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Anti‐inflammatory effects of açai (Euterpe oleracea Martius) extract on normal intestinal CCD‐18Co cells
Author(s) -
Santos Dias Manoela Maciel,
RoqueAndrade Andrea,
Talcott Susanne
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.846.11
Subject(s) - gallic acid , chemistry , polyphenol , reactive oxygen species , western blot , cyanidin , cell growth , lipopolysaccharide , inflammation , antioxidant , pharmacology , biochemistry , microbiology and biotechnology , immunology , biology , gene
Açai (Euterpe oleracea Mart.) has a growing demand due to its health benefits and antioxidant capacity. Another property of the fruit is its ability to potentially reduce inflammation leading to irritable bowel disease. This study evaluated the anti‐inflammatory effects of açai polyphenolic extract in non‐cancer human colon fibroblasts cells (CCD‐18). The polyphenolic profile of açai extract was analyzed by HPLC‐MS and it was assessed in CCD‐18 cells using the cell proliferation assay, the dichlorofluorescein diacetate assay for reactive oxygen species (ROS), qRT‐PCR for mRNA, and Western Blot for protein levels. The major compounds present in açai extract were cyanidin‐rutinoside (1395.3 mg/L) and cyanidin‐O‐glucoside (451.5 mg/L). The anti‐inflammatory and antiproliferative effects of the single compound cyanidin‐3‐O‐glucoside were evaluated to determine if the beneficial effects of açaí can be attributed to this compound. The extract (1–5 mg gallic acid equivalent/L) did not reduce cell growth significantly, but reduced ROS induced by lipopolysaccharide (LPS 0.53‐fold). Cyanidin‐3‐O‐glucoside (1–5 mg/L) did not inhibit cell proliferation in CCD‐18Co. Açai extract (5 mg GAE/L) downregulated the LPS‐induced expression of TNF‐α (to 0.42‐ fold), COX‐2 (to 0.61‐fold), TLR‐4 (to 0.52‐fold), TRAF‐6 (to 0.64‐fold), NF‐kB (to 0.76‐fold), VCAM‐1 (to 0.71‐fold) and ICAM‐1 (to 0.68‐fold). The protein levels of COX‐2, TLR‐4, p‐ NF‐kB and ICAM‐1 stimulated by LPS were also downregulated by the extract in a dose‐dependent manner. Cyanidin‐3‐O‐glucoside showed similar anti‐inflammatory effects. These results suggest the anti‐inflammatory effect of açai polyphenolic extract in intestinal cells, involving the inhibition of toll‐like receptor‐4 (TLR‐4) and factor nuclear kappa‐B (NF‐kB). Our results indicate the potential for acai polyphenolics in the prevention of intestinal inflammation.