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Inflammation

pp 1–12 | Cite as

Fraxin Alleviates LPS-Induced ARDS by Downregulating Inflammatory Responses and Oxidative Damages and Reducing Pulmonary Vascular Permeability

  • Xiaohong Ma
  • Xiangyong LiuEmail author
  • Jiali Feng
  • Dong Zhang
  • Lina Huang
  • Dongxiao Li
  • Liang Yin
  • Lan Li
  • Xiao-Zhi Wang
Original Article
  • 45 Downloads

Abstract

Acute respiratory distress syndrome (ARDS) is a severe acute disease that threatens human health, and few drugs that can effectively treat this disease are available. Fraxin, one of the main active ingredients of Cortex Fraxini, a Chinese herbal medicine, has presented various pharmacological and biological activities. However, the effects of fraxin on ARDS have yet to be reported. In the present study, the protective effect of fraxin in lipopolysaccharide (LPS)-induced ARDS in a mouse model was analyzed. Results from the hematoxylin and eosin staining showed that fraxin might alleviate pathological changes in the lung tissues of mice with ARDS. ELISA and Western blot results revealed that fraxin might inhibit the production of inflammatory factors, namely, IL-6, TNF-α, and IL-1β, and the activation of NF-κB and MAPK signaling pathways in the lungs. Thus, the inflammatory responses were reduced. Fraxin might inhibit the increase in reactive oxygen species (ROS) and malondialdehyde (MDA), a product of lipid peroxidation in lung tissues. Fraxin might increase the superoxide dismutase (SOD) activity to avoid oxidative damage. Vascular permeability was also assessed through Evans blue dye tissue extravasation and fluorescein isothiocyanate–labeled albumin (FITC-albumin) leakage. Fraxin might inhibit the increase in pulmonary vascular permeability and relieve pulmonary edema. Fraxin was also related to the inhibition of the increase in matrix metalloproteinase-9, which is a glycocalyx-degrading enzyme, and the relief of damages to the endothelial glycocalyx. Thus, fraxin elicited protective effects on mice with LPS-induced ARDS and might be used as a drug to cure ARDS induced by Gram-negative bacterial infection.

KEY WORDS

fraxin lipopolysaccharide ARDS inflammatory responses oxidative damages pulmonary vascular permeability 

Notes

Funding Information

This work was supported by funding from the Natural Science Foundation of Shandong Province, China (ZR2017MH065), Young Teachers’ Training and Funding Project of Binzhou Medical University, and the National Natural Science Foundation of China (No. 81670078).

Compliance with Ethical Standards

Conflict of Interest

The authors declare that they have no conflict of interest.

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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2019

Authors and Affiliations

  • Xiaohong Ma
    • 1
    • 2
  • Xiangyong Liu
    • 1
    Email author
  • Jiali Feng
    • 1
    • 2
  • Dong Zhang
    • 1
    • 2
  • Lina Huang
    • 1
  • Dongxiao Li
    • 1
    • 2
  • Liang Yin
    • 3
  • Lan Li
    • 1
  • Xiao-Zhi Wang
    • 2
  1. 1.Department of Cell BiologyBinzhou Medical UniversityYantaiChina
  2. 2.Department of Respirator Medicine and Intensive Care UnitAffiliated Hospital of Binzhou Medical UniversityBinzhouChina
  3. 3.Department of Immunology, the School of Basic Medical SciencesShandong UniversityJinanChina

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