醒脑静固体制剂对缺血性脑损伤大鼠恢复早期的保护作用

刘洋; 孙建宁; 董世芬; 刘明; 张易; 杜守颖

doi:10.13422/j.cnki.syfjx.2012.16.033

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醒脑静固体制剂对缺血性脑损伤大鼠恢复早期的保护作用

药理 | 更新时间：2024-09-23

- 醒脑静固体制剂对缺血性脑损伤大鼠恢复早期的保护作用
- Protective Effect of Solid Preparation of Xingnaojing from Neurological Defect and Oxidative Damage in pMCAO Model Rats in Early Convalescence
- 中国实验方剂学杂志 2012年18卷第16期页码：175-180
- 作者机构：
  
  1. 北京中医药大学中药学院
  2. 贵阳中医学院
- 作者简介：
- 基金信息：
  
  重大新药创制科技重大专项（2009ZX09502-008,2009ZX09308-003）
- DOI：10.13422/j.cnki.syfjx.2012.16.033
  中图分类号： R285.5
- 纸质出版日期：2012
- 稿件说明：
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[1]刘洋,孙建宁,董世芬,刘明,张易,杜守颖.醒脑静固体制剂对缺血性脑损伤大鼠恢复早期的保护作用[J].中国实验方剂学杂志,2012,18(16):175-180.

LIU Yang1, SUN Jian-ning1, DONG Shi-fen1, et al. Protective Effect of Solid Preparation of Xingnaojing from Neurological Defect and Oxidative Damage in pMCAO Model Rats in Early Convalescence[J]. Chinese journal of experimental traditional medical formulae, 2012, 18(16): 175-180.
[1]刘洋,孙建宁,董世芬,刘明,张易,杜守颖.醒脑静固体制剂对缺血性脑损伤大鼠恢复早期的保护作用[J].中国实验方剂学杂志,2012,18(16):175-180. DOI： 10.13422/j.cnki.syfjx.2012.16.033.

LIU Yang1, SUN Jian-ning1, DONG Shi-fen1, et al. Protective Effect of Solid Preparation of Xingnaojing from Neurological Defect and Oxidative Damage in pMCAO Model Rats in Early Convalescence[J]. Chinese journal of experimental traditional medical formulae, 2012, 18(16): 175-180. DOI： 10.13422/j.cnki.syfjx.2012.16.033.

摘要

目的:初步研究醒脑静固体制剂对缺血性脑损伤大鼠恢复早期的保护作用及其作用机制。方法:线拴法制备永久性局灶性中动脉阻断脑缺血（pMCAO）大鼠模型

分为模型组、醒脑静12

50 mg.kg-1剂量组

丁苯酞（NBP）70 mg.kg-1组

ig给药12 d并设假手术组。在术后3

14 d

检测动物平衡能力、缺血前肢触觉、前肢肌肉张力等指标的改善状况

取材并测定动物缺血侧脑组织超氧化物歧化酶（SOD）活性和丙二醛（MDA）含量。结果:与假手术组相比

pMCAO模型动物表现出神经功能缺损症状

在缺血后3 d横木行走评分降低65%

撕除胶布潜伏期增加13.9倍

前肢拉力减小39.7%（P<0.01）。其中

醒脑静12

50 mg.kg-1在缺血后6～14 d分别降低神经功能缺损评分（P<0.05或P<0.01）

提高横木行走能力评分（P<0.05或P<0.01）

缩短撕除潜伏期（P<0.05或P<0.01）

提高前肢抓握力（P<0.05或P<0.01）。同时醒脑静可显著降低缺血侧脑组织中MDA含量（P<0.01）。结论:醒脑静固体制剂对缺血性脑损伤恢复早期大鼠模型具有一定保护作用

其作用机制可能与抑制脂质过氧化反应产物MDA含量

从而减轻氧化损伤有关。

Abstract

Objective:To investigate protective effect of solid preparation of Xingnaojing（XNJ） in middle cerebral artery occlusion（MCAO） model in rats

and explore related mechanism.Method: Cerebral middle artery was occluded with nylon suture to establish permanent middle cerebral artery occlusion（pMCAO） model.Rats with occlusion were randomly divided into model group

XNJ 12

50 mg · kg-1 groups

and Butylphthalide（NBP） 70 mg · kg-1 group

which were ig administered for 12 days

taking rats underwent same procedure except artery occlusion as the sham group.At day of 3

14 from the occlusion

four different neurological tests were applied to all animals: neurological defects score

beam-walking test

tape-removal test

and pulling-force test

with regard to detection of sensorimotor defects

motor coordination defects

and strength of forelimbs.At the 14th day

superoxide dismutase（SOD） activity and malondialdehyde（MDA） content in ischemic cerebral tissues were measured after neurological tests.Result: Compared with the sham group

there were obvious neurological defects in pMCAO model rats.At the 3rd day after occlusion

score of beam-walking test in the model group reduced by 65%（P<0.01）

time for tape-removing increased 13.9 times（P<0.01）

as well as strength of forelimbs reduced to 39.7%（P<0.01）.From 6th day to 14th day after occlusion

compared with the model group

in the 12

50 mg · kg-1 dose-groups of XNJ

neurological defects scores reduced（P<0.05

P<0.01）

scores for beam-walking test improved（P<0.05

P<0.01）

time for tape-removing shortened（P<0.05

P<0.01）

strength of forelimbs increased（P<0.05

P<0.01）.In addition

content of MDA in the ischemic brain tissue of all dose-groups of XNJ significantly reduced（P<0.01）.Conclusion: Solid preparation of XNJ has protective effect on permanent cerebral ischemia model in rats.In early convalescence after pMCAO

it is able to improve recovery of neurological defects in rat

which might relate to its inhibition on generation of MDA to alleviate oxidative stress.

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