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中国临床药理学与治疗学 ›› 2007, Vol. 12 ›› Issue (9): 1032-1036.

• 基础研究 • 上一篇    下一篇

刺五加注射液对大鼠脑缺血损伤保护机制的研究

关利新1, 翟凤国1, 衣欣1, 苏云明2   

  1. 1牡丹江医学院药学系药理教研室, 牡丹江157011, 黑龙江;
    2黑龙江中医药大学药理教研室, 哈尔滨150040, 黑龙江
  • 收稿日期:2007-03-21 修回日期:2007-09-17 出版日期:2007-09-26 发布日期:2020-10-30
  • 通讯作者: 苏云明, 男, 教授, 博士生导师, 主要从事中药药理的研究。Tel:0451-82196314
  • 作者简介:关利新, 男, 在读博士, 教授, 研究方向:心脑血管药理学。Tel:13945327008 E-mail:glx1960@yahoo.com.cn

Study on protection of acanthopanax senticosus injection to focal cerebral ischemia in rats

GUAN Li-xin1, ZHAI Feng-guo1, YI Xin1, SU Yun-ming2   

  1. 1Department of Pharmacology, Mudanjiang Medical College, Mudanjiang 157011, Heilongjiang, China;
    2Department of Pharmacology, Heilongjiang University of Chinese Medicine, Harbin 150040, Heilongjiang, China
  • Received:2007-03-21 Revised:2007-09-17 Online:2007-09-26 Published:2020-10-30

摘要: 目的:研究刺五加注射液对大鼠脑缺血损伤的保护机制。方法:Wistar 大鼠随机分为假手术组、脑缺血模型组和刺五加注射液组(45、90 mg/kg), 腹腔注射给药, 连续7 d。末次给药后30 min, 采用大鼠大脑中动脉内栓线阻断法制备局灶性脑缺血损伤24 h 模型, 通过硫代巴比妥酸法、化学比色法、TUNEL 及免疫组化等方法, 观察刺五加注射液对脑缺血损伤大鼠脑组织丙二醛(MDA) 含量和超氧化物歧化酶(SOD) 活性、大脑皮质区细胞调亡及bcl-2、bax 和caspase-3 基因蛋白表达的影响。结果:刺五加注射液(45、90 mg/kg) 可明显降低MDA 含量, 提高SOD 活性, 抑制神经细胞调亡, 增加bcl-2 蛋白表达,减少bax 和caspase-3 蛋白表达。结论:刺五加注射液对脑缺血损伤的保护机制可能与抗自由基、抑制细胞调亡有关。

关键词: 刺五加注射液, 脑缺血, 自由基, 细胞凋亡

Abstract: AIM: To investigate the protective mechanism of acanthopanax senticosus injection (ASI) on focal cerebral ischemia injury in rats.METHODS: Wistar rats were randomly divided into sham operated group, model control group and two ASI groups, to which ASI of 45 and 90 mg/kg was intraperitoneally administered for 7d, and then subjected to cerebral ischemia injury induced by middle cerebral artery occlusion (MCAO) in rats, via string ligation of arteria carotis interna.The content of maleic dialdehyde (MDA) was determined by thibabituric acid (TBA) test and the activity of superoxide dismutase (SOD) was detected by chemical colorimetry test in cerebral tissues.Apoptosis in cortex region was measured with TUNEL method.Bcl-2, bax and caspase-3 protein expression of neurons was detected with immunohistochemistry staining in cortex region.RESULTS: ASI (45, 90 mg/kg) could significantly decrease the content of MDA and increase the activity of SOD, and inhibit the neuronal apoptosis.ASI (45, 90 mg/kg) could increase the expression of bcl-2 protein, and reduce the expression of bax and caspase-3 protein significantly.CONCLUSION: The protective mechanism of ASI on focal cerebral ischemia injury may be related to anti-free radical effect and inhibition of neuron apoptosis.

Key words: acanthopanax senticosus injection, cerebral ischemia, free radical, apoptosis

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