FSLLRY-NH2 Improves Neurological Outcome After Cardiac Arrest in Rats

Özet

AIM: To evaluate the effect of FSLLRY-NH2, a protease-activated receptor 2 (PAR2) inhibitor, on neurocognitive impairment andhippocampal neuronal degeneration in the setting of asphyxial cardiac arrest (ACA)-induced global cerebral ischemia (GCI) in rats.MATERIAL and METHODS: A total of 43 Sprague-Dawley male rats were used. Shams and rats resuscitated from 9 minutes ofACA were randomized to two separate experiments including time course and short-term neurological outcomes. FSLLRY-NH2 (50microgram [μg] per rat) was administered intranasally at 1 hour postresuscitation. Neurological function and hippocampal neuronaldegeneration were evaluated after ACA.RESULTS: Significant neurological function decline and hippocampal neuron degeneration were observed in ACA animals ascompared with the shams. Treatment with FSLLRY-NH2 significantly improved neurological outcome and reduced the number ofdegenerating hippocampal neurons after ACA.CONCLUSION: Targeting PAR2 may be a novel therapeutic approach in the management of neurological dysfunction after cardiacarrest-associated ischemic injury.