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高密度脂蛋白胆固醇在获得性主动脉瓣狭窄患者中的作用及其与氧化应激的关系。

HDL-C Role in Acquired Aortic Valve Stenosis Patients and Its Relationship with Oxidative Stress.

作者信息

Hofmanis Juris, Hofmane Dace, Svirskis Simons, Mackevics Vitolds, Tretjakovs Peteris, Lejnieks Aivars, Signorelli Salvatore Santo

机构信息

Faculty of Medicine, Department of Internal Diseases, Riga Stradins University and Riga East University Hospital, LV-1007 Riga, Latvia.

Zemgale Health Center, LV-3001 Jelgava, Latvia.

出版信息

Medicina (Kaunas). 2019 Jul 29;55(8):416. doi: 10.3390/medicina55080416.


DOI:10.3390/medicina55080416
PMID:31362438
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6723197/
Abstract

: Mechanical stress is currently considered as the main factor promoting calcific aortic valve stenosis (AS) onset. It causes endothelial damage and dysfunction. The chronic inflammatory process causes oxidative stress. Oxidative stress-induced high-density lipoprotein cholesterol (HDL-C) dysfunction is an important component of the development of AS. The aim of the study was to evaluate the role of HDL-C in AS patients in three severity grades and in relation to the biomarkers of oxidative stress, thioredoxin reductase 1 (TrxR1) and myeloperoxidase (MPO). : 18 patients with mild, 19 with moderate. and 15 with severe AS were included in the study, and 50 individuals were enrolled in the control group. Stenosis severity was determined by echocardiography. The TrxR1 and MPO were analyzed by ELISA, and HDL-C by commercially available tests. Data were analyzed using GraphPad Prism 8. : HDL-C in AS patients vs. control substantially decreases and this decline was observed in all three AS severity groups: mild ( = 0.018), moderate ( = 0.0002), and severe ( = 0.004). In both the control and the stenosis group, the HDL-C was higher in women than in men. In comparison to control, the HDL-C level was lower in the AS group, and more pronounced in women ( = 0.0001) than in men ( = 0.049). A higher TrxR1 level was observed in patients with mild ( = 0.0001) and severe AS ( = 0.047). However, a clear correlation between TrxR1 and HDL-C was not obtained. Analysis of MPO showed differences in all severity grades vs. control ( = 0.024 mild stenosis; = 0.002 moderate stenosis; = 0.0015 severe stenosis). A negative correlation ( = 0.047; = -0.28) was found between MPO and HDL-C, which confirms the adverse effects of MPO resulting in HDL-C dysfunction. : In this study, we justified HDL-C level association with AS development process. The results unequivocally substantiated the association between HDL-C and AS in all severity grades in women, but only in moderate AS for men, which we explained by the small number of men in the groups. The obtained correlation between the HDL-C and MPO levels, as well as the concurrent decrease in the HDL-C level and increase in the TrxR1 level, indicate in general an HDL-C association with oxidative stress in AS patients.

摘要

机械应力目前被认为是促进钙化性主动脉瓣狭窄(AS)发病的主要因素。它会导致内皮损伤和功能障碍。慢性炎症过程会引发氧化应激。氧化应激诱导的高密度脂蛋白胆固醇(HDL-C)功能障碍是AS发展的一个重要组成部分。本研究的目的是评估HDL-C在三个严重程度等级的AS患者中以及与氧化应激生物标志物硫氧还蛋白还原酶1(TrxR1)和髓过氧化物酶(MPO)相关的作用。:本研究纳入了18例轻度AS患者、19例中度AS患者和15例重度AS患者,对照组纳入了50名个体。通过超声心动图确定狭窄严重程度。采用酶联免疫吸附测定法(ELISA)分析TrxR1和MPO,采用市售检测方法分析HDL-C。使用GraphPad Prism 8软件分析数据。:AS患者的HDL-C与对照组相比显著降低,且在所有三个AS严重程度组中均观察到这种下降:轻度(P = 0.018)、中度(P = 0.0002)和重度(P = 0.004)。在对照组和狭窄组中,女性的HDL-C均高于男性。与对照组相比,AS组的HDL-C水平较低,且在女性中(P = 0.0001)比在男性中(P = 0.049)更明显。在轻度(P = 0.0001)和重度AS患者(P = 0.047)中观察到较高的TrxR1水平。然而,未获得TrxR1与HDL-C之间的明显相关性。MPO分析显示,与对照组相比,所有严重程度等级均存在差异(轻度狭窄P = 0.024;中度狭窄P = 0.002;重度狭窄P = 0.0015)。发现MPO与HDL-C之间存在负相关(P = 0.047;r = -0.28),这证实了MPO导致HDL-C功能障碍的不良影响。:在本研究中,我们证明了HDL-C水平与AS发展过程的关联。结果明确证实了HDL-C与所有严重程度等级女性的AS之间的关联,但仅在中度AS男性中得到证实,我们将其解释为各组中男性数量较少。HDL-C与MPO水平之间的相关性以及HDL-C水平的同时降低和TrxR1水平的升高,总体表明HDL-C与AS患者的氧化应激相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc8/6723197/ca0b00e19a78/medicina-55-00416-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc8/6723197/2735fb5848e5/medicina-55-00416-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc8/6723197/ca0b00e19a78/medicina-55-00416-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc8/6723197/88aafaac139d/medicina-55-00416-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc8/6723197/1be084228367/medicina-55-00416-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc8/6723197/0f48a4c814ec/medicina-55-00416-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc8/6723197/5110fe2a8340/medicina-55-00416-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc8/6723197/bc5a460bd007/medicina-55-00416-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc8/6723197/b618d6183f9c/medicina-55-00416-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc8/6723197/2735fb5848e5/medicina-55-00416-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dfc8/6723197/ca0b00e19a78/medicina-55-00416-g008.jpg

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