Green Tea @entity3978 @entity3089 Attenuates XXXX -Induced Intercellular Adhesion Molecule-1 Expression and Monocyte Adhesion to Retinal Pigment Epithelial Cells.

@entity3978 @entity32 @entity1 @entity310 @entity26 @entity3089 @entity3090 @entity989 @entity2071
UNASSIGNED: @entity3089 ( @entity3090 ) is a major @entity3978 component of green tea (Camellia sinensis) and demonstrates anti-oxidant, anticancer and anti-inflammatory properties. @entity3090 has been shown to protect @entity989 ( @entity989 ) against oxidative stress-induced cell death. The pathogenesis of diseases in the retina is usually initiated by local @entity32 at the @entity989 cell layer, and @entity32 is mostly associated with leukocyte migration and the secretion of pro-inflammatory cytokines. Whether @entity3090 can modulate the cytokine-induced inflammatory response of @entity989 , particularly leukocyte migration, has not been clearly elucidated, and was therefore the objective of this study. @entity1 cells were cultured with different concentrations of @entity310 in the presence or absence of @entity3090 to different time points. Intracellular reactive @entity26 species (ROS) levels were determined. @entity2071 and phosphor-NF-kB and IkB expression were determined by Western blot analysis. Phosphor-NF-kB nuclear translocation and monocyte- @entity989 adhesion were investigated using immunofluorescence confocal laser scanning microscopy. Scanning electron microscopy (SEM) was carried out to further determine the ultrastructure of monocyte- @entity989 adhesion. The results demonstrated that @entity310 modulated inflammatory effects in ARPE-19 by induction of ROS and up-regulation of @entity2071 expression. Moreover, @entity310 -induced phosphor-NF-kB nuclear translocation, increased phosphor-NF-kB expression and IkB degradation, and increased the degree of monocyte- @entity989 adhesion. Pretreating the cells with @entity3090 ameliorated the inflammatory effects of @entity310 . The results indicated that @entity3090 significantly exerts anti-inflammatory effects in @entity1 cells, partly as a suppressor of @entity310 signaling and that the inhibition was mediated via the NF-kB pathway.
