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F2-异前列腺素和F4-神经前列腺素作为颅内动脉瘤发展的标志物。

F2-isoprostanes and F4-neuroprostanes as markers of intracranial aneurysm development.

作者信息

Syta-Krzyżanowska Anna, Jarocka-Karpowicz Iwona, Kochanowicz Jan, Turek Grzegorz, Rutkowski Robert, Gorbacz Krzysztof, Mariak Zenon, Skrzydlewska Elżbieta

机构信息

Department of Invasive Neurology, Medical University of Bialystok, Poland.

Department of Analytical Chemistry, Medical University of Bialystok, Poland.

出版信息

Adv Clin Exp Med. 2018 May;27(5):673-680. doi: 10.17219/acem/68634.

DOI:10.17219/acem/68634
PMID:29790685
Abstract

BACKGROUND

Intracranial aneurysms are common, occurring in about 1-2% of the population. Saccular aneurysm is a pouch-like pathological dilatation of an intracranial artery that develops when the cerebral artery wall becomes too weak to resist hemodynamic pressure and distends.

OBJECTIVES

The aim of this study was to determine whether the development of intracranial aneurysms and subarachnoid hemorrhage (SAH) affects neuronal phospholipid metabolism, and what influence different invasive treatments have on brain free radical phospholipid metabolism.

MATERIAL AND METHODS

The level of polyunsaturated fatty acid (PUFA) cyclization products - F2-isoprostanes and F4-neuroprostanes - was examined using liquid chromatography - mass spectrometry (LC-MS) in the plasma of patients with brain aneurysm and resulting subarachnoid hemorrhage.

RESULTS

It was revealed that an aneurysm leads to the enhancement of lipid peroxidation with a significant increase in plasma F2-isoprostanes and F4-neuroprostanes (more than 3-fold and 11-fold, respectively) in comparison to healthy subjects. The rupture of an aneurysm results in hemorrhage and an additional increase in examined prostaglandin derivatives. The embolization and clipping of aneurysms contribute to a gradual restoration of metabolic homeostasis in brain cells, which is visible in the decrease in PUFA cyclization products.

CONCLUSIONS

The results indicate that aneurysm development is associated with enhanced inflammation and oxidative stress, factors which favor lipid peroxidation, particularly in neurons, whose membranes are rich in docosahexaenoic acid, a precursor of F4-neuroprostanes.

摘要

背景

颅内动脉瘤很常见,在大约1%-2%的人群中发生。囊状动脉瘤是颅内动脉的袋状病理性扩张,当脑动脉壁变得过于薄弱而无法抵抗血流动力学压力并扩张时就会形成。

目的

本研究的目的是确定颅内动脉瘤和蛛网膜下腔出血(SAH)的发生是否会影响神经元磷脂代谢,以及不同的侵入性治疗对脑自由基磷脂代谢有何影响。

材料和方法

使用液相色谱-质谱联用(LC-MS)检测脑动脉瘤及由此导致的蛛网膜下腔出血患者血浆中多不饱和脂肪酸(PUFA)环化产物——F2-异前列腺素和F4-神经前列腺素的水平。

结果

研究发现,与健康受试者相比,动脉瘤会导致脂质过氧化增强,血浆F2-异前列腺素和F4-神经前列腺素显著增加(分别增加超过3倍和11倍)。动脉瘤破裂会导致出血,并使所检测的前列腺素衍生物进一步增加。动脉瘤的栓塞和夹闭有助于脑细胞代谢稳态的逐渐恢复,这在PUFA环化产物的减少中可见。

结论

结果表明,动脉瘤的发生与炎症和氧化应激增强有关,这些因素有利于脂质过氧化,尤其是在神经元中,其细胞膜富含二十二碳六烯酸,即F4-神经前列腺素的前体。

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