Protective effect of cardamonin against acetic acid-induced ulcerative colitis in rats

Pharmacol Rep. 2017 Apr;69(2):268-275. doi: 10.1016/j.pharep.2016.11.002. Epub 2016 Nov 9.

Abstract

Background: Ulcerative colitis (UC) is an inflammatory bowel disease with significant morbidity. Cardamonin is a natural chalcone derivative with considerable anti-inflammatory activity. Herein, the potential protective effect of cardamonin against UC was tested in a rat model.

Methods: Rats were given 10 or 30mg/kg/day of cardamonin orally for 14days before induction of UC. On the 14th day of treatment, UC was induced by intrarectal instillation of 2ml 3% acetic acid. Twenty four h after acetic acid instillation, rats were sacrificed and colons were analyzed by macroscopic and histopathological examination. Colon lipid peroxidation was examined by biochemical evaluation of malondialdehyde (MDA). Myeloperoxidase (MPO), iNOS, NF-κB, TNFα levels were measured by ELISA. Moreover, caspase-3 and COX-2 were assessed by immunohistochemical analysis.

Results: Cardamonin at 10 and 30mg/kg decreased the disease activity index and macroscopic damage index scores, and significantly reduced histopathological deterioration. Additionally, cardamonin reduced levels of MPO, iNOS, NF-κB, TNFα and MDA (p<0.05). Immunohistochemistry revealed down-regulation of COX-2 and caspase-3 in groups treated with cardamonin.

Conclusion: Cardamonin has a protective effect against acetic acid-induced colitis. This effect may be due to reducing inflammation, oxidative stress and apoptosis.

Keywords: Apoptosis; Cardamonin; Inflammation; ROS; Ulcerative colitis.

MeSH terms

  • Acetic Acid / pharmacology*
  • Animals
  • Anti-Inflammatory Agents / pharmacology
  • Caspase 3 / metabolism
  • Chalcones / pharmacology*
  • Colitis, Ulcerative / chemically induced*
  • Colitis, Ulcerative / drug therapy*
  • Colitis, Ulcerative / metabolism
  • Colon / drug effects
  • Colon / metabolism
  • Cyclooxygenase 2 / metabolism
  • Inflammation / chemically induced
  • Inflammation / drug therapy
  • Inflammation / metabolism
  • Lipid Peroxidation / drug effects
  • Male
  • Malondialdehyde / metabolism
  • NF-kappa B / metabolism
  • Nitric Oxide Synthase Type II / metabolism
  • Peroxidase / metabolism
  • Protective Agents / pharmacology*
  • Rats
  • Rats, Sprague-Dawley
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Anti-Inflammatory Agents
  • Chalcones
  • NF-kappa B
  • Protective Agents
  • Tumor Necrosis Factor-alpha
  • Malondialdehyde
  • Peroxidase
  • Nitric Oxide Synthase Type II
  • Cyclooxygenase 2
  • Caspase 3
  • cardamonin
  • Acetic Acid