Rebamipide suppresses TNF-α mediated inflammation in vitro and attenuates the severity of dermatitis in mice.

Abstract

Rebamipide is a routine drug for the treatment of gastritis in a clinical setting. Recently, it has been shown to protect against various inflammatory diseases, and has provided a potential therapy for these diseases. However, whether rebamipide has a role in dermatitis remains to be elucidated. Here, we found that rebamipide alleviated the inflammatory reaction induced by tumor necrosis factor-α in RAW264.7, a stable macrophage cell line. Furthermore, rebamipide treatment repressed activation of nuclear factor-kappaB signaling, a well-established inflammatory signaling pathway. Moreover, an oxazolone-induced dermatitis mouse model was established to investigate the role of rebamipide in vivo. PBS control group exhibited typical skin inflammation, whereas treatment with rebamipide remarkably attenuated a dermatitis phenotype in this mouse model. The protective role of rebamipide in dermatitis in vivo was probably due to its inhibition of nuclear factor-kappaB signaling. Collectively, rebamipide may represent a promising molecular target for the prevention and treatment of inflammatory skin diseases.

• Authors: Weiwei Li, Yunpeng Zhao, Xiangling Xu, Weiyuan Ma, Peng Gao, Yan Wang, Ke Liang, Ruifeng Li
• Journal: The FEBS journal (FEBS J) Vol. 282 Issue 12 Pg. 2317-26 (Jun 2015) ISSN: 1742-4658 [Electronic] England
• PMID: 25817390 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: © 2015 FEBS.

Chemical References

• Anti-Inflammatory Agents, Non-Steroidal
• Inflammation Mediators
• NF-kappa B
• Quinolones
• Tumor Necrosis Factor-alpha
• Oxazolone
• rebamipide
• Alanine

Topics

• Alanine (analogs & derivatives, pharmacology, therapeutic use)
• Animals
• Anti-Inflammatory Agents, Non-Steroidal (pharmacology, therapeutic use)
• Cell Line, Transformed
• Dermatitis, Allergic Contact (drug therapy, immunology, metabolism, pathology)
• Disease Models, Animal
• Gene Expression Regulation (drug effects)
• Genes, Reporter (drug effects)
• Inflammation Mediators (metabolism)
• Lymph Nodes (drug effects, immunology, metabolism, pathology)
• Macrophage Activation (drug effects)
• Macrophages (drug effects, immunology, metabolism, pathology)
• Male
• Mice, Inbred C57BL
• NF-kappa B (antagonists & inhibitors, genetics, metabolism)
• Oxazolone
• Quinolones (pharmacology, therapeutic use)
• Severity of Illness Index
• Signal Transduction (drug effects)
• Skin (drug effects, immunology, metabolism, pathology)
• Tumor Necrosis Factor-alpha (antagonists & inhibitors, metabolism)