Ocak Umut, Eser Ocak Pinar, Huang Lei, Zhang John H
University of Health Sciences, Bursa Yuksek Ihtisas Training and Research Hospital, Department of Emergency Medicine, Bursa, Turkey.
Loma Linda University School of Medicine, Department of Physiology and Pharmacology, Loma Linda, California, USA
Turk Neurosurg. 2020;30(2):244-251. doi: 10.5137/1019-5149.JTN.27714-19.1.
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.
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.
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.
Targeting PAR2 may be a novel therapeutic approach in the management of neurological dysfunction after cardiac arrest-associated ischemic injury.
评估蛋白酶激活受体2（PAR2）抑制剂FSLLRY-NH2对大鼠窒息性心脏骤停（ACA）所致全脑缺血（GCI）引起的神经认知障碍和海马神经元变性的影响。
共使用43只雄性Sprague-Dawley大鼠。假手术组和从9分钟ACA复苏的大鼠被随机分为两个独立实验，包括时间进程和短期神经学结果。复苏后1小时经鼻给予FSLLRY-NH2（每只大鼠50微克[μg]）。在ACA后评估神经功能和海马神经元变性。
与假手术组相比，ACA动物出现明显的神经功能下降和海马神经元变性。FSLLRY-NH2治疗显著改善了ACA后的神经学结果，并减少了变性海马神经元的数量。
靶向PAR2可能是心脏骤停相关缺血性损伤后神经功能障碍管理中的一种新型治疗方法。
