PECAM-1、Bcl-2、Bax在各组大鼠脑组织中的表达变化。结果大鼠大脑中动脉闭塞后脑组织PECAM-1、Bcl-2、Bax的表达明显增高(均P<0.01)。奥扎格雷钠组缺血12h、24h、36h表达PECAM-1较生理盐水组增高,缺血12h、24h表达Bcl-2较生理盐水组增高,缺血24h、36h表达Bax较生理盐水组增高,均P<0.01。结论脑组织表达的PECAM-1、Bcl-2、Bax分别参与了脑缺血不同时期的病理生理作用;奥扎格雷钠可促进PE-CAM-1和Bcl-2的表达,抑制Bax的表达。 Objective To observe the changes of expressions of PECAM-1, Bcl-2, Bax in ischemic cerebrum of adult rats after focal cerebral isehemia, and the effect of Sodium Ozagrel. Methods Middle cerebral artery occlusion (MCAO) models were made by reforming Longa suture method in Wistar rats. The MCAO rats were randomly divided into Sodium Ozagrel group and normal saline group. The expression levels of PECAM-1 ,Bcl-2 ,Bax on 6h, 12h, 24h,48h after MCAO were detected by immunohistochemistry staining. Results The expression levels of PECAM-1, Bcl-2 and Bax in cerebrum were significantly increased after MCAO. The levels of PECAM-1 in Sodium Ozagrel group on 12h, 24h, 36h were higher than which of normal saline group,the levels of Bcl-2 on 12h,24h were higher than which of normal saline group, the levels of Bcl-2 on 24h, 36h were higher than which of normal saline group(all P〈0.01). Conclusion PECAM-1, Bcl-2 and Bax participates in the different pathological stages of focal cerebral ischemia. Sodium Ozagrel could promote the expression of PECAM-1 and Bcl-2,and inhibit the expression of Bax.
出处 《中国实用神经疾病杂志》 2009年第11期1-4,共4页 Chinese Journal of Practical Nervous Diseases
基金 济南市科技局计划项目〔2007〕5号
关键词 局灶性脑缺血 血小板内皮细胞黏附分子-1 BCL-2 BAX 奥扎格雷钠 Focal cerebral ischemia PECAM-1 Bcl-2 Bax Sodium Ozagrel
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参考文献14

  • 1Longa EZ, Weinstein PR, Carlson S, et al. Reversible middle cerebral artery occlusion without craniectomy in rats [J]. Stroke, 1989, 20:84-91.
  • 2Gross A, McDonnell JM, Korsmeyer SJ. Bcl-2 family members and the mitochondria in apoptosis[J]. Gnens Dev, 1999, 13(15): 1899-1911.
  • 3Vivier E,Daeron M. Immunoreceptor tyrosine-based inhibition motifs[J]. Immunol Today, 1997, 18(8):286-291.
  • 4Cambier JC. Inhibitory receptors abound? [J]. Proc Natl Acad Sci USA, 1997, 94(12) :5993-5995.
  • 5Newman PJ. Switched at birth: a new family for PECAM-1 [J]. J Clin Invest, 1999,103(1): 5-9.
  • 6Gao CJ, Sun WY, Christofidou-Solomidou M, et al. PECAM- 1 functions as a specific and potent inhibitor of mitochondrial-dependent apoptosis[J]. Blood, 2003,102(1) : 169-179.
  • 7Newman PJ, Newman DK. Signal transduction pathways mediated by PECAM-1 new roles for an old molecule in platelet and vascular cell biology[J]. Arterioscler Thromb Vasc Biol, 2003,23 (16) : 953-964.
  • 8Brown S, Heinisch I, Ross E, et al. Apoptosis disables CD31- mediated eell detachment from phagocytes promoting binding and engulfment[J]. Nature, 2002, 418: 200-203.
  • 9Zoechi MR,Poggi A. PECAM-1, apoptosis and CD34+ precursors[J]. Leuk Lymphoma, 2004,45(11) :2205-2213.
  • 10Vernon-Wilson EF, Frederic Aurade, Brown SB. CD31 promotes? 1 integrin-dependent engulfment of apoptotic Jurkat T lymphocytes opsonized for phagocytosis by fibronectin[J]. Journal of Leukocyte Biology, 2006,79 : 1260-1267.

二级参考文献17

  • 1各类脑血管疾病诊断要点[J].中华神经科杂志,1996,29(6):379-380. 被引量:33029
  • 2洪奇.奥扎格雷钠治疗脑梗死[N].中国医学论坛报,1997—4—24(7).
  • 3洪奇.奥扎格雷钠治疗脑梗塞[J].中国医学论坛报,1997,(7):22-24.
  • 4Pulsinelli WA, James BA. New model of bilateral hemispheric ischemia in the unanesthetized rat[J]. Stroke, 1979,10: 267.
  • 5Lrakewslos,Mai JK,Krajenski M,et al.Upregulation of Bcl-2 protein events in neurons following cerebral ischemia[J].J Neurosci,1995,15:6364-6365
  • 6永井肇.脑血栓急性期OKY—046临床检验[J].诊断新药,1991,28(3):162-162.
  • 7Johnston GI, Cook RG, McEver RP, et al. Cloning of GMP-140, a granule membrane protein ofplatelets and endothelium: sequence similarity to proteins involved in cell adhesion and inflammation [J]. Cell, 1989, 56: 1033-1044.
  • 8Patil S, Newman DK, Newman PJ. Platelet endothelial cell adhesion molecule-I serves as an inhibitory receptor that modulates platelet responses to collagen[J]. Blood, 2001, 97(6): 1727-1732.
  • 9Jones KL, Hughan SC, Dopheide SM, et al. Platelet endothelial cell adhesion molecule- I is a negative regulator of platelet-collagen interactions[J]. Blood, 2001, 98(5): 1456-1463.
  • 10Cicmil M, Thomas JM, Leduc M, et al. Platelet endothelial cell adhesion molecule-I signaling inhibits the activation of human platelets[J]. Blood, 2002, 99(1): 137-144.

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