神经损伤与功能重建2018，Vol.13Issue(5)：221-224,4.DOI:10.16780/j.cnki.sjssgncj.2018.05.002
尤瑞克林对心脏骤停后综合征兔脑保护作用的研究
Brain Protective Effects of Urinary Kallidinogenase in Rabbits with Post-cardiac Arrest Syndrome
摘要
Abstract
Objective: To investigate the brain protective effects and mechanism of urinary kallidinogenase (UK) in rabbits with post-cardiac arrest syndrome (PCAS). Methods: Japanese white rabbits were random divided into the sham group (n=6), PCAS group (n=12), UK high-dose group (UK-H group, n=12), and UK low-dose group(UK-L group,n=12).PCAS models were established by using asphyxia-induced cardiac arrest;the sham group was not subjected to asphyxia. Immediately after ROSC, UK-H and UK-L groups were given 17.5×10-3 PNAU/kg and 3.5×10-3 PNAU/kg doses of UK,and the PCAS group was injected with an equal amount of saline.Serum level of neuron specificity enolization enzyme(NSE)was examined before ROSC and 6 h,24 h, and 48 h after ROSC respectively. Functional outcomes were measured by neurological deficit score. Rabbit brain tissue was collected after 48 h, and Western blot was performed to determine brain tissue Caspase-3 and Caspase-9 expression.Results:Compared to the sham group,serum level of NSE was significantly elevated in the PCAS group,UK-L group,and UK-H group 6 h,24 h,and 48 h after ROSC(P<0.01).Compared to PCAS group,serum level of NSE and neurological deficit score was clearly decreased in the UK-L group and UK-H group 24 h and 48 h after ROSC;the expression level of Caspase-3 and Caspase-9 was significantly attenuated in the two groups 48 h after ROSC (P<0.05), with the UK-H group showing a greater reduction than the UK-L group (P<0.05). Conclusion: UK reduced brain inflammation and alleviated neurological deficit, and the mechanism may be related to inhibition of apoptosis.关键词
心脏骤停后综合征/尤瑞克林/炎症/凋亡Key words
post-cardiac arrest syndrome/urinary kallidinogenase/inflammation/apoptosis分类
医药卫生引用本文复制引用
李昌盛,闵喆,杨贤义,郭辉,柴林,肖敏..尤瑞克林对心脏骤停后综合征兔脑保护作用的研究[J].神经损伤与功能重建,2018,13(5):221-224,4.基金项目
湖北省自然科学基金面上项目(No.2010CDB09103) （No.2010CDB09103）
