RT Journal Article
SR Electronic
T1 Metformin-mediated mitochondrial protection post-cardiac arrest improves EEG activity and confers neuroprotection and survival benefit
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2021.10.07.460078
DO 10.1101/2021.10.07.460078
A1 Muhammad Shoaib
A1 Rishabh C. Choudhary
A1 Rupesh K. Chillale
A1 Nancy Kim
A1 Santiago J. Miyara
A1 Shabirul Haque
A1 Tai Yin
A1 Maya Frankfurt
A1 Ernesto P. Molmenti
A1 Stavros Zanos
A1 Junhwan Kim
A1 Lance B. Becker
YR 2021
UL http://biorxiv.org/content/early/2021/10/09/2021.10.07.460078.abstract
AB Cardiac arrest (CA) produces global ischemia/reperfusion injury resulting in substantial multiorgan damage. There are limited efficacious therapies to save lives despite CA being such a lethal disease process. Surviving patients suffer extensive brain damage with mitochondrial dysfunction implicated as a major source of injury. Metformin, a first-line treatment for diabetes, has also shown promising results in other diseases and is known to interact with mitochondria. In the present study, we evaluated the therapeutic benefits of metformin administration immediately after resuscitation using a 10 min asphxyial-CA rat model. This is the first study to show that metformin treatment post-CA a) improves survival and neurologic function, b) potentiates early normalization of brain electrophysiologic activity, and c) protects mitochondrial function with a reduction in apoptotic brain injury. Overall, as an effective and safe drug, metformin has the potential to be an easily translatable intervention for improving survival and preventing brain damage after CA.Summary Brain damage post-cardiac arrest is a major cause of death; metformin protects brain mitochondria and improved survival and brain function.Competing Interest StatementThe authors have declared no competing interest.