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].神经损伤功能重建,2018,13(5):221-224 |
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 ArrestSyndrome |
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DOI: |
中文关键词: 心脏骤停后综合征 尤瑞克林 炎症 凋亡 |
英文关键词: post-cardiac arrest syndrome urinary kallidinogenase inflammation apoptosis |
基金项目:湖北省自然科学基
金 面 上 项 目
(No.2010CDB0910
3) |
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中文摘要: |
目的:探讨尤瑞克林(UK)对心脏骤停后综合征(PCAS)兔脑的保护作用及机制。 方法:将42只日本
大耳白兔随机分为假手术组(n=6)、PCAS组(n=12)、UK大剂量(UK-H)组(n=12)、UK小剂量(UK-L)组(n=
12)。采用窒息性心脏骤停法制备兔PCAS模型,假手术组不造成窒息。复苏成功后UK-H、UK-L组立即给
予UK 17.5×10- 3
PNAU/kg、3.5×10- 3
PNAU/kg,PCAS组注射等量生理盐水。分别于复苏前、复苏后6 h、24 h、
48 h检测血清神经元特异性烯醇化酶(NSE),并进行神经功能缺损评分。48 h后取兔脑组织,应用Western
blot方法测定脑组织Caspase-3、Caspase-9表达。结果:与假手术组比,PCAS组、UK-H组、UK-L组血清NSE
水平在复苏后6 h、24 h、48 h均明显升高(P<0.01)。与PCAS组比,UK-H组、UK-L组血清NSE水平、神经功
能损伤评分在复苏后24 h、48 h明显减少,复苏后48 h Caspase-3、Caspase-9表达水平减低(P<0.05),且在复
苏后48 h UK-H组较UK-L组减低更为明显(P<0.05)。结论:UK能减少复苏后脑炎性因子表达,改善神经
功能,其机制可能与抑制细胞凋亡有关。 |
英文摘要: |
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 |
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