Eclipta prostrata Improves DSS-Induced Colitis through Regulation of Inflammatory Response in Intestinal Epithelial Cells

Am J Chin Med. 2017;45(5):1047-1060. doi: 10.1142/S0192415X17500562. Epub 2017 Jun 28.

Abstract

Eclipta prostrata (EP) and its compounds are known to have several pharmacological effects including anti-inflammatory effects. In the present study, we demonstrated that EP improves the dextran sulfate sodium (DSS)-induced colitis symptoms such as body weight loss, colon length shortening and disease activity index. In DSS-induced colitis tissue, EP controls the protein expressions of cyclooxygenase-2 (COX-2) and hypoxia inducible factor-1[Formula: see text] (HIF-1[Formula: see text]). In addition, the release of prostaglandin E2 and vascular endothelial growth factor-A were significantly reduced by EP administration. EP also inhibited COX-2 and HIF-1[Formula: see text] expressions in the tumor necrosis factor-[Formula: see text] stimulated HT-29 cells. These inhibitory effects of EP occurred by reducing the phosphorylation of I[Formula: see text]B and the translocation of the nuclear factor-[Formula: see text]B (NF-[Formula: see text]B). Additionally, we found through HPLC analysis that wedelolactone, which is an inhibitor of NF-[Formula: see text]B transcription, was contained in water extract of EP. These results indicate that EP can improve colitis symptoms through the modulation of immune function in intestinal epithelial cells and suggests that EP has the potential therapeutic effect to intestinal inflammation.

Keywords: Eclipta prostrata; Intestinal Epithelial Cell; Nuclear Factor-B; Ulcerative Colitis.

MeSH terms

  • Acute Disease
  • Animals
  • Anti-Inflammatory Agents*
  • Cells, Cultured
  • Colitis / chemically induced*
  • Colitis / drug therapy*
  • Colitis / metabolism
  • Cyclooxygenase 2 / metabolism
  • Dextran Sulfate / adverse effects*
  • Dinoprostone / metabolism
  • Disease Models, Animal
  • Eclipta / chemistry*
  • Epithelial Cells / immunology*
  • Epithelial Cells / metabolism*
  • Female
  • HT29 Cells
  • Humans
  • Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • Inflammation Mediators / metabolism*
  • Intestinal Mucosa / cytology
  • Intestinal Mucosa / immunology
  • Intestinal Mucosa / metabolism
  • Mice, Inbred BALB C
  • NF-kappa B / metabolism
  • Phytotherapy*
  • Plant Extracts / pharmacology*
  • Plant Extracts / therapeutic use*
  • Severity of Illness Index
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Anti-Inflammatory Agents
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Inflammation Mediators
  • NF-kappa B
  • Plant Extracts
  • Tumor Necrosis Factor-alpha
  • Dextran Sulfate
  • Cyclooxygenase 2
  • Dinoprostone