Effect of oxymatrine on the expression of BDNF and its receptor TrkB after focal cerebral ischemia-reperfusion in rats

FU Yan-yan1; DUAN Jing-yu2; DUAN Chang-zhu3

doi:10.13406/j.cnki.cyxb.2011.09.003

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Effect of oxymatrine on the expression of BDNF and its receptor TrkB after focal cerebral ischemia-reperfusion in rats

更新时间：2024-01-17

- Effect of oxymatrine on the expression of BDNF and its receptor TrkB after focal cerebral ischemia-reperfusion in rats
- Journal of Chongqing Medical University Vol. 36, Issue 9, Pages: 1047-1050(2011)
- 作者机构：
  
  1. 徐州医学院生物学教研室
  2. 徐州医学院中药学教研室
  3. 重庆医科大学基础医学院生物学教研室
- 作者简介：
- 基金信息：
- DOI：10.13406/j.cnki.cyxb.2011.09.003
  CLC： R285.5
- Published：2011，
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[1]付燕燕,段静雨,段昌柱.氧化苦参碱对大鼠局灶性脑缺血再灌注损伤BDNF及其受体TrkB表达的影响[J].重庆医科大学学报,2011,36(09):1047-1050.

FU Yan-yan1, DUAN Jing-yu2, DUAN Chang-zhu3. Effect of oxymatrine on the expression of BDNF and its receptor TrkB after focal cerebral ischemia-reperfusion in rats. [J]. Journal of Chongqing Medical University 36(9):1047-1050(2011)
[1]付燕燕,段静雨,段昌柱.氧化苦参碱对大鼠局灶性脑缺血再灌注损伤BDNF及其受体TrkB表达的影响[J].重庆医科大学学报,2011,36(09):1047-1050. DOI： 10.13406/j.cnki.cyxb.2011.09.003.

FU Yan-yan1, DUAN Jing-yu2, DUAN Chang-zhu3. Effect of oxymatrine on the expression of BDNF and its receptor TrkB after focal cerebral ischemia-reperfusion in rats. [J]. Journal of Chongqing Medical University 36(9):1047-1050(2011) DOI： 10.13406/j.cnki.cyxb.2011.09.003.

摘要

目的:观察氧化苦参碱（Oxymatrine

OMT）对大鼠局灶性脑缺血再灌注后皮质脑源性神经生长因子（Brain-derivedneurotrophic factor

BDNF）及其受体酪氨酸激酶B（Tyrosine kinase B

TrkB）表达的影响

探讨OMT神经保护作用的机制。方法:采用线栓法建立大鼠大脑中动脉缺血再灌注模型。SD雄性大鼠随机分为假手术组、模型组、阳性药尼莫地平组和OMT低、中、高剂量给药组6组

缺血2 h再灌注24 h后进行神经功能评分。免疫组化法检测BDNF阳性细胞

Western blot检测BDNF和TrkB蛋白表达。结果:与模型组比

OMT中、高剂量组神经学评分均减低

BDNF阳性细胞数以及BDNF和其受体TrkB蛋白表达显著增加

差异有统计学意义（P<0.05

P<0.01）。结论:OMT对大鼠局灶性脑缺血再灌注损伤的恢复有一定促进作用

其机制可能与上调BDNF及受体TrkB的表达有关。

Abstract

Objective:To study the effects of oxymatrine(OMT) on brain-derived neurotrophic factor(BDNF) and its receptor tyrosine kinase(TrkB) in cerebral cortex after focal cerebral ischemia-reperfusion in rats

and explore the neuroprotective mechanism of oxymatrine.Methods:The rat middle cerebral artery occlusion models with filament of focal cerebral ischemia-reperfusion were established.SD male rats were divided randomly into sham group

cerebral ischemia-reperfusion model group

nimodipine(Nim) group and the oxymatrine group.the oxymatrine group was futher divided into three sub-groups which were dealt with the low

middle and high dose of oxymatrine.The neurological scores were used after 2 h ischemia followed by 24 h reperfusion.The expression of BDNF positive neurons

BDNF and TrkB proteins were respectively detected by immunohistochemistry and western blot.Results:Compared with the sham group

the neurological scores decreased

while the expression of BDNF positive neurons

BDNF and its receptor TrkB protein significantly increased in middle and high dose of oxymatrine groups(P<0.05;P<0.01).Conclusion:OMT protects the rats from the ischemia injury following focal cerebral ischemia-reperfusion

the mechanism of which may partly be due to up-regulating the expression of BDNF and TrkB.

关键词

氧化苦参碱脑缺血再灌注脑源性神经生长因子酪氨酸激酶B

Keywords

oxymatrineischemia-reperfusionbrain-derived neurotrophic factor(BDNF)TrkB

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