Protective effects of hesperetin on lipopolysaccharide-induced acute lung injury by targeting MD2

Eur J Pharmacol. 2019 Jun 5:852:151-158. doi: 10.1016/j.ejphar.2019.02.042. Epub 2019 Feb 23.

Abstract

Inflammation plays an important role in acute lung injury (ALI). Hesperetin (HES), a natural flavanone and an aglycone of hesperidin, has established potent anti-inflammatory activity. The aim of this study was to evaluate the potential protective effect of HES on lipopolysaccharide (LPS)-induced ALI in mice and to illuminate its possible directly target. Results indicated that HES pretreatment significantly attenuated LPS-induced pulmonary pathological injury, total protein concentration, markedly decreased the number of neutrophils and the levels of inflammatory cytokines, TNF-α and IL-6, in ALI model in vivo and in vitro. Meanwhile, pretreatment with HES dramatically reduced myeloperoxidase (MPO) activity in LPS-induced ALI mice. Additionally, using molecular docking and co-immunoprecipitation assay, HES showed a directly bind with myeloid differentiation 2 (MD2), in which HES could inhibit MAPK activation, regulate IκB degradation, block the interaction MD2 and its co-receptor Toll-like receptor 4 (TLR4). Taken together, HES showed a significantly protective effect against LPS-induced ALI, which might be associated with MD2 protein. These results attested HES worthy of further progress into an adjunctive potential drug for the treatment for ALI.

Keywords: Acute lung injury; Hesperetin; Inflammation; Myeloid differentiation 2.

MeSH terms

  • Acute Lung Injury / chemically induced*
  • Acute Lung Injury / drug therapy*
  • Acute Lung Injury / metabolism
  • Acute Lung Injury / pathology
  • Animals
  • Cytoprotection / drug effects*
  • Gene Expression Regulation / drug effects
  • Hesperidin / metabolism
  • Hesperidin / pharmacology*
  • Hesperidin / therapeutic use
  • Humans
  • Lipopolysaccharides / pharmacology*
  • Lung / drug effects
  • Lung / metabolism
  • Lung / pathology
  • Lymphocyte Antigen 96 / chemistry
  • Lymphocyte Antigen 96 / metabolism*
  • MAP Kinase Signaling System / drug effects
  • Mice
  • Mice, Inbred C57BL
  • Molecular Docking Simulation
  • Molecular Targeted Therapy*
  • Protein Conformation
  • RAW 264.7 Cells
  • Toll-Like Receptor 4 / metabolism

Substances

  • Lipopolysaccharides
  • Ly96 protein, mouse
  • Lymphocyte Antigen 96
  • Tlr4 protein, mouse
  • Toll-Like Receptor 4
  • Hesperidin
  • hesperetin