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CJAP ›› 2020, Vol. 36 ›› Issue (5): 452-455.doi: 10.12047/j.cjap.6001.2020.096

• ORIGINAL ARTICLES • Previous Articles     Next Articles

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

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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