4.7 Article

Caffeic Acid Modulates Processes Associated with Intestinal Inflammation

期刊

NUTRIENTS
卷 13, 期 2, 页码 -

出版社

MDPI
DOI: 10.3390/nu13020554

关键词

inflammation; caffeic acid; antiglycative; antioxidant; myofibroblasts; ACE inhibitory activity; colon; COX-2; PGE(2)

资金

  1. National Science Center (Poland) [5056/B/P01/2011/40]
  2. project REFRESH-Unlocking the potential of the Institute of Animal Reproduction and Food Research for strengthening integration [FP7-REGPOT-2010-1-264103]
  3. European Research Area and region development
  4. area of Research Potential of the 7th Framework Program
  5. Standard European Marie Curie Fellowship from the European Commission
  6. European Union's Horizon 2020 research and innovation program under the Marie Sklodowska-Curie grant [838991]
  7. Ramon y Cajal contract [RyC-2015-18083]
  8. Marie Curie Actions (MSCA) [838991] Funding Source: Marie Curie Actions (MSCA)

向作者/读者索取更多资源

The study showed that caffeic acid can modulate mechanisms related to intestinal inflammation by targeting COX-2, PGE(2) synthesis, and IL-8 biosynthesis. Additionally, it inhibits AGE formation, possibly due to its high chelating activity.
Caffeic acid is one of the most abundant hydroxycinnamic acids in fruits, vegetables, and beverages. This phenolic compound reaches relevant concentrations in the colon (up to 126 mu M) where it could come into contact with the intestinal cells and exert its anti-inflammatory effects. The aim of this investigation was to study the capacity of caffeic acid, at plausible concentrations from an in vivo point of view, to modulate mechanisms related to intestinal inflammation. Consequently, we tested the effects of caffeic acid (50-10 mu M) on cyclooxygenase (COX)-2 expression and prostaglandin (PG)E-2, cytokines, and chemokines (IL-8, monocyte chemoattractant protein-1 -MCP-1-, and IL-6) biosynthesis in IL-1 beta-treated human myofibroblasts of the colon, CCD-18Co. Furthermore, the capacity of caffeic acid to inhibit the angiotensin-converting enzyme (ACE) activity, to hinder advanced glycation end product (AGE) formation, as well as its antioxidant, reducing, and chelating activity were also investigated. Our results showed that (i) caffeic acid targets COX-2 and its product PGE(2) as well as the biosynthesis of IL-8 in the IL-1 beta-treated cells and (ii) inhibits AGE formation, which could be related to (iii) the high chelating activity exerted. Low anti-ACE, antioxidant, and reducing capacity of caffeic acid was also observed. These effects of caffeic acid expands our knowledge on anti-inflammatory mechanisms against intestinal inflammation.

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