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3-硝基丙酸预处理对大鼠局灶性脑缺血神经元凋亡的抑制作用 被引量:4

Effect of 3-nitropropionic acid preconditioning on the apoptotic cells death and expression of bcl-2/bax following transient local cerebral ischemia in rats
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摘要 目的 探讨小剂量线粒体毒素 3-硝基丙酸 (3-nitropropionicacid ,3-NPA)对大鼠局灶性脑缺血神经细胞凋亡和bcl- 2 /bax表达的影响。方法 大鼠腹腔注射 3-NPA 2 0mg·kg- 1 或生理盐水后 3d制作大脑中动脉闭塞模型 ,分别采用TTC染色、流式细胞术、免疫组织化学方法 ,观察 3-NPA预处理对脑缺血 2h再灌注 2 4h脑梗死体积、神经细胞凋亡率、bcl- 2和bax表达的影响。结果  3-NPA预处理组较对照组脑梗死体积减小 ,神经细胞凋亡减少 ,bcl- 2表达增强 ,bax表达降低。结论  3-NPA预处理可以诱导脑缺血耐受 ,增强bcl- 2的表达 ,降低bax的表达 。 Objective To investigate the effects of 3-nitropropionic acid (3-NPA) preconditioning on the apoptotic cells death and expression of bcl-2/bax.Methods Rats were administrated either saline water or 3-NPA at dose of 20 mg·kg -1 intraperitoneally for 3 days to produce cerebral artery occlusion model. Infarction volumes were assessed by a 2, 3, 5 triphenylte trazolinmchloride staining (TTC) . The neural cells apoptotic percentage in cerebral ischemic penumbra were measured by flow cytometry methods(FCM). Meanwhile, immunohistochemistry was used for the expression of bcl-2 and bax. Results Treatment with 3-NPA showed a reduction in infarct volume compared with the control group.The neural cells apoptotic percentage had a significant reduction. 3-NPA pretreated group showed an elevated bcl-2 and decreased bax.Conclusion 3-NPA preconditioning may induce ischemic tolerance to transient local cerebral ischemia in rats. The inhibition of apoptosis is the underlying pathophysiologic mechanism.
出处 《中华急诊医学杂志》 CAS CSCD 2004年第7期457-459,共3页 Chinese Journal of Emergency Medicine
基金 教育部留学回国人员基金项目 ( 2 0 0 13 45 )
关键词 3-硝基丙酸 预处理 大鼠 局灶性脑缺血 神经元凋亡 抑制作用 分子机制 nitropropionic acid Cerebral ischemia Apoptosis bcl-2 Bax
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  • 1Horiguchi T, Kis B, Rajapakse N, et al.Opening of mitochondrial ATP-sensitive potassium channels is a trigger of 3-nitropropionic acid-induced tolerance to transient focal cerebral ischemia in rats. Stroke,2003, 34 :1015-1020.
  • 2Zhao H, Yenari MA, Cheng D, et al. Bcl-2 overexpression protects against neuron loss within the ischemic margin following experimental stroke and inhibits cytochrome c transtocation and Caspase-3 activity. J Neurochem, 2003, 85: 1026- 1036.
  • 3Brambrink AM,Schneider A,Noga H,et al. Tolerance-inducing dose of 3-nitropropionic acid modulates bcl-2 and bax. Balance in the rat brain: a potential mechanism of chemical preconditioning.J Cerebblood Flow Metab, 2000, 20 :1425-1436.
  • 4Sugino T,Nozaki K,Takagi Y, et al.3-nitropropionic acid induces ischemic tolerance in gerbil hippocampus in vivo. Neurosci Lett, 1999,259:9-12.
  • 5Yao H, Takasawa R, Fukudu K, et al. DNA fragmentation in ischemic core and penumbra in focal cerebral ischemia in rats.Mol Brain Res,2001, 91:112-118.
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