首页> 中文期刊> 《中国老年学杂志》 >电针对局灶性脑缺血大鼠神经行为学及酪氨酸激酶JAK2的影响

电针对局灶性脑缺血大鼠神经行为学及酪氨酸激酶JAK2的影响

         

摘要

目的:研究电针对局灶性脑缺血大鼠神经行为学及缺血侧皮质JAK2 mRNA表达的影响。方法按区组随机化法将250只SD大鼠分为假手术组、模型组、电针组、AG490组、电针+AG490组,根据不同缺血时间段又分为2 h、1、3、7和21 d五个小组。采用热凝闭大脑中动脉建立局灶性脑缺血模型,电针取“百会”、“大椎”穴,AG490采用侧脑室注射。通过原位杂交的方法检测缺血侧皮质JAK2 mRNA表达变化。结果在假手术组大鼠脑组织中未发现明显JAK2 mRNA表达;模型组JAK2 mRNA同时间段与假手术组比较表达量均增多(P<0.01),其中以1 d组表达量增高最为显著;电针治疗与AG490干预可降低JAK2 mRNA表达(P<0.05),以1 d、3 d较为显著。 JAK2 mRNA表达变化上与脑缺血大鼠的神经行为学评分改变基本呈一致性。结论脑缺血后JAK2的超量表达及其活化,可能为脑损伤加重的机制之一。脑缺血后电针治疗可下调JAK2的表达水平,降低其磷酸化活性,阻断JAK2诱导的信号转导通路的异常激活。%Objective To explore the electro-acupuncture effect on neuroethology and the expression of tyrosine kinase-JAK 2 of is-chemic cortex in rats with the focal cerebral ischemia .Methods The 250 SD rats were randomly divided into sham , model, electroa acu-puncture ( EA) , AG490 and EA+AG490 groups.The model of focal cerebral ischemia was established by the heat-coagulation induced the occlusion of the middle cerebral artery.The electro-acupuncture were applied on Baihui (GV20) and Dazhui (GV14), and AG490 were ap-plied by intracerebroventricular infusion .The expression of JAK2 mRNA in the ischemic cortex was observed by in situ hybridization .Results There was no obvious expression of JAK 2 mRNA found in sham group.In the model group, the expression of JAK2 mRNA was increased (P<0.01).After 1d of cerebral ischemia, the expression of JAK2 mRNA had reached the peak.Electro-acupuncture treatment and AG490 intervention could down-regulate the expression of JAK 2 mRNA ( P<0.05 ) , especially in 1 d and 3 d groups.After cerebral ischemia , the expression of JAK2 mRNA was consistent with the neurological deficits score and cerebral pathomorphological changes .Conclusions After cerebral ischemia, the excessive expression of JAK2, and the JAK2 phosphorylation would be one of mechanisms which the brain injury gets worse.The therapy of electro-acupuncture could reduce the expression of JAK 2, and inhibit JAK2 phosphorylated activation , so as to block the abnormal activation of signal transduction pathway which induced by JAK 2.

著录项

相似文献

  • 中文文献
  • 外文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号