• Scot Med J · Feb 2021

    Retracted Publication

    Metformin prevents brain injury after cardiopulmonary resuscitation by inhibiting the endoplasmic reticulum stress response and activating AMPK-mediated autophagy.

    • Libo Chuan, Lei Zhang, Hao Fu, Ying Yang, Quanyu Wang, Xingpeng Jiang, Zhengchao Li, Kuang Ni, and Li Ding.
    • Attending Physician, Faculty of Life Science and Biotechnology, Kunming University of Science and Technology, P.R. China.
    • Scot Med J. 2021 Feb 1; 66 (1): 162216-22.

    Background And AimsThe neurological damage caused by cardiac arrest (CA) can seriously affect quality of life. We investigated the effect of metformin pretreatment on brain injury and survival in a rat CA/cardiopulmonary resuscitation (CPR) model.Methods And ResultsAfter 14 days of pretreatment with metformin, rats underwent 9 minutes of asphyxia CA/CPR. Survival was evaluated 7 days after restoration of spontaneous circulation; neurological deficit scale (NDS) score was evaluated at days 1, 3, and 7. Proteins related to the endoplasmic reticulum (ER) stress response and autophagy were measured using immunoblotting. Seven-day survival was significantly improved and NDS score was significantly improved in rats pretreated with metformin. Metformin enhanced AMPK-induced autophagy activation. AMPK and autophagy inhibitors removed the metformin neuroprotective effect. Although metformin inhibited the ER stress response, its inhibitory effect was weaker than 4-PBA.ConclusionIn a CA/CPR rat model, 14-day pretreatment with metformin has a neuroprotective effect. This effect is closely related to the activation of AMPK-induced autophagy and inhibition of the ER stress response. Long-term use of metformin can reduce brain damage following CA/CPR.

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