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NLRP3炎性小体在抑郁症与心肌梗死共病中的潜在作用

The Possible Role of NLRP3 Inflammasome in Depression and Myocardial Infarction Comorbidity.

作者信息

Baysak Erensu, Yildirim Cagan, Sayar Nurten, Sayar Mustafa Kemal, Halaris Angelos, Aricioglu Feyza

机构信息

Department of Psychiatry, School of Medicine, Marmara University, Istanbul 34854, Turkey.

Department of Cardiology, School of Medicine, Marmara University, Istanbul 34854, Turkey.

出版信息

J Pers Med. 2023 Aug 25;13(9):1295. doi: 10.3390/jpm13091295.

DOI:10.3390/jpm13091295
PMID:37763063
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10533058/
Abstract

It is well-established that cardiovascular disease and depression are highly comorbid. This study aimed to assess the possible role of the NOD-like receptor protein 3 (NLRP3) inflammasome pathway and the high-sensitivity C-reactive protein (CRP) in patients with incident myocardial infarction in the presence or absence of depression. Sixty-eight consecutive patients with incident ST-elevation myocardial infarction and twenty healthy subjects were included. The patients were assessed using the Structured Clinical Interview for DSM-5 Disorders-Clinician Version during their 1-4-day-long hospitalization and were divided into two groups: with and without comorbid depression. Blood samples for the determination of NLRP3, interleukin-18 (IL-18), interleukin-1β (IL-1β), and CRP levels were analyzed using ELISA. NLRP3, IL-1β, IL-18, and CRP levels were significantly higher in myocardial infarction patients compared to the healthy group ( = 0.02, < 0.001, < 0.001, and < 0.001, respectively). No significant difference was found between the myocardial groups with and without depression. However, in the logistic regression analysis, the NLRP3 variable in myocardial infarction patients was found to have a significant contribution to the likelihood of depression ( = 0.015, OR = 1.72, and CI = 1.11-2.66). The likelihood of depression is associated with increasing NLRP3 levels in myocardial infarction patients. However, this potential role should be further explored in a larger sample.

摘要

心血管疾病与抑郁症高度共病,这一点已得到充分证实。本研究旨在评估核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)炎性小体途径和高敏C反应蛋白(CRP)在新发心肌梗死患者伴或不伴抑郁症情况下可能发挥的作用。纳入了68例连续的新发ST段抬高型心肌梗死患者和20名健康受试者。在患者住院1至4天期间,使用《精神疾病诊断与统计手册》第5版障碍的结构化临床访谈——临床医生版对患者进行评估,并将其分为两组:合并抑郁症组和未合并抑郁症组。采用酶联免疫吸附测定法分析用于测定NLRP3、白细胞介素18(IL-18)、白细胞介素1β(IL-1β)和CRP水平的血样。与健康组相比,心肌梗死患者的NLRP3、IL-1β、IL-18和CRP水平显著更高(分别为P = 0.02、P < 0.001、P < 0.001和P < 0.001)。合并抑郁症和未合并抑郁症的心肌梗死组之间未发现显著差异。然而,在逻辑回归分析中,发现心肌梗死患者的NLRP3变量对抑郁症的发生可能性有显著贡献(P = 0.015,OR = 1.72,CI = 1.11 - 2.66)。抑郁症的发生可能性与心肌梗死患者NLRP3水平升高有关。然而,这一潜在作用应在更大样本中进一步探索。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9618/10533058/bfb10560ef34/jpm-13-01295-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9618/10533058/bfb10560ef34/jpm-13-01295-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9618/10533058/bfb10560ef34/jpm-13-01295-g001.jpg

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2
Serum NLRP3 Inflammasome and BDNF: Potential Biomarkers Differentiating Reactive and Endogenous Depression.血清NLRP3炎性小体与脑源性神经营养因子:区分反应性抑郁和内源性抑郁的潜在生物标志物
Front Psychiatry. 2022 Feb 28;13:814828. doi: 10.3389/fpsyt.2022.814828. eCollection 2022.
3
Four clinical profiles of adult outpatients with somatic Symptom Disorders and Related Disorders (SSRD). A latent class analysis.
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J Psychosom Res. 2022 May;156:110775. doi: 10.1016/j.jpsychores.2022.110775. Epub 2022 Mar 1.
4
Targeting the NLRP3 inflammasome in cardiovascular diseases.针对心血管疾病中的 NLRP3 炎性小体。
Pharmacol Ther. 2022 Aug;236:108053. doi: 10.1016/j.pharmthera.2021.108053. Epub 2021 Dec 11.
5
Crosstalk Among NLRP3 Inflammasome, ETR Signaling, and miRNAs in Stress-Induced Depression-Like Behavior: a Modulatory Role for SGLT2 Inhibitors.NLRP3 炎性小体、ETR 信号与应激诱导的抑郁样行为中的 miRNAs 之间的串扰:SGLT2 抑制剂的调节作用。
Neurotherapeutics. 2021 Oct;18(4):2664-2681. doi: 10.1007/s13311-021-01140-4. Epub 2021 Oct 18.
6
Endothelial dysfunction in people with depressive disorders: A systematic review and meta-analysis.抑郁障碍患者的血管内皮功能障碍:系统评价和荟萃分析。
J Psychiatr Res. 2021 Sep;141:152-159. doi: 10.1016/j.jpsychires.2021.06.045. Epub 2021 Jun 26.
7
The interaction between autophagy and neuroinflammation in major depressive disorder: From pathophysiology to therapeutic implications.自噬与神经炎症在重度抑郁症中的相互作用:从病理生理学到治疗意义。
Pharmacol Res. 2021 Jun;168:105586. doi: 10.1016/j.phrs.2021.105586. Epub 2021 Mar 31.
8
Statins for major depressive disorder: A systematic review and meta-analysis of randomized controlled trials.他汀类药物治疗重度抑郁症:随机对照试验的系统评价和荟萃分析。
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9
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