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中国应用生理学杂志 ›› 2020, Vol. 36 ›› Issue (5): 452-455.doi: 10.12047/j.cjap.6001.2020.096

• 研究论文 • 上一篇    下一篇

利格列汀对小鼠脑缺血/再灌注损伤的神经保护作用*

赵波1, 魏海萍2△   

  1. 1.甘肃省平凉市第二人民医院神经内科, 平凉 744000;
    2.兰州大学第二医院神经内科, 兰州 730030
  • 收稿日期:2020-01-06 修回日期:2020-07-24 发布日期:2021-02-25
  • 通讯作者: Tel: 15117243002; E-mail: haipingwei11@sina.com
  • 基金资助:
    *兰州大学第二医院萃英科技创新计划应用基础研究(CY2018-QN04)

Neuroprotective effects of linagliptin on ischemia/reperfusion in mice

ZHAO Bo1, WEI Hai-ping2△   

  1. 1. Department of Neurology, the Second People's Hospital of Pingliang City, Pingliang 744000;
    2. Department of Neurology, the Second Hospital of Lanzhou University, Lanzhou 730030, China
  • Received:2020-01-06 Revised:2020-07-24 Published:2021-02-25

摘要: 目的: 评估二肽基肽酶4(DPP-4)抑制剂利格列汀对小鼠脑缺血/再灌注(I/R)损伤的神经保护作用。方法: BALB/c小鼠随机分为Sham组、I/R组和利格列汀(2.5、5和10 mg/kg) +I/R组,每组均为8只小鼠。不同剂量利格列汀组小鼠均在I/R前3周连续灌胃给药。采用小鼠脑中动脉闭塞(MCAO)1 h诱导I/R损伤模型,再灌注24 h评估神经功能缺损(n=8)和及梗死体积(n=4);再灌注48 h处死小鼠,检测脑组织中谷胱甘肽(GSH)、丙二醛(MDA)、磷酸化肌醇3激酶(PI3K)、磷酸化蛋白激酶 B(p-Akt)和雷帕霉素靶蛋白(mTOR)含量(n=4)。结果: 与I/R组相比,利他列汀预处理组小鼠再灌注24 h后,神经功能缺损评分和梗死体积明显降低(P<0.05);小鼠再灌注48 h后,脑内MDA含量明显降低(P<0.05),而GSH、PI3K、p-Akt和mTOR水平明显升高(P<0.05)。结论: 利格列汀对I/R小鼠具有神经保护作用,可能是通过激活PI3K/AKT/mTOR通路发挥的作用。

关键词: 利格列汀, 缺血/再灌注损伤, 磷脂酰肌醇3-激酶/蛋白激酶B/哺乳动物雷帕霉素靶蛋白通路, 小鼠

Abstract: Objective: To evaluate the neuroprotective effects of linagliptin, a dipeptidyl peptidase-4(DPP-4) inhibitor, on cerebral ischemia/reperfusion(I/R) injury in mice. Methods: BALB/c mice were randomly divided into Sham group, I/R group and linagliptin (2.5, 5 and 10 mg/kg) +I/R group, 8 mice in each group. The mice in the linagliptin group were administrated by gavage 3 weeks before I/R. I/R injury model was induced by MCAO, neurological deficit scores(n=8) and infarct volume(n=4) were assessed 24 h following reperfusion. Forty-eight hours following reperfusion, mice were euthanized, the contents of glutathione (GSH), malondialdehyde (MDA), phosphoinositide 3 kinase (PI3K), phosphoprotein kinase B (p-Akt) and rapamycin target protein (mTOR) in brain tissue were measured (n=4). Results: Compared with the I/R group, the neurological deficit score and infarct volume were significantly decreased in the linagliptin pretreatment group after 24 h reperfusion (P<0.05); the MDA content in the brain was significantly decreased (P<0.05), while the GSH, PI3K, p-Akt and mTOR levels were significantly increased (P<0.05). Conclusion: This study proves that linagliptin exerted a neuroprotective effect in I/R mice, which may be mediated by activation of the PI3K/AKT/mTOR pathway.

Key words: linagliptin, ischemia/reperfusion, PI3K/AKT/mTOR pathway, mice

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