eISSN: 1644-4124
ISSN: 1426-3912
Central European Journal of Immunology
Current issue Archive Manuscripts accepted About the journal Special Issues Editorial board Abstracting and indexing Subscription Contact Instructions for authors Publication charge Ethical standards and procedures
Editorial System
Submit your Manuscript
SCImago Journal & Country Rank
Search
3/2019
vol. 44
 
Share:
Send email
Share:
abstract:
Experimental immunology

Sulfur dioxide reduces lipopolysaccharide-induced acute lung injury in rats

Yu Zhai
1
,
Xin-Li Huang
2
,
Hui-Jie Ma
3
,
Xiao-Hong Zhou
1
,
Jun-Lin Zhou
4
,
Ya-Min Fan
2

  1. Department of Basic Medicine, Hebei University of Chinese Medicine, Shijiazhuang, China
  2. Department of Pathophysiology, Hebei Medical University, Shijiazhuang, China
  3. Department of Physiology, Hebei Medical University, Shijiazhuang, China
  4. Department of Orthopedics, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China
(Centr Eur J Immunol 2019; 44 (3): 226-236)
DOI: https://doi.org/10.5114/ceji.2019.89593
Online publish date: 2019/09/30
View full text Get citation
 
PlumX metrics:
Introduction
Recent studies suggested that sulfur dioxide (SO2) can be produced endogenously by pulmonary vessels and attenuate acute lung injury (ALI) with vasorelaxant effects. This study was conducted to determine whether SO2 can inhibit lung inflammation and relax pulmonary arteries via inhibition of the mitogen-activated protein kinase (MAPK) pathway.

Material and methods
Forty-eight adult male Sprague Dawley rats (250~300 g) were randomly divided into six treatment groups: control (n = 8), control + SO2 (n = 8), control + L-aspartic acid--hydroxamate (HDX) (n = 8), LPS (n = 8), LPS + SO2 (n = 8) and LPS + HDX (n = 8).

Results
Six hours after LPS treatment, rats exhibited elevated pulmonary artery hypertension (PAH), marked pulmonary structure injury with elevated pulmonary myeloperoxidase (MPO) activity and increased expression of intercellular adhesion molecule 1 (ICAM-1) and CD11b, along with decreased pulmonary SO2 production and reduced pulmonary aspartate aminotransferase (AAT) activity. Pretreatment with SO2 saline solution significantly reduced, while HDX (AAT inhibitor) aggravated, the pathogenesis of LPS-induced ALI. Moreover, SO2 saline solution significantly down-regulated expression of Raf-1, MEK-1 and phosphorylated ERK (p-ERK). It also prevented pulmonary hypertension in association with an up-regulated SO2/AAT pathway. However, HDX advanced pulmonary hypertension and inflammatory responses in the lung were associated with a down-regulated SO2/AAT pathway.

Conclusions
Our results suggest that SO2 markedly relieved inflammatory responses, in association with Raf-1, MEK-1 and p-ERK during ALI induced by LPS. The down-regulation of the SO2/AAT pathway may be involved in the mechanism(s) of LPS-induced lung injury.

keywords:

sulfur dioxide, acute lung injury, interleukin, inflammation
Termedia
About us Contact
Copyright notice Privacy policy Advertising policy Contact us
Quick links
Journals Books eBooks Events
© 2024 Termedia Sp. z o.o.
Developed by Bentus.