Lipid peroxidation in stroke patients

Lipid peroxidation in stroke patients
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DOI:
10.1515/cclm.2008.011
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发表时间:
2008-01-01
影响因子:
6.8
通讯作者:
Provinciali, Leandro
Provinciali, Leandro
中科院分区:
医学2区
文献类型:
--
作者:
Ferretti, Gianna;Bacchetti, Tiziana;Provinciali, Leandro

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背景:对氧磷酶是高密度脂蛋白相关的酯/内酯酶,在高密度脂蛋白的抗氧化和抗炎作用中发挥重要作用。越来越多的证据支持自由基和氧化应激在缺血再灌注所致的神经元损伤中所起的作用。本研究的目的是进一步探讨脂蛋白氧化损伤与卒中的关系。方法:比较50例健康人和49例卒中患者血浆中对氧磷酶活性和过氧化脂质水平。结果:首次发现卒中患者血浆对氧磷酶活性显著低于正常对照组(p<0.001),而血浆过氧化脂质水平显著高于对照组(p<0.001)。此外,通过线性回归分析发现,对氧磷酶活性和脂质过氧化水平与入院时神经功能缺失程度显著相关。结论:这些结果进一步证明氧化应激和抗氧化系统受损可能在卒中中起作用。血浆的抗氧化活性可能是防止中风相关氧化应激引起的神经损伤的一个重要因素。
Background: Paraoxonase is high-density lipoprotein (HDL)-associated esterase/lactonase implicated to play a role in the antioxidant and anti-inflammatory properties exerted by HDL. Increasing evidence support a role of free radicals and oxidative stress in neuronal damage induced by ischemia-reperfusion. The aim of this study was to further investigate the relationship between lipoprotein oxidative damage and stroke.Methods: We compared the paraoxonase activity and levels of lipid hydroperoxides in plasma isolated from healthy subjects (n=50) and from stroke patients (n = 49). Moreover, the correlations between biochemical markers and the National Institute of Health Stroke Scale (NIHSS), which is widely used to study neurological severity, were evaluated.Results: Our results demonstrated, for the first time, that the activity of paraoxonase in plasma of stroke subjects was significantly lower than controls (p < 0.001) and the levels of lipid hydroperoxides were significantly higher in plasma from patients (p < 0.001). Moreover, using linear regression analysis, significant correlations between the activity of paraoxonase, lipid peroxidation and the severity of neurological deficit at admission were observed.Conclusions: These results provide further evidence that oxidative stress and impairment of the antioxidant system may play a role in stroke. Antioxidant activity of plasma may be an important factor providing protection from neurological damage caused by stroke-associated oxidative stress.