Rosmarinic acid suppresses colonic inflammation in dextran sulphate sodium (DSS)-induced mice via dual inhibition of NF-[kappa]B and STAT3 activation

Ulcerative colitis (UC), a type of inflammatory bowel disease (IBD), is a chronic inflammatory disorder of the colon. Although UC is generally treated with anti-inflammatory drugs or immunosuppressants, most of these treatments often prove to be inadequate. Rosmarinic acid (RA) is a phenolic ester i...

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Bibliographic Details
Published in:Scientific reports 2017-04, Vol.7, p.46252
Main Authors: Jin, Bo-ram, Chung, Kyung-sook, Cheon, Se-yun, Lee, Minho, Hwang, Soonjae, Noh Hwang, Sam, Rhee, Ki-jong, An, Hyo-jin
Format: Article
Language:English
Subjects:
Antiinflammatory agents
Colon
Cyclooxygenase-2
Dextran
Herbal medicine
Immunosuppressive agents
Inflammatory bowel disease
Inflammatory bowel diseases
Inflammatory diseases
Interleukin 22
Interleukin 6
Intestine
NF-κB protein
Nitric-oxide synthase
Rodents
Rosmarinic acid
Sodium
Stat3 protein
Transcription activation
Transcription factors
Ulcerative colitis
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Summary:Ulcerative colitis (UC), a type of inflammatory bowel disease (IBD), is a chronic inflammatory disorder of the colon. Although UC is generally treated with anti-inflammatory drugs or immunosuppressants, most of these treatments often prove to be inadequate. Rosmarinic acid (RA) is a phenolic ester included in various medicinal herbs such as Salvia miltiorrhiz and Perilla frutescens. Although RA has many biological and pharmacological activities, the anti-inflammatory effect of RA in colonic tissue remains unclear. In this study, we investigated the anti-inflammatory effects and underlying molecular mechanism of RA in mice with dextran sulphate sodium (DSS)-induced colitis. In the DSS-induced colitis model, RA significantly reduced the severity of colitis, as assessed by disease activity index (DAI) scores, colonic damage, and colon length. In addition, RA resulted in the reduction of the inflammatory-related cytokines, such as IL-6, IL-1β, and IL-22, and protein levels of COX-2 and iNOS in mice with DSS-induced colitis. Furthermore, RA effectively and pleiotropically inhibited nuclear factor-kappa B and signal transducer and activator of transcription 3 activation, and subsequently reduced the activity of pro-survival genes that depend on these transcription factors. These results demonstrate that RA has an ameliorative effect on colonic inflammation and thus a potential therapeutic role in colitis.
ISSN:2045-2322
DOI:10.1038/srep46252