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循环系统中的脂多糖会引起 1 型心肾综合征中炎症反应和氧化应激的激活。

Lipopolysaccharide in systemic circulation induces activation of inflammatory response and oxidative stress in cardiorenal syndrome type 1.

机构信息

Department of Nephrology, Dialysis and Transplantation, St Bortolo Hospital, International Renal Research Institute Vicenza, Via Rodolfi, 37, 36100, Vicenza, Italy.

IRRIV-International Renal Research Institute Vicenza, Vicenza, Italy.

出版信息

J Nephrol. 2019 Oct;32(5):803-810. doi: 10.1007/s40620-019-00613-2. Epub 2019 Apr 20.


DOI:10.1007/s40620-019-00613-2
PMID:31006081
Abstract

BACKGROUND: Cardiorenal syndrome type 1 (CRS type 1) is characterized by a rapid worsening of cardiac function leading to acute kidney injury. In this study, we evaluate the role of lipopolysaccharide (LPS) and various inflammatory markers in the developing acute kidney injury (AKI) in acute heart failure (AHF) patients. METHODS: We enrolled 31 AHF patients and 20 CRS type 1 (the cause of AKI was presumed to be related to cardiac dysfunction) and 17 healthy volunteers without AHF, AKI or CKD, as control group (CTR). We assessed levels of LPS, proinflammatory cytokines (TNF-α, IL-6, IL-18), and oxidative stress marker (myeloperoxidase, MPO). RESULTS: We observed a significant increase in LPS, TNF-α, IL-6, IL-18 and MPO levels in CRS type 1 and AHF group compared to CTR. LPS levels resulted significantly higher in CRS type 1 patients compared with AHF (118.2 pg/mL, IQR 77.8-217.6 versus 13.5 pg/mL, IQR 12.0-17.0, p = 0.008). We found a cytokines and oxidative stress dysregulation in CRS type 1 patients compared with AHF. Furthermore, we observed a strong positive significant correlation between LPS levels and IL-6 (Spearman's rho = 0.79, p < 0.001), and IL-18 (Spearman's rho = 0.77, p < 0.001) and MPO (Spearman's rho = 0.80, p < 0.001), all confirm by simple linear regression analysis. CONCLUSION: CRS type 1 patients presented an increased level of LPS, pro-inflammatory cytokines, and MPO. Furthermore, there is a direct correlation between LPS and pro-inflammatory cytokines and stress oxidative marker. LPS may play a role in the pathophysiology of CRS type 1 inducing inflammation, oxidative stress and finally kidney damage.

摘要

背景:1 型心肾综合征(CRS 型 1)的特征是心脏功能迅速恶化,导致急性肾损伤。在这项研究中,我们评估了脂多糖(LPS)和各种炎症标志物在急性心力衰竭(AHF)患者发展为急性肾损伤(AKI)中的作用。

方法:我们纳入了 31 名 AHF 患者和 20 名 CRS 型 1 患者(AKI 的原因被认为与心功能障碍有关)以及 17 名无 AHF、AKI 或 CKD 的健康志愿者作为对照组(CTR)。我们评估了 LPS、促炎细胞因子(TNF-α、IL-6、IL-18)和氧化应激标志物(髓过氧化物酶,MPO)的水平。

结果:我们观察到 CRS 型 1 和 AHF 组的 LPS、TNF-α、IL-6、IL-18 和 MPO 水平显著升高,与 CTR 相比。CRS 型 1 患者的 LPS 水平明显高于 AHF 患者(118.2 pg/mL,IQR 77.8-217.6 与 13.5 pg/mL,IQR 12.0-17.0,p=0.008)。与 AHF 相比,我们发现 CRS 型 1 患者存在细胞因子和氧化应激失调。此外,我们观察到 LPS 水平与 IL-6(Spearman's rho=0.79,p<0.001)和 IL-18(Spearman's rho=0.77,p<0.001)以及 MPO(Spearman's rho=0.80,p<0.001)之间存在强正相关,所有这些都通过简单线性回归分析得到证实。

结论:CRS 型 1 患者的 LPS、促炎细胞因子和 MPO 水平升高。此外,LPS 与促炎细胞因子和氧化应激标志物之间存在直接相关性。LPS 可能在 CRS 型 1 的病理生理学中发挥作用,导致炎症、氧化应激和最终的肾损伤。

相似文献

[1]
Lipopolysaccharide in systemic circulation induces activation of inflammatory response and oxidative stress in cardiorenal syndrome type 1.

J Nephrol. 2019-4-20

[2]
Levels of Proinflammatory Cytokines, Oxidative Stress, and Tissue Damage Markers in Patients with Acute Heart Failure with and without Cardiorenal Syndrome Type 1.

Cardiorenal Med. 2018-9-11

[3]
Plasma Lipopolysaccharide Concentrations in Cardiorenal Syndrome Type 1.

Cardiorenal Med. 2019-6-25

[4]
[Type 1 cardiorenal syndrome and its possible pathophysiological mechanisms].

G Ital Nefrol. 2012

[5]
Oxidative stress: dual pathway induction in cardiorenal syndrome type 1 pathogenesis.

Oxid Med Cell Longev. 2015

[6]
The Role of Cell-Free Plasma DNA in Patients with Cardiorenal Syndrome Type 1.

Cardiorenal Med. 2021

[7]
Determinants of Monocyte Apoptosis in Cardiorenal Syndrome Type 1.

Cardiorenal Med. 2018-5-30

[8]
Qiliqiangxin Protects against Renal Injury in Rat with Cardiorenal Syndrome Type I through Regulating the Inflammatory and Oxidative Stress Signaling.

Biol Pharm Bull. 2018

[9]
Is circulating endotoxin the trigger for the systemic inflammatory response syndrome seen after injury?

Ann Surg. 1997-5

[10]
Acute coronary syndrome and acute kidney injury: role of inflammation in worsening renal function.

BMC Cardiovasc Disord. 2017-7-26

引用本文的文献

[1]
The Role of Oxidative Stress as a Mechanism in the Pathogenesis of Acute Heart Failure in Acute Kidney Injury.

Diagnostics (Basel). 2024-9-23

[2]
Endogenous Dysregulation of Thromboinflammatory Biomarkers in End-Stage Renal Disease, and Their Amplification by Heart Failure.

Clin Appl Thromb Hemost. 2024

[3]
Gut microbiota metabolites, redox status, and the related regulatory effects of probiotics.

Heliyon. 2023-10-29

[4]
Perfusate Neutrophil Gelatinase-Associated Lipocalin, Kidney Injury Molecular-1, Liver-Type Fatty Acid Binding Protein, and Interleukin-18 as Potential Biomarkers to Predict Delayed Graft Function and Long-Term Prognosis in Kidney Transplant Recipients: A Single-Center Retrospective Study.

Med Sci Monit. 2023-3-4

[5]
Endotoxin in Sepsis: Methods for LPS Detection and the Use of Omics Techniques.

Diagnostics (Basel). 2022-12-27

[6]
Insights of Worsening Renal Function in Type 1 Cardiorenal Syndrome: From the Pathogenesis, Biomarkers to Treatment.

Front Cardiovasc Med. 2021-12-14

[7]
Fibrosis, the Bad Actor in Cardiorenal Syndromes: Mechanisms Involved.

Cells. 2021-7-19

[8]
Grb2 Induces Cardiorenal Syndrome Type 3: Roles of IL-6, Cardiomyocyte Bioenergetics, and Akt/mTOR Pathway.

Front Cell Dev Biol. 2021-3-22

本文引用的文献

[1]
Cardiorenal Syndrome: Classification, Pathophysiology, Diagnosis, and Treatment Strategies: A Scientific Statement From the American Heart Association.

Circulation. 2019-4-16

[2]
Levels of Proinflammatory Cytokines, Oxidative Stress, and Tissue Damage Markers in Patients with Acute Heart Failure with and without Cardiorenal Syndrome Type 1.

Cardiorenal Med. 2018-9-11

[3]
Determinants of Monocyte Apoptosis in Cardiorenal Syndrome Type 1.

Cardiorenal Med. 2018-5-30

[4]
Endotoxin Effects on Cardiac and Renal Functions and Cardiorenal Syndromes.

Blood Purif. 2017-11-22

[5]
The Role of Endotoxin in the Setting of Cardiorenal Syndrome Type 5.

Cardiorenal Med. 2017-10

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Epigenetics: a potential key mechanism involved in the pathogenesis of cardiorenal syndromes.

J Nephrol. 2017-8-5

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Cardiorenal Syndrome Type 5 in Sepsis: Role of Endotoxin in Cell Death Pathways and Inflammation.

Kidney Blood Press Res. 2016

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Pro-Apoptotic Effects of Plasma from Patients with Cardiorenal Syndrome on Human Tubular Cells.

Am J Nephrol. 2015

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Cardiorenal syndrome type 1: a defective regulation of monocyte apoptosis induced by proinflammatory and proapoptotic factors.

Cardiorenal Med. 2015-4

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Oxidative stress: dual pathway induction in cardiorenal syndrome type 1 pathogenesis.

Oxid Med Cell Longev. 2015

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