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Differentional effect of black raspberry extract on two primary human microvascular endothelial cells isolated from intestine and esophagus (669.2)
Author(s) -
Medda Rituparna,
Nie Linghui,
Link Benjamin,
Lyros Orestis,
Otterson Mary,
Rafiee Parvaneh
Publication year - 2014
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.28.1_supplement.669.2
Subject(s) - angiogenesis , apoptosis , interleukin 8 , cancer research , carcinogenesis , inflammatory bowel disease , microbiology and biotechnology , chemistry , in vitro , biology , inflammation , biochemistry , pathology , immunology , medicine , gene , disease
BACKGROUND: Polyphenolic compounds (anthocyanins, flavonoid glycosides) in berries have been shown to prevent the carcinogenesis and tumorigenesis in esophagus and digestive tract. Angiogenesis has been implicated in the pathogenesis of inflammatory bowel disease (IBD). In this study, we aimed to determine the effects of black raspberry extract (BRE) on human primary microvascular endothelial cells isolated from intestine (HIMEC) and esophagus (HEMEC). METHODS: HIMEC and HEMEC monolayer were activated with either with VEGF or TNF‐α/IL‐1β with or without BRE. Effects of BRE on cells survival, apoptosis, proliferation, migration and tube formation were determined. COX‐2, ICAM‐1 and VCAM‐1 genes and proteins expression were assessed by qPCR and immunobloting and nuclear localization of p65 was observed by immunofluorescence staining. RESULTS: VEGF increased cell migration, proliferation and in vitro tube formation and BRE treatment of cells suppressed these effects in both HIMEC and HEMEC. TNF‐α/IL‐1β treatment translocated the p65 subunit of NFκB to nucleus, increased COX‐2, ICAM‐1 and VCAM‐1 gene and protein expression and the PGE2 activity in HIMEC and HEMEC. However, BRE treatment only was effective in inhibiting the COX2, NFκB and ICAM‐1 and VCAM‐1 in HEMEC, but exerted no inhibitory effect on HIMEC. CONCLUSIONS: Taken together, BRE is a potent anti‐inflammatory agent for HEMEC but not HIMEC. Grant Funding Source : MCW Digestive Disease