Pomegranate fruit extract suppresses PMACI-,induced expression of pro-inflammatory cytokines .....

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Polyphenol-rich pomegranate fruit extract (POMx) suppresses PMACI-

induced expression of pro-inflammatory cytokines by inhibiting the

activation of MAP Kinases and NF-kappaB in human KU812 cells

Rasheed Z, Akhtar N, Anbazhagan A, Ramamurthy S, Shukla M, Haqqi T

Journal of Inflammation, 2009 6:1 ( 8 January 2009 )

Abstract

Background Mast cells and basophils are multifunctional effector cells

and contain plentiful

secretary granules in their cytoplasm. These cell types are involved in

several inflammatory and immune events and are known to produce an< BR>array

of mediators including a broad spectrum of cytokines. Pomegranate fruit

is rich in anthocyanins and hydrolysable tannins; a group of

polyphenolic compounds shown to be potent antioxidant with

anti-inflammatory activity.

However, no studies have been undertaken to investigate whether a

polyphenol-rich pomegranate

fruit extract (POMx) inhibits the inflammatory activity of activated

human mast cells and

basophils. The aim of this study was to examine whether POMx modulates

inflammatory

reactions using human basophilic cell line KU812.

Methods KU812 cells were stimulated with phorbol-12-myristat e

13-acetate

plus ca lcium

inophore A23187 (PMACI). The inhibitory effect of POMx on

pro-inflammatory cytokine gene

expression and production by stimulated KU812 cells was measured by

quantitative RT-PCR,

and cytokine-specific ELISA assays, respectively. Western blotting was

used to analyze the

effect of POMx on the activation of mitogen-activated protein kinases

(MAPKs), and the nuclear factor (NF)-?B in PMACI stimulated KU812

cells.

Effect on the activity of NF-?B was

determined using Luciferase reporter assay. Significance of differences

from control values were analyzed by means of & nb sp;standard statistical

m ethods .

Results POMx significantly decreased PMACI stimulated inflammatory gene

expression and

production of interleukin (IL)-6 and IL-8 in KU812 cells. The

inhibitory

effect of POMx on the pro-inflammatory cytokines was MAPK subgroups

c-jun N-terminal kinase (JNK)- and

extracellular-regulated kinase (ERK) dependent. In addition, POMx

suppressed the NF-?B

activation induced by PMACI by inhibiting I?B-degradation in human

basophil cells. POMx also

suppressed the powerful induction of NF-?B promoter-mediated luciferase

activity in transiently transfected KU812 cells.

Conclusion These & nb sp;novel pharmacological actions of POMx provide

new

suggestion that POMx

or POMx-derived compounds may be of therapeutic use for the treatment

of

inflammatory

diseases by suppressing mast cells/basophils activation.

http://www.journal-inflammation.com/content/pdf/1476-9255-6-1.pdf

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