The protective effect of icariin and phosphorylated icariin against LPS-induced intestinal goblet cell dysfunction

Innate Immun. 2020 Feb;26(2):97-106. doi: 10.1177/1753425919867746. Epub 2019 Aug 7.

Abstract

In this study, we used LS174T cells as a model to investigate the protective effects of icariin and phosphorylated icariin on LPS-induced goblet cell dysfunction. Our results indicated that icariin and phosphorylated icariin increased the cell viability and decreased lactate dehydrogenase activity in LPS-treated LS174T cells. Icariin and phosphorylated icariin attenuated LPS-induced changes in mucin 2 synthesis and secretion. Besides, Icariin and phosphorylated icariin reduced the levels of ROS, MDA, and H2O2 and increased the activity of SOD, GPx, CAT, and T-AOC in LPS-treated LS174T cells. Moreover, the levels of IL-1β, IL-6, IL-8, and TNF-α were reduced in the Icariin and phosphorylated icariin group. Furthermore, Icariin and phosphorylated icariin decreased gene abundance or enzyme activity of Bip, XBP1, GRP78, CHOP, caspase-3, and caspase-4 in LPS-treated LS174T cells. Our data suggest that Icariin and phosphorylated icariin effectively attenuate LPS-induced intestinal goblet cell function damage through regulating oxidative stress, inflammation, apoptosis, and mucin expression.

Keywords: Icariin; LPS; LS174T cells; mucus barrier; phosphorylated icariin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects*
  • Apoptosis / genetics
  • Caspase 3 / genetics
  • Caspase 3 / metabolism
  • Caspases, Initiator / genetics
  • Caspases, Initiator / metabolism
  • Catalase / metabolism
  • Cell Proliferation / drug effects*
  • Cell Survival / drug effects
  • Endoplasmic Reticulum Chaperone BiP
  • Flavonoids / metabolism
  • Flavonoids / pharmacology*
  • Glutathione Peroxidase / metabolism
  • Goblet Cells / drug effects*
  • Goblet Cells / enzymology
  • Goblet Cells / metabolism
  • Heat-Shock Proteins / genetics
  • Heat-Shock Proteins / metabolism
  • Humans
  • Hydrogen Peroxide / metabolism
  • Inflammation / genetics
  • Inflammation / metabolism*
  • Interleukin-1beta / metabolism
  • Interleukin-6 / metabolism
  • Interleukin-8 / metabolism
  • L-Lactate Dehydrogenase / metabolism
  • Lipopolysaccharides / pharmacology
  • Malondialdehyde / metabolism
  • Mucin-2 / biosynthesis
  • Mucin-2 / metabolism
  • Phosphorylation
  • Reactive Oxygen Species / metabolism
  • Superoxide Dismutase-1 / metabolism
  • Transcription Factor CHOP / genetics
  • Transcription Factor CHOP / metabolism
  • Tumor Necrosis Factor-alpha / metabolism
  • X-Box Binding Protein 1 / genetics
  • X-Box Binding Protein 1 / metabolism

Substances

  • DDIT3 protein, human
  • Endoplasmic Reticulum Chaperone BiP
  • Flavonoids
  • Heat-Shock Proteins
  • Interleukin-1beta
  • Interleukin-6
  • Interleukin-8
  • Lipopolysaccharides
  • Mucin-2
  • Reactive Oxygen Species
  • Tumor Necrosis Factor-alpha
  • X-Box Binding Protein 1
  • XBP1 protein, human
  • Transcription Factor CHOP
  • Malondialdehyde
  • Hydrogen Peroxide
  • L-Lactate Dehydrogenase
  • Catalase
  • Glutathione Peroxidase
  • Superoxide Dismutase-1
  • CASP4 protein, human
  • Caspase 3
  • Caspases, Initiator
  • icariin