FSLLRY-NH2 improves neurological outcome after cardiac arrest in rats

Ocak U., Ocak P. E., Huang L., Zhang J. H.

Turkish Neurosurgery, cilt.30, sa.2, ss.244-251, 2020 (SCI-Expanded, Scopus, TRDizin) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 30 Sayı: 2
  • Basım Tarihi: 2020
  • Doi Numarası: 10.5137/1019-5149.jtn.27714-19.1
  • Dergi Adı: Turkish Neurosurgery
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, EMBASE, MEDLINE, TR DİZİN (ULAKBİM)
  • Sayfa Sayıları: ss.244-251
  • Anahtar Kelimeler: Cardiac arrest, Cognitive, Global cerebral ischemia, PAR2
  • Samsun Üniversitesi Adresli: Hayır

Özet

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.