Sinomenine Attenuates Chronic Intermittent Hypoxia-Induced Lung Injury by Inhibiting Inflammation and Oxidative Stress

Med Sci Monit. 2018 Mar 17:24:1574-1580. doi: 10.12659/msm.906577.

Abstract

BACKGROUND In the present study, we aimed to investigate the effects of sinomenine (SIN) on chronic intermittent hypoxia (CIH)- induced lung injury in rats, and to explore the underlying mechanisms. MATERIAL AND METHODS To perform the investigation, a CIH rat model was established. ELISA assay was applied to detect the level of inflammatory cytokines. Oxidative stress bio-markers (MDA, SOD, and CAT) were determined in lung tissues. In addition, the expression level of NADPH oxidase 2 (Nox2) was analyzed by Western blotting and qRT-PCR, respectively. RESULTS The results showed that compared with other groups, more obvious pulmonary pathological changes were observed in the CIH group. The level of inflammatory cytokines in the CIH group was markedly higher than that in the control and Con-S groups. Compared with the control and Con-S groups, oxidative stress was notably increased in the CIH group. Expression of Nox2 was also increased in the CIH group. The effects caused by CIH in rats were attenuated by SIN treatment. CONCLUSIONS SIN can reverse chronic intermittent hypoxia-induced lung injury through inhibiting inflammation and oxidative stress.

MeSH terms

  • Animals
  • Chronic Disease
  • Cytokines / metabolism
  • Down-Regulation / drug effects
  • Hypoxia / complications*
  • Hypoxia / pathology
  • Inflammation / drug therapy*
  • Inflammation / pathology*
  • Inflammation Mediators / metabolism
  • Lung / drug effects
  • Lung / metabolism
  • Lung / pathology
  • Lung Injury / drug therapy*
  • Lung Injury / etiology*
  • Lung Injury / pathology
  • Male
  • Mice
  • Morphinans / pharmacology
  • Morphinans / therapeutic use*
  • NADPH Oxidases / metabolism
  • NF-E2-Related Factor 2 / metabolism
  • Oxidative Stress*
  • Rats, Sprague-Dawley
  • Signal Transduction / drug effects

Substances

  • Cytokines
  • Inflammation Mediators
  • Morphinans
  • NF-E2-Related Factor 2
  • sinomenine
  • NADPH Oxidases