Irisolidone attenuates ethanol-induced gastric injury in mice by inhibiting the infiltration of neutrophils.

Abstract

SCOPE:

This study was designed to determine whether irisolidone and its glycoside kakkalide, which are the major constituents of the flower of Pueraria lobata (Kudzu) can attenuate ethanol-induced gastritic injury in mice.

METHODS AND RESULTS:

Irisolidone and kakkalide inhibited IL-8 secretion and NF-κB activation in lipopolysaccharide-stimulated KATO III cells. Therefore, we investigated their protective effects against ethanol-induced gastric injury in mice. Pretreatment with kakkalide or irisolidone decreased the area of hemorrhagic ulcerative lesions caused by ethanol and suppressed stomach myeloperoxidase activity, CXCL4 secretion, and NF-κB activation. The ameliorating effect of irisolidone was more potent than that of kakkalide.

CONCLUSION:

Irisolidone may attenuate ethanol-induced gastritis by inhibiting the infiltration of immune cells, particularly neutrophils, through the regulation of CXCL-4 or IL-8 secretion.

• Authors: Geum-Dan Kang, Sang-Yoon Lee, Se-Eun Jang, Myung Joo Han, Dong-Hyun Kim
• Journal: Molecular nutrition & food research (Mol Nutr Food Res) Vol. 61 Issue 2 (02 2017) ISSN: 1613-4133 [Electronic] Germany
• PMID: 27546737 (Publication Type: Journal Article)
• Copyright: © 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Chemical References

• Flavonoids
• Glycosides
• Interleukin-8
• Isoflavones
• Lipopolysaccharides
• NF-kappa B
• Protective Agents
• Tumor Necrosis Factor-alpha
• irisolidone
• Platelet Factor 4
• Ethanol
• kakkalide
• Peroxidase

Topics

• Animals
• Cell Line
• Ethanol (adverse effects)
• Flavonoids (pharmacology)
• Gastritis (chemically induced, drug therapy, metabolism)
• Glycosides (pharmacology)
• Interleukin-8 (metabolism)
• Isoflavones (pharmacology)
• Lipopolysaccharides (pharmacology)
• Male
• Mice, Inbred ICR
• NF-kappa B (metabolism)
• Neutrophils (drug effects)
• Peroxidase (metabolism)
• Platelet Factor 4 (metabolism)
• Protective Agents (pharmacology)
• Tumor Necrosis Factor-alpha (metabolism)