Authors:
Lei Zhang Department of Critical Care Medicine, The First Hospital of Lanzhou University, The First School of Clinical Medicine of Lanzhou University, Lanzhou City 730000, Gansu, China

Search for other papers by Lei Zhang in
Current site
Google Scholar
PubMed
Close
,
Bin Li Department of Critical Care Medicine, The First Hospital of Lanzhou University, The First School of Clinical Medicine of Lanzhou University, Lanzhou City 730000, Gansu, China

Search for other papers by Bin Li in
Current site
Google Scholar
PubMed
Close
,
Degang Zhang Department of Respiratory Medicine, Lanzhou University Second Hospital, Lanzhou City 730000, China

Search for other papers by Degang Zhang in
Current site
Google Scholar
PubMed
Close
,
Zhuo Wang Department of Pathology, Gansu Provincial Hospital, Lanzhou City 730050, Gansu, China

Search for other papers by Zhuo Wang in
Current site
Google Scholar
PubMed
Close
,
Ye Zhao Department of Critical Care Medicine, The First Hospital of Lanzhou University, The First School of Clinical Medicine of Lanzhou University, Lanzhou City 730000, Gansu, China

Search for other papers by Ye Zhao in
Current site
Google Scholar
PubMed
Close
, and
Qin Yu Department of Critical Care Medicine, The First Hospital of Lanzhou University, The First School of Clinical Medicine of Lanzhou University, Lanzhou City 730000, Gansu, China

Search for other papers by Qin Yu in
Current site
Google Scholar
PubMed
Close
https://orcid.org/0000-0002-5703-8646
Restricted access

Abstract

Acute respiratory distress syndrome (ARDS) refers to the injury of alveolar epithelial cells and capillary endothelial cells due to various injury factors. Research on the pathogenesis of ARDS has made great progress, but the exact pathogenesis of ARDS has not been fully elucidated. Up to now, the prevention and treatment of ARDS is still an important scientific problem that needs to be solved urgently. In this work, we analyzed the effect of uridine on ARDS. An ARDS model was successfully constructed by lipopolysaccharide (LPS) stimulation. Western-blotting, IFA, ELISA, RT-PCT and CLSM were conducted to investigate the effect of uridine on ARDS and insulin resistance, and the results showed that lung histopathological alterations were significantly attenuated by uridine treatment. Further work showed that the levels of proinflammatory cytokines were significantly down-regulated in the lung tissue after treatment with uridine. Additionally, the numbers of total cells and neutrophils in the bronchoalveolar lavage fluid (BALF) were also decreased in the uridine-treated ARDS mice. We further explored the potential mechanism by which uridine could treat ARDS, and the results indicated that NF-κB signaling was down-regulated by uridine treatment. Next, we studied insulin sensitivity in the ARDS mice, and found that insulin signaling was significantly down-regulated, and uridine could enhance insulin sensitivity in the ARDS mice model. Furthermore, we found that the levels of inflammation and oxidative stress were decreased by uridine treatment, which may be the potential mechanism by which uridine could improve insulin sensitivity. Taken together, the current work provides evidence that uridine can serve as a potential drug to treat ARDS and insulin resistance.

  • 1.

    Ji M , Chen M , Hong X , Chen T , Zhang N . The effect of diabetes on the risk and mortality of acute lung injury/acute respiratory distress syndrome: a meta-analysis. Medicine (Baltimore) 2019; 98(13): e15095. https://doi.org/10.1097/MD.0000000000015095.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 2.

    Chen X , Tang J , Shuai W , Meng J , Feng J , Han Z . Macrophage polarization and its role in the pathogenesis of acute lung injury/acute respiratory distress syndrome. Inflamm Res. 2020; 69(9): 883895. https://doi.org/10.1007/s00011-020-01378-2.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 3.

    Deshpande R , Zou C . Pseudomonas aeruginosa induced cell death in acute lung injury and acute respiratory distress syndrome. Int J Mol Sci. 2020; 21(15): 5356. https://doi.org/10.3390/ijms21155356.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 4.

    Lew TW , Kwek TK , Tai D , Earnest A , Loo S , Singh K , et al. Acute respiratory distress syndrome in critically ill patients with severe acute respiratory syndrome. JAMA 2003; 290(3): 374380. https://doi.org/10.1001/jama.290.3.374.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5.

    Stapleton RD , Wang BM , Hudson LD , Rubenfeld GD , Caldwell ES , Steinberg KP . Causes and timing of death in patients with ARDS. Chest 2005; 128(2): 525532. https://doi.org/10.1378/chest.128.2.525.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 6.

    Wu C , Chen X , Cai Y , Xia Ja , Zhou X , Xu S , et al. Risk factors associated with acute respiratory distress syndrome and death in patients with coronavirus disease 2019 Pneumonia in Wuhan, China. JAMA Intern Med. 2020; 180(7): 934943. https://doi.org/10.1001/jamainternmed.2020.0994.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 7.

    Kong G , Huang X , Wang L , Li Y , Sun T , Han S , et al. Astilbin alleviates LPS-induced ARDS by suppressing MAPK signaling pathway and protecting pulmonary endothelial glycocalyx. Int Immunopharmacol. 2016; 36: 5158. https://doi.org/10.1016/j.intimp.2016.03.039.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 8.

    Hetzel M , Bachem M , Anders D , Trischler G , Faehling M . Different effects of growth factors on proliferation and matrix production of normal and fibrotic human lung fibroblasts. Lung 2005; 183(4): 225237. https://doi.org/10.1007/s00408-004-2534-z.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 9.

    Liu XY , Xu HX , Li JK , Zhang D , Ma XH , Huang LN , et al. Neferine protects endothelial glycocalyx via mitochondrial ROS in lipopolysaccharide-induced acute respiratory distress syndrome. Front Physiol. 2018; 9: 102. https://doi.org/10.3389/fphys.2018.00102.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 10.

    Ma X , Liu X , Feng J , Zhang D , Huang L , Li D , et al. Fraxin alleviates LPS-induced ARDS by downregulating inflammatory responses and oxidative damages and reducing pulmonary vascular permeability. Inflammation. 2019; 42(5): 19011912. https://doi.org/10.1007/s10753-019-01052-8.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11.

    Jeengar MK , Thummuri D , Magnusson M , Naidu VGM , Uppugunduri S . Uridine ameliorates dextran Sulfate Sodium (DSS)-Induced colitis in mice. Sci Rep. 2017; 7(1): 3924. https://doi.org/10.1038/s41598-017-04041-9.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 12.

    Simon HU , Haj-Yehia A , Levi-Schaffer F . Role of reactive oxygen species (ROS) in apoptosis induction. Apoptosis 2000; 5(5): 415418. https://doi.org/10.1023/a:1009616228304.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13.

    Pan L , Yao DC , Yu YZ , Li SJ , Chen BJ , Hu GH , et al. Necrostatin-1 protects against oleic acid-induced acute respiratory distress syndrome in rats. Biochem Biophys Res Commun. 2016; 478(4): 16021608. https://doi.org/10.1016/j.bbrc.2016.08.163.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 14.

    Tang PS , Mura M , Seth R , Liu M . Acute lung injury and cell death: how many ways can cells die? Am J Physiol Lung Cell Mol Physiol. 2008; 294(4): L632L641. https://doi.org/10.1152/ajplung.00262.2007.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 15.

    Kitamura Y , Hashimoto S , Mizuta N , Kobayashi A , Kooguchi K , Fujiwara I , et al. Fas/FasL-dependent apoptosis of alveolar cells after lipopolysaccharide-induced lung injury in mice. Am J Respir Crit Care Med. 2001; 163(3 Pt 1): 762769. https://doi.org/10.1164/ajrccm.163.3.2003065.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 16.

    Chen L , Li W , Qi D , Wang D . Lycium barbarum polysaccharide protects against LPS-induced ARDS by inhibiting apoptosis, oxidative stress, and inflammation in pulmonary endothelial cells. Free Radic Res. 2018; 52(4): 480490. https://doi.org/10.1080/10715762.2018.1447105.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 17.

    Mironova GD , Khrenov MO , Talanov EY , Glushkova OV , Parfenyuk SB , Novoselova TV , et al. The role of mitochondrial KATP channel in anti-inflammatory effects of uridine in endotoxemic mice. Arch Biochem Biophys. 2018; 654: 7076. https://doi.org/10.1016/j.abb.2018.07.006.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 18.

    Rozova EV , Mankovskaya IN , Belosludtseva NV , Khmil NV , Mironova GD . Uridine as a protector against hypoxia-induced lung injury. Sci Rep. 2019; 9(1): 9418. https://doi.org/10.1038/s41598-019-45979-2.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 19.

    Krylova IB , Selina EN , Bulion VV , Rodionova OM , Evdokimova NR , Belosludtseva NV , et al. Uridine treatment prevents myocardial injury in rat models of acute ischemia and ischemia/reperfusion by activating the mitochondrial ATP-dependent potassium channel. Sci Rep. 2021; 11(1): 16999. https://doi.org/10.1038/s41598-021-96562-7.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 20.

    Krylova IB , Kachaeva EV , Rodionova OM , Negoda AE , Evdokimova NR , Balina MI , et al. The cardioprotective effect of uridine and uridine-5′-monophosphate: the role of the mitochondrial ATP-dependent potassium channel. Exp Gerontol. 2006; 41(7): 697703. https://doi.org/10.1016/j.exger.2006.03.005.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • Collapse
  • Expand

Editor-in-Chief

László ROSIVALL (Semmelweis University, Budapest, Hungary)

Managing Editor

Anna BERHIDI (Semmelweis University, Budapest, Hungary)

Co-Editors

  • Gábor SZÉNÁSI (Semmelweis University, Budapest, Hungary)
  • Ákos KOLLER (Semmelweis University, Budapest, Hungary)
  • Zsolt RADÁK (University of Physical Education, Budapest, Hungary)
  • László LÉNÁRD (University of Pécs, Hungary)
  • Zoltán UNGVÁRI (Semmelweis University, Budapest, Hungary)

Assistant Editors

  • Gabriella DÖRNYEI (Semmelweis University, Budapest, Hungary)
  • Zsuzsanna MIKLÓS (Semmelweis University, Budapest, Hungary)
  • György NÁDASY (Semmelweis University, Budapest, Hungary)

Hungarian Editorial Board

  • György BENEDEK (University of Szeged, Hungary)
  • Zoltán BENYÓ (Semmelweis University, Budapest, Hungary)
  • Mihály BOROS (University of Szeged, Hungary)
  • László CSERNOCH (University of Debrecen, Hungary)
  • Magdolna DANK (Semmelweis University, Budapest, Hungary)
  • László DÉTÁRI (Eötvös Loránd University, Budapest, Hungary)
  • Zoltán GIRICZ (Semmelweis University, Budapest, Hungary and Pharmahungary Group, Szeged, Hungary)
  • Zoltán HANTOS (Semmelweis University, Budapest and University of Szeged, Hungary)
  • Zoltán HEROLD (Semmelweis University, Budapest, Hungary) 
  • László HUNYADI (Semmelweis University, Budapest, Hungary)
  • Gábor JANCSÓ (University of Pécs, Hungary)
  • Zoltán KARÁDI (University of Pecs, Hungary)
  • Miklós PALKOVITS (Semmelweis University, Budapest, Hungary)
  • Gyula PAPP (University of Szeged, Hungary)
  • Gábor PAVLIK (University of Physical Education, Budapest, Hungary)
  • András SPÄT (Semmelweis University, Budapest, Hungary)
  • Gyula SZABÓ (University of Szeged, Hungary)
  • Zoltán SZELÉNYI (University of Pécs, Hungary)
  • Lajos SZOLLÁR (Semmelweis University, Budapest, Hungary)
  • József TOLDI (MTA-SZTE Neuroscience Research Group and University of Szeged, Hungary)
  • Árpád TÓSAKI (University of Debrecen, Hungary)

International Editorial Board

  • Dragan DJURIC (University of Belgrade, Serbia)
  • Christopher H.  FRY (University of Bristol, UK)
  • Stephen E. GREENWALD (Blizard Institute, Barts and Queen Mary University of London, UK)
  • Tibor HORTOBÁGYI (University of Groningen, Netherlands)
  • George KUNOS (National Institutes of Health, Bethesda, USA)
  • Massoud MAHMOUDIAN (Iran University of Medical Sciences, Tehran, Iran)
  • Tadaaki MANO (Gifu University of Medical Science, Japan)
  • Luis Gabriel NAVAR (Tulane University School of Medicine, New Orleans, USA)
  • Hitoo NISHINO (Nagoya City University, Japan)
  • Ole H. PETERSEN (Cardiff University, UK)
  • Ulrich POHL (German Centre for Cardiovascular Research and Ludwig-Maximilians-University, Planegg, Germany)
  • Andrej A. ROMANOVSKY (University of Arizona, USA)
  • Anwar Ali SIDDIQUI (Aga Khan University, Karachi, Pakistan)
  • Csaba SZABÓ (University of Fribourg, Switzerland)
  • Eric VICAUT (Université de Paris, UMRS 942 INSERM, France)

 

Editorial Correspondence:
Physiology International
Semmelweis University
Faculty of Medicine, Institute of Translational Medicine
Nagyvárad tér 4, H-1089 Budapest, Hungary
Phone/Fax: +36-1-2100-100
E-mail: pi@semmelweis.hu

Indexing and Abstracting Services:

  • Biological Abstracts
  • BIOSIS Previews
  • CAB Abstracts
  • CABELLS Journalytics
  • EMBASE/Excerpta Medica
  • Global Health
  • Index Copernicus
  • Index Medicus
  • Medline
  • Referativnyi Zhurnal
  • SCOPUS
  • WoS - Science Citation Index Expanded

 

2023  
Web of Science  
Journal Impact Factor 2.2
Rank by Impact Factor Q3 (Physiology)
Journal Citation Indicator 0.58
Scopus  
CiteScore 3.4
CiteScore rank Q2 (Physical Therapy, Sports Therapy and Rehabilitation)
SNIP 0.508
Scimago  
SJR index 0.407
SJR Q rank Q2

Physiology International
Publication Model Hybrid
Submission Fee none
Article Processing Charge 1100 EUR/article
Printed Color Illustrations 40 EUR (or 10 000 HUF) + VAT / piece
Regional discounts on country of the funding agency World Bank Lower-middle-income economies: 50%
World Bank Low-income economies: 100%
Further Discounts Editorial Board / Advisory Board members: 50%
Corresponding authors, affiliated to an EISZ member institution subscribing to the journal package of Akadémiai Kiadó: 100%
Subscription fee 2025 Online subsscription: 752 EUR / 828 USD
Print + online subscription: 880 EUR / 968 USD
Subscription Information Online subscribers are entitled access to all back issues published by Akadémiai Kiadó for each title for the duration of the subscription, as well as Online First content for the subscribed content.
Purchase per Title Individual articles are sold on the displayed price.

Physiology International
Language English
Size B5
Year of
Foundation
2006 (1950)
Volumes
per Year
1
Issues
per Year
4
Founder Magyar Tudományos Akadémia
Founder's
Address
H-1051 Budapest, Hungary, Széchenyi István tér 9.
Publisher Akadémiai Kiadó
Publisher's
Address
H-1117 Budapest, Hungary 1516 Budapest, PO Box 245.
Responsible
Publisher
Chief Executive Officer, Akadémiai Kiadó
ISSN 2498-602X (Print)
ISSN 2677-0164 (Online)

Monthly Content Usage

Abstract Views Full Text Views PDF Downloads
Aug 2024 104 0 0
Sep 2024 56 0 0
Oct 2024 250 1 1
Nov 2024 160 1 2
Dec 2024 102 0 0
Jan 2025 66 0 0
Feb 2025 0 0 0