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本文引用的文献

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PGE(2) -EP(2) signalling in endothelium is activated by haemodynamic stress and induces cerebral aneurysm through an amplifying loop via NF-κB.内皮细胞中的 PGE(2)-EP(2)信号由血流动力应激激活,并通过 NF-κB 诱导的放大环导致脑动脉瘤。
Br J Pharmacol. 2011 Jul;163(6):1237-49. doi: 10.1111/j.1476-5381.2011.01358.x.
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Lack of complement inhibitors in the outer intracranial artery aneurysm wall associates with complement terminal pathway activation.颅内动脉壁缺乏补体抑制剂与补体末端途径激活有关。
Am J Pathol. 2010 Dec;177(6):3224-32. doi: 10.2353/ajpath.2010.091172. Epub 2010 Oct 22.
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Trends in case-fatality rates in hospitalized nontraumatic subarachnoid hemorrhage: results of a population-based study in Dijon, France, from 1985 to 2006.法国第戎地区 1985 年至 2006 年人群住院非创伤性蛛网膜下腔出血病例病死率趋势的研究结果。
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Aspirin inhibits MMP-2 and MMP-9 expression and activity through PPARalpha/gamma and TIMP-1-mediated mechanisms in cultured mouse celiac macrophages.阿司匹林通过PPARα/γ和TIMP-1介导的机制抑制培养的小鼠腹腔巨噬细胞中MMP-2和MMP-9的表达及活性。
Inflammation. 2009 Aug;32(4):233-41. doi: 10.1007/s10753-009-9125-3.
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Impact of monocyte chemoattractant protein-1 deficiency on cerebral aneurysm formation.单核细胞趋化蛋白-1缺乏对脑动脉瘤形成的影响。
Stroke. 2009 Mar;40(3):942-51. doi: 10.1161/STROKEAHA.108.532556. Epub 2009 Jan 22.
7
Aspirin inhibits MMP-2 and MMP-9 expressions and activities through upregulation of PPARalpha/gamma and TIMP gene expressions in ox-LDL-stimulated macrophages derived from human monocytes.阿司匹林通过上调人单核细胞来源的氧化型低密度脂蛋白(ox-LDL)刺激的巨噬细胞中PPARα/γ和金属蛋白酶组织抑制因子(TIMP)基因的表达,抑制基质金属蛋白酶-2(MMP-2)和基质金属蛋白酶-9(MMP-9)的表达及活性。
Pharmacology. 2009;83(1):18-25. doi: 10.1159/000166183. Epub 2008 Oct 30.
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NF-kappaB is a key mediator of cerebral aneurysm formation.核因子-κB是脑动脉瘤形成的关键介质。
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10
Endothelial injury and inflammatory response induced by hemodynamic changes preceding intracranial aneurysm formation: experimental study in rats.颅内动脉瘤形成前血流动力学变化诱导的内皮损伤和炎症反应:大鼠实验研究
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阿司匹林作为降低颅内动脉瘤破裂发生率的有前途的药物。

Aspirin as a promising agent for decreasing incidence of cerebral aneurysm rupture.

机构信息

Department of Neurosurgery, Carver College of Medicine, University of Iowa, Iowa City, USA.

出版信息

Stroke. 2011 Nov;42(11):3156-62. doi: 10.1161/STROKEAHA.111.619411. Epub 2011 Oct 6.

DOI:10.1161/STROKEAHA.111.619411
PMID:21980208
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3432499/
Abstract

BACKGROUND AND PURPOSE

Chronic inflammation is postulated as an important phenomenon in intracranial aneurysm wall pathophysiology. This study was conducted to determine if aspirin use impacts the occurrence of intracranial aneurysm rupture.

METHODS

Subjects enrolled in the International Study of Unruptured Intracranial Aneurysms (ISUIA) were selected from the prospective untreated cohort (n=1691) in a nested case-control study. Cases were subjects who subsequently had a proven aneurysmal subarachnoid hemorrhage during a 5-year follow-up period. Four control subjects were matched to each case by site and size of aneurysm (58 cases, 213 control subjects). Frequency of aspirin use was determined at baseline interview. Aspirin frequency groups were analyzed for risk of aneurysmal hemorrhage. Bivariable and multivariable analyses were performed using conditional logistic regression.

RESULTS

A trend of a protective effect for risk of unruptured intracranial aneurysm rupture was observed. Patients who used aspirin 3× weekly to daily had an OR for hemorrhage of 0.40 (95% CI, 0.18-0.87); reference group, no use of aspirin), patients in the "< once a month" group had an OR of 0.80 (95% CI, 0.31-2.05), and patients in the "> once a month to 2×/week" group had an OR of 0.87 (95% CI, 0.27-2.81; P=0.025). In multivariable risk factor analyses, patients who used aspirin 3 times weekly to daily had a significantly lower odds of hemorrhage (adjusted OR, 0.27; 95% CI, 0.11-0.67; P=0.03) compared with those who never take aspirin.

CONCLUSIONS

Frequent aspirin use may confer a protective effect for risk of intracranial aneurysm rupture. Future investigation in animal models and clinical studies is needed.

摘要

背景与目的

慢性炎症被认为是颅内动脉瘤壁病理生理学中的一个重要现象。本研究旨在确定阿司匹林的使用是否会影响颅内动脉瘤破裂的发生。

方法

本研究从一项嵌套病例对照研究的前瞻性未治疗队列(n=1691)中选择了参加国际未破裂颅内动脉瘤研究(ISUIA)的受试者。病例组是在 5 年随访期间发生证实的颅内动脉瘤蛛网膜下腔出血的受试者。每个病例匹配 4 个对照组,匹配的因素包括动脉瘤的部位和大小(58 例,213 例对照组)。在基线访谈时确定阿司匹林的使用频率。分析阿司匹林使用频率与未破裂颅内动脉瘤破裂风险的关系。采用条件 logistic 回归进行单变量和多变量分析。

结果

阿司匹林使用与未破裂颅内动脉瘤破裂风险呈负相关。每周使用阿司匹林 3 次至每日的患者发生出血的 OR 为 0.40(95%CI,0.18-0.87);参考组为未使用阿司匹林;每月使用阿司匹林<1 次的患者 OR 为 0.80(95%CI,0.31-2.05),每月使用阿司匹林>1 次至每周 2 次的患者 OR 为 0.87(95%CI,0.27-2.81;P=0.025)。多变量危险因素分析显示,每周使用阿司匹林 3 次至每日的患者出血风险显著降低(调整 OR,0.27;95%CI,0.11-0.67;P=0.03),与从不服用阿司匹林的患者相比。

结论

频繁使用阿司匹林可能对颅内动脉瘤破裂风险具有保护作用。需要进一步在动物模型和临床研究中进行探索。