Protective effects of escin against indomethacin-induced gastric ulcer in mice

Toxicol Mech Methods. 2014 Dec;24(8):560-6. doi: 10.3109/15376516.2014.951815.

Abstract

Escin, a natural mixture of triterpenoid saponin isolated from the seed of the horse chestnut, is reported to have a potent antiulcer activity against ethanol-induced gastric mucosal lesions. This study investigated the possible mechanisms underlying the gastroprotective effect of escin against indomethacin-induced gastric ulcer in mice. Gastric ulceration was induced by a single intragastric administration of indomethacin (18 mg/kg). The mice underwent intragastric treatment with escin at doses of 0.45, 0.9 or 1.8 mg/kg. Gastric lesion was estimated morphometrically and histopathologically 6 h after the indomethacin administration. The antioxidative parameters in gastric mucosa were measured. Moreover, the activity of myeloperoxidase and the contents of TNF-α, P-selectin and VCAM-1 in gastric tissues were determined. The results showed that escin protected gastric tissues against indomethacin-induced gastropathy as demonstrated from a reduction in the ulcer index and an attenuation of histopathologic changes. Escin caused significant reductions of the contents of malondialdehyde, TNF-α, P-selectin, VCAM-1 and myeloperoxidase activity. The altered activities of superoxide dismutase, catalase and glutathione peroxidase in the stomach tissues were also ameliorated by escin treatment. The present study demonstrated that escin had a protective effect against indomethacin-induced gastric ulcer in mice, not only by virtue of its antioxidant potential, but also due to its anti-inflammatory effect.

Keywords: Anti-inflammatory; antioxidant; escin; gastric ulcer; indomethacin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / administration & dosage
  • Anti-Inflammatory Agents, Non-Steroidal / adverse effects
  • Anti-Inflammatory Agents, Non-Steroidal / antagonists & inhibitors*
  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
  • Anti-Ulcer Agents / administration & dosage
  • Anti-Ulcer Agents / therapeutic use*
  • Antioxidants / administration & dosage
  • Antioxidants / therapeutic use
  • Dose-Response Relationship, Drug
  • Escin / administration & dosage
  • Escin / therapeutic use*
  • Gastric Mucosa / drug effects*
  • Gastric Mucosa / immunology
  • Gastric Mucosa / metabolism
  • Gastric Mucosa / pathology
  • H(+)-K(+)-Exchanging ATPase / chemistry
  • H(+)-K(+)-Exchanging ATPase / metabolism
  • Indomethacin / adverse effects
  • Indomethacin / antagonists & inhibitors*
  • Lipid Peroxidation / drug effects
  • Mice
  • Oxidoreductases / antagonists & inhibitors
  • Oxidoreductases / metabolism
  • P-Selectin / antagonists & inhibitors
  • P-Selectin / chemistry
  • P-Selectin / metabolism
  • Protective Agents / administration & dosage
  • Protective Agents / therapeutic use*
  • Random Allocation
  • Severity of Illness Index
  • Stomach / drug effects
  • Stomach / immunology
  • Stomach / pathology
  • Stomach Ulcer / chemically induced
  • Stomach Ulcer / metabolism
  • Stomach Ulcer / pathology
  • Stomach Ulcer / prevention & control*
  • Tumor Necrosis Factor-alpha / agonists
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Tumor Necrosis Factor-alpha / metabolism
  • Vascular Cell Adhesion Molecule-1 / chemistry
  • Vascular Cell Adhesion Molecule-1 / metabolism

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Anti-Ulcer Agents
  • Antioxidants
  • P-Selectin
  • Protective Agents
  • Tumor Necrosis Factor-alpha
  • Vascular Cell Adhesion Molecule-1
  • Escin
  • Oxidoreductases
  • H(+)-K(+)-Exchanging ATPase
  • Indomethacin