FSLLRY-NH2 Improves Neurological Outcome After Cardiac Arrest in Rats

  • Turk Neurosurg. 2020;30(2):244-251. doi: 10.5137/1019-5149.JTN.27714-19.1.
Umut Ocak  1  2 ,  Pinar Eser Ocak  2  3 ,  Lei Huang  2 ,  John H Zhang  2
Affiliations
  • 1. University of Health Sciences, Bursa Yuksek Ihtisas Training and Research Hospital, Department of Emergency Medicine, Bursa, Turkey.
  • 2. Loma Linda University School of Medicine, Department of Physiology and Pharmacology, Loma Linda, California, USA
  • 3. Uludag University, School of Medicine, Department of Neurosurgery, Bursa, Turkey
PMID: 32020571 DOI: 10.5137/1019-5149.JTN.27714-19.1
Abstract

Aim: To evaluate the effect of FSLLRY-NH2, a Protease-activated Receptor 2 (PAR2) inhibitor, on neurocognitive impairment and hippocampal 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 of ACA were randomized to two separate experiments including time course and short-term neurological outcomes. FSLLRY-NH2 (50 microgram [μg] per rat) was administered intranasally at 1 hour postresuscitation. Neurological function and hippocampal neuronal degeneration were evaluated after ACA.

Results: Significant neurological function decline and hippocampal neuron degeneration were observed in ACA Animals as compared with the shams. Treatment with FSLLRY-NH2 significantly improved neurological outcome and reduced the number of degenerating hippocampal neurons after ACA.

Conclusion: Targeting PAR2 may be a novel therapeutic approach in the management of neurological dysfunction after cardiac arrest-associated ischemic injury.

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