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精胺预处理对急性脑缺血/再灌注损伤的作用

Pre-treatment with spermine for acute cerebral ischemia/reperfusion injuries.

作者信息

Du Hai, Ming Xing, Zhou Shengkui

机构信息

Department of Neurosurgery, Xuzhou Central Hospital, Xuzhou, Jiangsu 221009, P.R. China.

出版信息

Exp Ther Med. 2017 Jul;14(1):169-172. doi: 10.3892/etm.2017.4455. Epub 2017 May 12.

DOI:10.3892/etm.2017.4455
PMID:28672910
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5488636/
Abstract

Acute cerebral ischemia/reperfusion injury (ACIR) rat model was used to investigate the effect of spermine on oxidative stress and apoptosis. Sixty healthy and clean male Sprague-Dawley rats were randomly divided into 3 groups: The sham-operated group (n=12), the model group (n=12) and the experiment group (n=36). The experiment group was further divided into 3 subgroups: The SPE-10 group (n=12), the SPE-25 group (n=12) and the SPE-50 group (n=12). Rats in the experimental sub-groups SPE-10, SPE-25 and SPE-50 were injected with 10, 25 and 50 mg/kg of spermine, respectively, one week before the establishment of rat models. Rats in the sham-operated and model groups were injected with 0.9% NaCl solution. We evaluated the effect of spermine on malondialdehyde (MDA) level and superoxide dismutase (SOD) activity using ELISA kits. Bax and Bcl-2 levels were measured using western blot analysis. Our results showed that after spermine injection, MDA levels markedly decreased, while SOD activity increased significantly. The variations in MDA levels and SOD activity were dose (spermine)-dependent. Bax protein levels increased significantly, while Bcl-2 levels decreased significantly after the onset of ACIR injuries. After spermine injection, there was a significant decrease in Bax levels. Bcl-2 levels in these rats markedly increased. The observed decline in Bax levels and the increase in Bcl-2 levels in the experimental groups were dose-dependent. We concluded that spermine protected nerve tissues in rats with ACIR by decreasing the MDA level, increasing SOD activity and modifying the balance between Bax and Bcl-2 proteins.

摘要

采用急性脑缺血/再灌注损伤(ACIR)大鼠模型研究精胺对氧化应激和细胞凋亡的影响。将60只健康清洁级雄性Sprague-Dawley大鼠随机分为3组:假手术组(n = 12)、模型组(n = 12)和实验组(n = 36)。实验组进一步分为3个亚组:精胺10mg/kg组(n = 12)、精胺25mg/kg组(n = 12)和精胺50mg/kg组(n = 12)。在建立大鼠模型前一周,分别给精胺10mg/kg组、精胺25mg/kg组和精胺50mg/kg组的大鼠注射10、25和50mg/kg的精胺。假手术组和模型组大鼠注射0.9%氯化钠溶液。使用酶联免疫吸附测定试剂盒评估精胺对丙二醛(MDA)水平和超氧化物歧化酶(SOD)活性的影响。采用蛋白质免疫印迹分析测定Bax和Bcl-2水平。结果显示,注射精胺后,MDA水平显著降低,而SOD活性显著增加。MDA水平和SOD活性的变化呈剂量(精胺)依赖性。ACIR损伤发生后,Bax蛋白水平显著升高,而Bcl-2水平显著降低。注射精胺后,Bax水平显著降低。这些大鼠的Bcl-2水平显著升高。实验组中观察到的Bax水平下降和Bcl-2水平升高呈剂量依赖性。我们得出结论,精胺通过降低MDA水平、增加SOD活性以及调节Bax和Bcl-2蛋白之间的平衡来保护ACIR大鼠的神经组织。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e811/5488636/8ac14a5d6aa7/etm-14-01-0169-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e811/5488636/edab228dc1b8/etm-14-01-0169-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e811/5488636/8ac14a5d6aa7/etm-14-01-0169-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e811/5488636/edab228dc1b8/etm-14-01-0169-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e811/5488636/8ac14a5d6aa7/etm-14-01-0169-g01.jpg

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