• 早期强化运动训练与电针治疗对脑缺血再灌注后大鼠神经功能恢复的作早期强化运动训练与电针治疗对脑缺血再灌注后大鼠神经功能恢复的作用
  • A comparative study on neural functional recovery between early intensive training and electroacupuncture treatment after cerebral ischemia reperfusion in rats
  • 马冉冉.早期强化运动训练与电针治疗对脑缺血再灌注后大鼠神经功能恢复的作早期强化运动训练与电针治疗对脑缺血再灌注后大鼠神经功能恢复的作用[J].内科急危重症杂志,2019,25(3):227-231
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    DOI:10.11768/nkjwzzzz20190316
    中文关键词:  脑卒中  康复  电针  轴突再生  GAP-43  Neurocan
    英文关键词:
    基金项目:西安市科技计划项目[No:SF1319(4)]
    作者单位E-mail
    马冉冉 西安市第九医院 junxiangao45266@sohu.com 
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    中文摘要:
          目的:观察早期强化运动训练与电针治疗对局部脑缺血大鼠再灌注后神经功能恢复的疗效并探讨其机制。方法:将65只健康成年SD雄性大鼠随机分为假手术组(5只)、大脑中动脉闭塞再灌注(MCAO)模型组(20只)、电针组(20只)、强化运动训练组(20只)。用线栓法建立右侧MCAO模型,电针组选取人中、百会穴给予电针刺激。强化运动训练组采用跑笼运动试验,观察4组大鼠的运动功能。选取24h、3d、7d、14d4个时间点,应用免疫组化方法检测脑缺血区皮层GAP-43及Neurocan阳性细胞的表达情况。采用神经症状评分评价造模情况及神经功能的恢复情况,TTC(2,3,5-三苯基氯化四氮唑)染色观察大鼠局部脑缺血再灌注后梗死体积的大小。结果: 2周后,强化运动训练组及电针组的神经症状评分明显低于模型组(P<0.05),并高于假手术组(P<0.05);强化运动训练组及电针组的脑梗死体积明显小于模型组(P<0.05),电针组与运动训练组比较差异无统计学意义。结论:脑缺血再灌注后早期强化运动训练或电针刺激能够减小脑梗死体积,促进脑缺血大鼠神经功能的恢复。早期康复治疗可上调脑缺血区GAP-43表达与下调Neurocan表达,可能是其促进脑损伤区中枢神经修复的重要机制之一。
    英文摘要:
          Objective: To compare the effects of the early intensive training (EIT) and electroacupuncture (EA) therapy on the nerve functional recovery and infarction volume after local cerebral ischemia reperfusion in rats, and investigate the mechanism of promoting the functional recovery. Methods: Sixty-five healthy adult male SD rats were randomly divided into sham-operated group (n=5), MCAO group (n=20), EA group (n=20), and EIT group (n=20). MCAO was made by nylon monofilament suture. The rats in the EA group received EA treatment at the acupoints Renzhong+Baihui after MCAO. The animals in the EIT group received treadmill running to observe the recovery of motor function. The rats were randomly fallen into different time points (24h, 3days, 7days, and 14days after reperfusion). The successful establishment of models and the neural functional recovery were evaluated by Longa's score. TTC staining was used to observe the size of the infarct volume after local cerebral ischemia reperfusion in rats. Immunohistochemistry was used to detect the expression of GAP-43 and Neurocan in the ischemic cortex. Results: The Longa scores were significantly lower in both EIT group and EA group than in model group (P<0.05), but significantly higher than in sham-operated group (P<0.05). The infarct volume in EIT group and EA group was significantly smaller than in model group (P<0.05), but there was no significant difference between EA group and EIT group. Conclusion: The EIT or EA therapy can reduce the size of the infarct volume and promote the recovery of neurological function after local cerebral ischemia reperfusion in rats. Early rehabilitation treatment could up-regulate the expression of GAP-43, and down-regulate the Neurocan expression, which may be one of the important mechanisms of promoting the axon regeneration in the cerebral injured area after cerebral infarction.