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Journals / Turkish Neurosurgery / 2020 / Cilt: 30 - Sayı: 2

FSLLRY-NH2 Improves Neurological Outcome After Cardiac Arrest in Rats

Umut OCAK
Pinar ESER OCAK
Lei HUANG
John H. ZHANG
Pages
244–251
DOI
—
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⚡ TL;DR(Too Long; Didn't Read)

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.

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Objective & Hypothesis: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.
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Key Findings & Data:Shams and rats resuscitated from 9 minutes ofACA were randomized to two separate experiments including time course and short-term neurological outcomes.
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Conclusion & Impact: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.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

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.

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Cite This Article

OCAK, U., OCAK, P. E., HUANG, L., ZHANG, J. H. (2020). FSLLRY-NH2 Improves Neurological Outcome After Cardiac Arrest in Rats. Turkish Neurosurgery, Cilt: 30 - Sayı: 2, 244–251. https://ajindex.com/articles/399190

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References (1)

  1. Afkhami-Goli A, Noorbakhsh F, Keller AJ, Vergnolle N, Westaway D, Jhamandas JH, Andrade-Gordon P, Hollenberg MD, Arab H, Dyck RH, Power C: Proteinase-activated receptor-2 exerts protective and pathogenic cell type-specific effects in Alzheimer’s disease. J Immunol 179:5493-5503, 2007 2. Bendel O, Bueters T, von Euler M, Ove Ogren S, Sandin J, von Euler G: Reappearance of hippocampal CA1 neurons after ischemia is associated with recovery of learning and memory. J Cereb Blood Flow Metab 25:1586-1595, 2005 3. Benjamin EJ, Virani SS, Callaway CW, Chamberlain AM, Chang AR, Cheng S, Chiuve SE, Cushman M, Delling FN, Deo R, de Ferranti SD, Ferguson JF, Fornage M, Gillespie C, Isasi CR, Jimenez MC, Jordan LC, Judd SE, Lackland D, Lichtman JH, Lisabeth L, et al: Heart disease and stroke statistics-2018 update: A report from the american heart association. Circulation 137:e67-e492, 2018 4. Chu K, Yin B, Wang J, Peng G, Liang H, Xu Z, Du Y, Fang M, Xia Q, Luo B: Inhibition of P2X7 receptor ameliorates transient global cerebral ischemia/reperfusion injury via modulating inflammatory responses in the rat hippocampus. J Neuroinflammation 9:69, 2012 5. Cuenca L, Gil-Martinez AL, Cano-Fernandez L, SanchezRodrigo C, Estrada C, Fernandez-Villalba E, Herrero MT: Parkinson’s disease: A short story of 200 years. Histol Histopathol 34:573-591, 2019 6. Delattre C, Bournonville C, Auger F, Lopes R, Delmaire C, Henon H, Mendyk AM, Bombois S, Devedjian JC, Leys D, Cordonnier C, Bordet R, Bastide M: Hippocampal deformations and entorhinal cortex atrophy as an anatomical signature of long-term cognitive impairment: From the MCAO rat model to the stroke patient. Transl Stroke Res 9:294-305, 2018 7. Field JM, Hazinski MF, Sayre MR, Chameides L, Schexnayder SM, Hemphill R, Samson RA, Kattwinkel J, Berg RA, Bhanji F, Cave DM, Jauch EC, Kudenchuk PJ, Neumar RW, Peberdy MA, Perlman JM, Sinz E, Travers AH, Berg MD, Billi JE, Eigel B, et al: Part 1: Executive summary: 2010 American Heart Association Guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 122:S640-656, 2010 8. Globus MY, Busto R, Martinez E, Valdes I, Dietrich WD, Ginsberg MD: Comparative effect of transient global ischemia on extracellular levels of glutamate, glycine, and gammaaminobutyric acid in vulnerable and nonvulnerable brain regions in the rat. J Neurochem 57:470-478, 1991 9. Hanusova Z, Mosko T, Matej R, Holada K: Precision in the design of an experimental study deflects the si