纳洛酮对大鼠脑缺血再灌注后JNK3蛋白表达的影响

中国临床药理学与治疗学 ›› 2013, Vol. 18 ›› Issue (3): 258-262.

纳洛酮对大鼠脑缺血再灌注后JNK3蛋白表达的影响

田和平, 褚正民, 金成胜, 沈建国

嘉兴市第二医院神经外科,嘉兴 314000, 浙江

收稿日期:2012-05-25 修回日期:2012-09-04 出版日期:2013-03-26 发布日期:2013-04-02
通讯作者: 褚正民,通信作者,男,主任医师,研究方向:脑损伤与修复的临床研究。Tel: 13505730668 E-mail: chuzhengmin@msn.com
作者简介:田和平,男,医学硕士,研究方向:中枢神经损伤与修复的基础研究。Tel: 15825707125 E-mail: grantnw@163.com

Effects of naloxone on the expressions of JNK3 protein in rats after ischemia-reperfusion

TIAN He-ping, CHU Zheng-min, JIN Cheng-shen, SHEN Jian-guo

Department of Neurosurgery, the Second Hospital of Jiaxing, Jiaxing 314000, Zhejiang, China

Received:2012-05-25 Revised:2012-09-04 Online:2013-03-26 Published:2013-04-02

摘要/Abstract

摘要： 目的: 观察纳洛酮对脑缺血再灌注损伤后海马区c-jun氨基末端激酶3(JNK3)表达的影响,探讨纳洛酮的脑保护作用机制。方法: 采用线栓法制造大鼠局灶性脑缺血再灌注模型,将SD大鼠随机分为假手术组、缺血再灌注对照组、小剂量纳洛酮给药组、高剂量纳洛酮给药组、SP600125(JNK3抑制剂)给药组及其溶剂组;采用氯化三苯基四氮唑(TTC)染色法检测大鼠缺血再灌注后脑梗死范围;采用免疫印迹法检测海马区JNK3的磷酸化水平。结果: 高剂量纳洛酮干预组、SP600125干预组与缺血再灌注组相比脑梗死范围缩小,蛋白JNK3磷酸化水平显著降低;随着干预剂量增加,纳洛酮抑制蛋白JNK3磷酸化水平作用增强。结论: 纳洛酮通过抑制脑缺血再灌注损伤后JNK3的磷酸化激活参与了对脑组织的部分保护性作用,其作用呈剂量依赖性。

关键词: 纳洛酮, 脑缺血再灌注, c-jun氨基末端激酶3

Abstract: AIM: To investigate the effect of naloxone on the expression of JNK3 protein in Hippocampus during transient focal cerebral ischemia reperfusion, and to discuss the probable mechanism of its protective effect.METHODS: The model of focal cerebral ischemia-reperfusion injury was established in rats by suture-occluded method. Rats were randomly divided into several groups, including Sham-operation, ischemia-reperfusion, low dose naloxone treated ischemia-reperfusion, high dose naloxone treated schemia-reperfusion, SP600125 treated ischemia-reperfusion and respective Vehicle treated ischemia-reperfusion. The infarction volume was detected by TTC staining. Western Blot was operated to detect expression of p-JNK3 in Hippocampus.RESULTS: Both groups of high dose naloxone treated ischemia-reperfusion and SP600125 treated ischemia-reperfusion, not only ischemia-reperfusion infarction volume was reduced, but also expression of p-JNK3 was down-regulated, compared with ischemia-reperfusion only group. As the dose increase, the effect of naloxone on inhibiting expression of p-JNK3 was obviously improved.CONCLUSION: Naloxone inhibits the expression of p-JNK3 in a dose-dependent manner during focal ischemia reperfusion which may be one of the mechanisms of its neuroprotective function.

Key words: Naloxone, Cerebral ischemia-reperfusion, c-Jun N-terminal kinase 3

中图分类号:

R965.2

田和平, 褚正民, 金成胜, 沈建国. 纳洛酮对大鼠脑缺血再灌注后JNK3蛋白表达的影响[J]. 中国临床药理学与治疗学, 2013, 18(3): 258-262.

TIAN He-ping, CHU Zheng-min, JIN Cheng-shen, SHEN Jian-guo. Effects of naloxone on the expressions of JNK3 protein in rats after ischemia-reperfusion[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2013, 18(3): 258-262.

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