Key result
Ac2-26 significantly improved neurological function, decreased blood-brain barrier permeability, and reduced neuroinflammation after cardiac arrest and CPR in rats compared to saline (P<0.05).
Why the study?
Brain injury is the leading cause of death following cardiac arrest and cardiopulmonary resuscitation, and this study aimed to determine the mechanism by which Ac2-26 protects against inflammation during post-resuscitation brain injury.
Does Ac2-26 reduce brain injury after cardiac arrest and cardiopulmonary resuscitation in rats?
RCT (n=64)
randomized
Does Ac2-26 reduce brain injury after cardiac arrest and cardiopulmonary resuscitation in rats?
p-value: p=<0.05
Ac2-26 reduces brain injury after cardiac arrest and CPR in rats by inhibiting oxidative stress and neuroinflammation via the eNOS pathway.
Hypothesis-generating for Ac2-26 neuroprotection after cardiac arrest; human trials required before clinical consideration.
Background. Brain injury is the leading cause of death following cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). Ac2-26 and endothelial nitric oxide synthase (eNOS) have been shown to reduce neuroinflammation. This study is aimed at determining the mechanism by which Ac2-26 protects against inflammation during brain injury following CA and CPR.Methods. Sixty-four rats were randomized into sham, saline, Ac2-26, and Ac2-26+L-NIO (endothelial nitric oxide synthase (eNOS) inhibitor) groups. Rats received Ac2-26, Ac2-26+L-NIO, or saline after CPR. Neurologic function was assessed at baseline, 24, and 72 hours after CPR. At 72 hours after resuscitation, serum and brain tissues were collected.Results. Blood-brain barrier (BBB) permeability increased, and the number of surviving neurons and neurological function decreased in the saline group compared to the sham group. Anti-inflammatory and proinflammatory factors, neuron-specific enolase (NSE) levels, and the expression of eNOS, phosphorylated (p)-eNOS, inducible nitric oxide synthase (iNOS), and oxidative stress-related factors in the three CA groups significantly increased ( P<0.05 ). BBB permeability decreased, and the number of surviving neurons and neurological function increased in the Ac2-26 group compared to the saline group ( P<0.05 ). Ac2-26 increased anti-inflammatory and reduced proinflammatory markers, raised NSE levels, increased the expression of eNOS and p-eNOS, and reduced the expression of iNOS and oxidative stress-related factors compared to the saline group ( P<0.05 ). The effect of Ac2-26 on brain injury was reversed by L-NIO ( P<0.05 ).Conclusions. Ac2-26 reduced brain injury after CPR by inhibiting oxidative stress and neuroinflammation and protecting the BBB. The therapeutic effect of Ac2-26 on brain injury was largely dependent on the eNOS pathway.
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Gong et al. (2020) conducted an RCT in Brain injury following cardiac arrest and cardiopulmonary resuscitation (n=64). Ac2-26 vs. Saline was evaluated on Neurologic function, blood-brain barrier permeability, and surviving neurons (p=<0.05). Ac2-26 significantly improved neurological function, decreased blood-brain barrier permeability, and reduced neuroinflammation after cardiac arrest and CPR in rats compared to saline (P<0.05).
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