The Role of Tryptophan Catabolism along the Kynurenine Pathway in Acute Ischemic Stroke

The Role of Tryptophan Catabolism along the Kynurenine Pathway in Acute Ischemic Stroke
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DOI:
10.1007/s11064-010-0187-2
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发表时间:
2010-09-01
影响因子:
4.4
通讯作者:
De Deyn, Peter P.
De Deyn, Peter P.
中科院分区:
医学3区
文献类型:
--
作者:
Brouns, Raf;Verkerk, Robert;De Deyn, Peter P.

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中风后炎症可诱导色氨酸(TRP)氧化的犬尿氨酸(KYN)途径上调,导致神经保护性(犬尿烯酸,KA)和神经毒性代谢物(3-羟基邻氨基苯甲酸,3-HAA)。我们研究了急性缺血性卒中中犬尿氨酸通路的活性是否与初始卒中严重程度、长期卒中结局和缺血诱导的炎症反应相关。测定了149例脑卒中患者入院时、发病后24 h、72 h和第7天血浆TRP及其代谢产物的浓度。我们评估了KYN/TRP比值、KA/3-HAA比值与卒中严重程度、预后和炎症参数(C-反应蛋白(CRP)、红细胞沉降率(ESR)和中性粒细胞/淋巴细胞比值(NLR))之间的关系。KYN/TRP与NIHSS评分和梗死体积相关,KA/3 HAA与NIHSS评分和梗死体积无关。结果较差的患者的平均KYN/TRP比值高于结果较好的患者。入院时KYN/TRP比值与CRP水平、ESR和NLR相关。急性缺血性卒中中色氨酸降解的犬尿氨酸途径活性与卒中严重程度和长期卒中结局相关。色氨酸氧化与脑卒中诱导的炎症反应有关。
Post-stroke inflammation may induce upregulation of the kynurenine (KYN) pathway for tryptophan (TRP) oxidation, resulting in neuroprotective (kynurenic acid, KA) and neurotoxic metabolites (3-hydroxyanthranillic acid, 3-HAA). We investigated whether activity of the kynurenine pathway in acute ischemic stroke is related to initial stroke severity, long-term stroke outcome and the ischemia-induced inflammatory response. Plasma concentrations of TRP and its metabolites were measured in 149 stroke patients at admission, at 24 h, at 72 h and at day 7 after stroke onset. We evaluated the relation between the KYN/TRP ratio, the KA/3-HAA ratio and stroke severity, outcome and inflammatory parameters (C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and neutrophil/lymphocyte ratio (NLR)). KYN/TRP but not KA/3HAA correlated with the NIHSS score and with the infarct volume. Patients with poor outcome had higher mean KYN/TRP ratios than patients with more favourable outcome. The KYN/TRP ratio at admission correlated with CRP levels, ESR and NLR. The activity of the kynurenine pathway for tryptophan degradation in acute ischemic stroke correlates with stroke severity and long-term stroke outcome. Tryptophan oxidation is related to the stroke-induced inflammatory response.