基础医学与临床 ›› 2018, Vol. 38 ›› Issue (3): 340-343.

• 研究论文 • 上一篇    下一篇

食欲素-B抑制大鼠脑缺血再灌注损伤

徐超1,王春梅2,白波2   

  1. 1. 山东大学
    2. 济宁医学院
  • 收稿日期:2017-10-11 修回日期:2017-12-19 出版日期:2018-03-05 发布日期:2018-02-27
  • 通讯作者: 白波 E-mail:bbai@mail.jnmc.edu.cn
  • 基金资助:
    国家自然青年基金;山东省自然基金项目

Orexin-B inhibits cerebral ischemia reperfusion injury in rats

  • Received:2017-10-11 Revised:2017-12-19 Online:2018-03-05 Published:2018-02-27
  • Supported by:
    The National Natural Youth Fund;Shandong Province Natural Science Foundation Project

摘要: 目的 研究食欲素-B(Orexin-B,OXB)对大鼠脑缺血再灌注的神经保护作用及其分子机制。方法 制备大鼠大脑中动脉栓塞模型(MCAO),将大鼠随机分为:假手术组(contral)、缺血再灌注组(I/R)、缺血再灌注+PBS组(I/R+PBS)和缺血再灌注+Orexin-B组(I/R+OXB);通过神经功能评分确定模型是否成功;TTC染色法测定大鼠脑梗死体积;Western blot检测海马区食欲素受体2(OX2R)、p-AKT和p-GSK-3β蛋白表达;跳台实验检测大鼠学习与记忆。结果 I/R组海马中OX2R及p-AKT蛋白表达较对照组减少(p<0.05),p-GSK-3β蛋白表达增加(p<0.05),而I/R+OXB组上述变化明显减轻(p<0.05);I/R+OXB组脑梗死体积明显减少I/R组潜伏期时间减少,错误次数增多(p<0.05),而I/R+OXB组上述变化显著减小(p<0.05)。结论 食欲素-B抑制脑缺血再灌注损伤,可能与增强p-AKT活性、抑制p-GSK-3β活性有关。

关键词: 食欲素B, 脑缺血再灌注, 神经保护, 磷酸化蛋白激酶B, 糖原合成酶激酶3β

Abstract: Objective To study the neuroprotective effect of Orexin-B on rat model of cerebral ischemia-reperfusion injury and its molecular mechanism. Methods The artery occlusion model of male Wister rats (Middle cerebral artery occlusion, MCAO) was established which has been ischemic 2h and reperfusion 24h. Rats were randomly divided into Sham group (Sham), ischemia-reperfusion group (I/R), ischemia-reperfusion +PBS group (I/R+PBS), and ischemia-reperfusion +Orexin -B group (I/R+OXB). The neurological deficit scores were processed to inclusion and exclusion. Infarct size was determined by TTC staining; Using western blot, the expressions of Orexin receptor 2,p-AKT, p-GSK-3β proteins in hippocampus were detected; Jumping test was used to detect learning and memory abilities in rats. Results Orexin-B significantly reduce the volume of cerebral infarction in TTC staining; Orexin-B group was significantly increased the expression of Orexin Receptor 2as well as p-AKT,which decreased p-GSK-3β (P<0.05), compared with the untreated group. Furthmore, the Orexin-B treated group can improve the latency period and decline the mistakes in rat Jumping test (P<0.05). Conclusions The neuroprotective effect of Orexin-B in cerebral ischemia-reperfusion injury may enhance p-AKT activity and inhibit p-GSK-3β activity, which might increase the proliferation of neurons and improve the cerebral blood glucose concentration.

Key words: Orexin-B, brain ischemia-reperfusion, neuroprotection, phosphorylation of protein kinase b, glycogen synthase kinase 3β

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