Polysaccharides from Dendrobium officinale ameliorate colitis-induced lung injury via inhibiting inflammation and oxidative stress

Chem Biol Interact. 2021 Sep 25:347:109615. doi: 10.1016/j.cbi.2021.109615. Epub 2021 Aug 5.

Abstract

It has been reported that Dendrobium officinale polysaccharides (DOPS) could alleviate colitis in animal model and suppress the activation of NLRP3 inflammasome and β-arrestin1 in vitro. However, it remains unclear whether DOPS has effect on protecting against colitis-induced pulmonary injury. The purpose of this study was to explore the protective effect and mechanism of DOPS on colitis-induced lung injury. A dextran sodium sulfate (DSS)-induced mice colitis model and lipopolysaccharide (LPS)-stimulated BEAS-2B cells model were applied in this study. The results showed that DOPS treatment restored histopathological changes, reduced inflammatory cells infiltration, pro-inflammatory cytokines levels, reactive oxygen species (ROS) formation and MDA generation, and increased anti-oxidative enzymes activities including SOD and GSH-Px in colitis mice. Further investigation showed that DOPS significantly inhibited the protein expression of TLR4, and apparently up-regulated proteins expressions of nuclear-Nrf2, HO-1 and NQO-1 in lung tissues of colitis mice and in BEAS-2B cells. These results indicated that DOPS significantly inhibited inflammation and oxidative stress to alleviate colitis-induced secondary lung injury, and its mechanisms are closely related to the inhibition of TLR4 signaling pathway and the activation of Nrf2 signaling pathway. DOPS may be a promising drug for alleviating colitis-induced lung injury.

Keywords: Colitis-induced lung injury; Dendrobium officinale polysaccharides; Inflammation; Oxidative stress; TLR4/Nrf2.

MeSH terms

  • Animals
  • Cell Line
  • Colitis / complications*
  • Dendrobium / chemistry
  • Humans
  • Inflammation / drug therapy*
  • Inflammation / pathology
  • Intestinal Mucosa / metabolism
  • Lipopolysaccharides / metabolism
  • Lung / metabolism
  • Lung / pathology
  • Lung Injury / drug therapy*
  • Lung Injury / etiology
  • Lung Injury / pathology
  • Male
  • Mice
  • Mice, Inbred BALB C
  • NF-E2-Related Factor 2 / metabolism
  • Oxidative Stress / drug effects*
  • Permeability / drug effects
  • Polysaccharides / therapeutic use*
  • Protective Agents / therapeutic use*
  • Signal Transduction / drug effects
  • Toll-Like Receptor 4 / metabolism
  • Zonula Occludens-1 Protein / metabolism

Substances

  • Lipopolysaccharides
  • NF-E2-Related Factor 2
  • NFE2L2 protein, human
  • Nfe2l2 protein, mouse
  • Polysaccharides
  • Protective Agents
  • TLR4 protein, human
  • Tjp1 protein, mouse
  • Tlr4 protein, mouse
  • Toll-Like Receptor 4
  • Zonula Occludens-1 Protein