基础医学与临床 ›› 2019, Vol. 39 ›› Issue (9): 1239-1242.

• 研究论文 • 上一篇    下一篇

食欲素-A降低大鼠脑缺血-再灌注损伤

孔婷婷1,刘明慧2,王琴琴2,姜云璐2,王春梅2   

  1. 1. 山东大学
    2. 济宁医学院
  • 收稿日期:2018-09-17 修回日期:2018-12-24 出版日期:2019-09-05 发布日期:2019-09-06
  • 通讯作者: 王春梅 E-mail:wangchunmei410@163.com
  • 基金资助:
    Orexin-A/B对缺血性脑中风的神经保护作用及其机制研究;济宁医学院教师科研扶持基金;山东省自然科学基金;济宁医学院教师扶持基金

Orexin-A reduces cerebral ischemia-reperfusion injury in rats

  • Received:2018-09-17 Revised:2018-12-24 Online:2019-09-05 Published:2019-09-06

摘要: 目的 探讨食欲素-A(orexin-A, OA)对大鼠脑缺血-再灌注(I/R)损伤的保护作用及其可能的机制。方法 将大鼠随机分为假手术组(sham)、缺血-再灌注组(I/R)、10 、30 和50 μg/kg OA干预组;用2,3,5-氯化三苯基四氮唑(TTC)染色法检测脑梗死体积;用ELISA检测脑皮层组织中IL-6、TNF-α 和超氧化物歧化酶SOD水平;用Western blot检测p-JNK的表达。结果 与sham组相比,I/R组出现明显的梗死灶,30和50 μg/kg OA干预后,脑梗死灶体积明显降低(p<0.001)。与sham组相比,I/R组IL-6和TNF-α的含量明显升高(p<0.05),30和50 μg/kg OA干预后,IL-6和TNF-α的含量均明显降低(p<0.05);I/R组SOD的活性也明显降低(p<0.05),30和50 μg/kg OA干预后,SOD的活性均明显增加(p<0.05)。与sham组相比,I/R组p-JNK的表达增高(p<0.05),30和50 μg/kg OA干预后均降低了p-JNK的表达(p<0.05)。结论 OA可能是通过抑制炎性反应因子和增强抗氧化而发挥对大鼠脑I/R损伤的神经保护作用。

关键词: 关键词:脑缺血-再灌注损伤, Orexin-A, 炎症反应, 氧化应激

Abstract: Objective To investigate the protective effect of orexin-A (OA) on cerebral ischemia-reperfusion (I/R) injury in rats and its possible mechanism. Methods Rats were randomly divided into sham operation group (sham), ischemia-reperfusion group (I/R), 10, 30 and 50 μg/kg OA intervention group. 2,3,5-triphenylte-trazolium chloride (TTC) staining method was used to detect the cerebral infarction volume. ELISA method was used to detect the level of IL-6, TNF-α and SOD in cerebral cortex of rats, and Western blot was used to detect the expression of p-JNK. Results The I/R group had obvious infarct foci compared with the sham group, but the cerebral infarct volume significantly decreased after 30 and 50 μg/kg OA intervention (p<0.001), respectively. Compared with sham group, the levels of IL-6 and TNF-α in I / R group were significantly higher than those in sham group (p<0.05). After 30 and 50 μg/kg OA intervention, IL-6 and TNF-α levels were significantly decreased (p<0.05). The activity of SOD in I/R group was also significantly decreased (p<0.05). After 30 and 50 μg/kg OA intervention, the activity of SOD was significantly increased (p<0.05). Compared with sham group, the expression of p-JNK in I/R group was higher than that in sham group (p<0.05), yet the expression of p-JNK was decreased after 30 and 50 μg/kg OA intervention (p<0.05). Conclusion OA may play a neuroprotective role in cerebral I/R injury by inhibiting inflammatory factors and enhancing antioxidant activity.

Key words: Key words: Cerebral ischemia-reperfusion injury, Orexin-A, Inflammatory reactions, Oxidative stress

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