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一项关于Takotsubo综合征患者氢核磁共振血清代谢谱的初步研究揭示了对氧化应激的全身反应。

A Pilot Study on the H-NMR Serum Metabolic Profile of Takotsubo Patients Reveals Systemic Response to Oxidative Stress.

作者信息

Vanni Domitilla, Viceconte Nicola, Petrella Greta, Biccirè Flavio Giuseppe, Pelliccia Francesco, Tanzilli Gaetano, Cicero Daniel Oscar

机构信息

Department of Chemical Science and Technology, University of Rome "Tor Vergata", 00133 Rome, Italy.

Department of Internal Medicine, Anesthesiologic and Cardiovascular Sciences, Sapienza University of Rome, Policlinic Umberto I, 00161 Rome, Italy.

出版信息

Antioxidants (Basel). 2021 Dec 13;10(12):1982. doi: 10.3390/antiox10121982.

DOI:10.3390/antiox10121982
PMID:34943085
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8750825/
Abstract

Takotsubo syndrome (TTS) presents as an acute coronary syndrome characterized by severe left ventricular (LV) dysfunction and non-obstructive coronary artery disease that typically shows spontaneous recovery within days or weeks. The mechanisms behind TTS are mainly related to beta-adrenergic overstimulation and acute endogenous catecholamine surge, both of which could increase oxidative status that may induce further deterioration of cardiac function. Although several studies reported evidence of inflammation and oxidative stress overload in myocardial tissue of TTS models, systemic biochemical evidence of augmented oxidant activity in patients with TTS is lacking. In this study, serum samples of ten TTS patients and ten controls have been analyzed using H-NMR spectroscopy. The results of this pilot study show a marked alteration in the systemic metabolic profile of TTS patients, mainly characterized by significant elevation of ketone bodies, 2-hydroxybutyrate, acetyl-L-carnitine, and glutamate levels, in contrast with a decrease of several amino acid levels. The overall metabolic fingerprint reflects a systemic response to oxidative stress caused by the stressor that triggered the syndrome's onset.

摘要

应激性心肌病(TTS)表现为一种急性冠状动脉综合征,其特征是严重的左心室(LV)功能障碍和非阻塞性冠状动脉疾病,通常在数天或数周内可自发恢复。TTS背后的机制主要与β-肾上腺素能过度刺激和急性内源性儿茶酚胺激增有关,这两者均可增加氧化状态,进而可能导致心脏功能进一步恶化。尽管多项研究报告了TTS模型心肌组织中存在炎症和氧化应激过载的证据,但TTS患者体内氧化剂活性增强的系统性生化证据仍然缺乏。在本研究中,我们使用氢核磁共振波谱(H-NMR)对10例TTS患者和10例对照者的血清样本进行了分析。这项初步研究的结果显示,TTS患者的全身代谢谱有明显改变,主要表现为酮体、2-羟基丁酸、乙酰-L-肉碱和谷氨酸水平显著升高,同时几种氨基酸水平降低。整体代谢指纹反映了机体对引发该综合征发作的应激源所导致的氧化应激的系统性反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/8750825/d5119ebe55bf/antioxidants-10-01982-sch001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/8750825/622d1e84d09f/antioxidants-10-01982-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/8750825/64c548096db4/antioxidants-10-01982-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/8750825/4a1e6e867d27/antioxidants-10-01982-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/8750825/b0bb1e23087d/antioxidants-10-01982-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/8750825/4dee7126dabe/antioxidants-10-01982-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/8750825/d5119ebe55bf/antioxidants-10-01982-sch001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/8750825/622d1e84d09f/antioxidants-10-01982-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/8750825/64c548096db4/antioxidants-10-01982-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/8750825/4a1e6e867d27/antioxidants-10-01982-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/8750825/b0bb1e23087d/antioxidants-10-01982-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/8750825/4dee7126dabe/antioxidants-10-01982-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/8750825/d5119ebe55bf/antioxidants-10-01982-sch001.jpg

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