[1]张会芳),卢宏)#,焦淑洁),等.丁基苯酞对慢性脑缺血老龄大鼠脑组织TRPM2和核酸内切酶G的影响[J].郑州大学学报(医学版),2011,(06):872.
 ZHANG Huifang),LU Hong),JIAO Shujie),et al.Effects of dlbutylphthalide on expressions of TRPM2 and EndoG in brain tissues of aged rats with chronic cerebral ischemia[J].JOURNAL OF ZHENGZHOU UNIVERSITY(MEDICAL SCIENCES),2011,(06):872.
点击复制

丁基苯酞对慢性脑缺血老龄大鼠脑组织TRPM2和核酸内切酶G的影响
分享到:

《郑州大学学报(医学版)》[ISSN:1671-6825/CN:41-1340/R]

卷:
期数:
2011年06期
页码:
872
栏目:
论著
出版日期:
2011-11-20

文章信息/Info

Title:
Effects of dlbutylphthalide on expressions of TRPM2 and EndoG in brain tissues of aged rats with chronic cerebral ischemia
作者:
张会芳1) 卢宏1)#焦淑洁1)刘希2)
1)郑州大学第一附属医院神经内科 郑州 450052 2)郑州大学第五附属医院神经内科 郑州 450052
Author(s):
ZHANG Huifang1)LU Hong1)JIAO Shujie1)LIU Xi2)
1)Department of Neurology,the First Affiliated Hospital,Zhengzhou University,Zhengzhou 450052 2)Department of Neurology,the Fifth Affiliated Hospital,Zhengzhou University,Zhengzhou 450052
关键词:
瞬时感受器电位M2型核酸内切酶G慢性脑缺血丁基苯酞大鼠
Keywords:
transient receptor potential melastain 2endonuclease Gchronic cerebral ischemiadlbutylphthaliderat
分类号:
R743
摘要:
目的:研究丁基苯酞(NBP)对老龄大鼠慢性脑缺血脑组织瞬时感受器电位M2型(TRPM2)及核酸内切酶G(EndoG)表达的影响。方法:80只老龄Wistar大鼠随机分为4组,每组20只,分别为假手术组、模型组、NBP低剂量治疗组和NBP高剂量治疗组。采用双侧颈总动脉永久结扎建立慢性脑缺血模型。3个月后,HE染色观察脑组织形态学变化,免疫组化SP法染色检测TRPM2 和 EndoG的表达变化。结果:各组大鼠脑皮层与海马区组织TRPM2和EndoG表达比较,差异有统计学意义(F=310.046、127.115、49.959和80.292,P均<0.05)。模型组皮质和海马TRPM2、EndoG表达较假手术组增多(P<0.05),而NBP低剂量和高剂量治疗组较模型组减少(P<0.05),NBP高剂量组较低剂量治疗组降低更加明显(P<0.05)。结论:NBP可能通过下调TRPM2和EndoG的表达,抑制细胞损伤和死亡,发挥对慢性缺血性脑组织的神经保护作用。
Abstract:
Aim:To investigate the influences of dlbutylphthalide(NBP) on the expressions of transient receptor potential melastain 2(TRPM2) and endonuclease G (EndoG) after chronic cerebral ischemia in aged rats. Methods:A total of 80 aged male Wistar rats were randomly divided into 4 groups,shamoperated group, model group,lowdose NBPtreated group and highdose NBPtreated group. Chronic cerebral ischemia model was based on permanent bilateral occlusion of both common carotid arteries.The rats were sacrificed after 3 months.The changes of morphology of brain were observed by HE staining and the expressions of TRPM2 and EndoG were observed by immunohistochemistry.Results:The expressions of TRPM2 and EndoG in cortex and hippocampus of the four groups were significantly different (F=310.046,127.115,49.959,and 8.292,P<0.05). The expressions of TRPM2 and EndoG in cortex and hippocampus of model group were more than those of shamoperated group,and those of low and high dose NBPtreated groups were significantly less than those of model group(P<0.05),and the high dose group changed more apparently.Conclusion:NBP may have neuroprotective effects,which may result from its decreasing the expression of TRPM2 and EndoG after chronic ischemia,thus inhibiting the injury and death of the cells.

参考文献/References:

[1]吴航宇,梁华平.TRP离子通道在炎症反应中的调控作用[J].中国急救医学杂志,2009,29(10):944 [2]Lorenzo HK,Susin SA.Mitochondrial effectors in caspaseindependent cell death[J]. Febs Letters,2004,557(1/3):14 [3]Chong ZZ,Feng YP.Dl3nbutylphthalide attenuates reperfusioninduced bloodbrain barrier damage after focal cerebral ischemia in rats[J].Zhongguo Yao Li Xue Bao,1999,20(8):696 [4]Ohta H,Nishikawa H,Kimura H,et al.Chronic cerebral hypoperfusion by permanent internal carotid ligation produces learning impairment without brain damage in rats[J].Neuroscience,1997,79(4):1039 [5]Naziroglu M.TRPM2 cation channels,oxidative stress and neurological diseases:where are we now?[J].Neurochem Res,2011,36(3):355 [6]Ikonomidou C,Turski L.Why did NMDA receptor antagonists fail clinical trials for stroke and traumatic brain injury?[J].Lancet Neurol,2002,1(6):383 [7]PartidaSanchez S, Cockayne DA, Monard S, et al. Cyclic ADPribose production by CD38 regulates intracellular calcium release, extracellular calcium influx and chemotaxis in neutrophils and is required for bacterial clearance in vivo[J].Nat Med,2001,7(11):1209 [8]Hou ST, MacManus JP. Molecular mechanisms of cerebral ischemiainduced neuronal death[J]. Int Rev Cytol,2002,221:93 [9]LI LY,Luo X,Wang X.Endonuclease G is an apoptotic DNase when released from mitochondia[J].Nature,2001,412(6842):95 [10]Hara Y,Wakamori M,Ishii M,et al.LTRPC2 Ca2+ permeable channel activated by changes in redox status confers susceptibility to cell death[J].Mol Cell,2002,9(1):163 [11]韩恩吉,韩淑英.神经细胞凋亡与胞浆钙离子[J].中风与神经疾病杂志,1999,16(3):131 [12]Ishitsuka K,Hideshima T,Hamasaki M,et al.Novel inosine monophosphate dehydrogenase inhibitor VX944 induces apoptosis in multiple myeloma cells primarily via caspaseindependent AIF/Endo G pathway[J].Oncogene,2005,24(38):5888 [13]Kim JS, Lee JH,Jeong WW,et al.Reactive oxygen speciesdependent EndoG release mediates cisplatininduced caspaseindependent apoptosis in human head and neck squamous carcinoma cells[J].Int J Cancer,2008,122(3):672 [14]Wang X.The expanding role mitochondria in apoptosis[J].Genes Dev,2001,15(22):2922

备注/Memo

备注/Memo:
#通讯作者,女,1965年4月生,博士,教授 ,研究方向:脑血管及多发性硬化等神经系统疾病,Email:zhiyusong@yeah.net
更新日期/Last Update: 1900-01-01