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Ellagic acid, a polyphenol compound present in berries and pomegranate, has received attention as an agent that may have potential bioactivities preventing chronic diseases. This study examined photoprotective effects of ellagic acid on collagen breakdown and inflammatory responses in UV (ultraviolet)-B irradiated human skin cells and hairless mice. Ellagic acid attenuated the UV-B-induced toxicity of HaCaT keratinocytes and human dermal fibroblasts. Non-toxic ellagic acid markedly prevented collagen degradation by blocking matrix metalloproteinase production in UV-B-exposed fibroblasts. Antiwrinkle activity of ellagic acid was further investigated in hairless mice exposed to UV-B, in which it attenuated UV-B-triggered skin wrinkle formation and epidermal thickening. Topical application of 10 lmol ⁄ l ellagic acid diminished production of pro-inflammatory cytokines IL-1b and IL-6, and blocked infiltration of inflammatory macrophages in the integuments of SKH-1 hairless mice exposed to UV-B for 8 weeks. In addition, this compound mitigated inflammatory intracellular cell adhesion molecule-1 expression in UV-B-irradiated keratinocytes and photoaged mouse epidermis. These results demonstrate that ellagic acid prevented collagen destruction and inflammatory responses caused by UV-B. Therefore, dietary and pharmacological interventions with berries rich in ellagic acid may be promising treatment strategies interrupting skin wrinkle and inflammation associated with chronic UV exposure leading to photoageing.

The airway epithelium is thought to play an important role in the pathogenesis of asthma. Airway epithelial activation may contribute to inflammatory and airway-remodeling events characteristic of asthma. Kaempferol, a flavonoid with antioxidative and antitumor properties, has been studied as an antiinflammatory agent. However, little is known regarding its effects on allergic asthma. Human airway epithelial BEAS-2B cells and eosinophils were used to investigate the effects of kaempferol on endotoxin- or cytokine-associated airway inflammation. Kaempferol, nontoxic at 1-20 μmol/L, suppressed LPS-induced eotaxin-1 protein expression that may be mediated, likely via Janus kinase 2 (JAK2) JAK2 signaling. Additionally, 1-20 μmol/L kaempferol dose-dependently attenuated TNFα-induced expression of epithelial intracellular cell adhesion molecule-1 and eosinophil integrin β2, thus encumbering the eosinophil-airway epithelium interaction. Kaempferol blunted TNFα-induced airway inflammation by attenuating monocyte chemoattractant protein-1 transcription, possibly by disturbing NF-κB signaling. This study further investigated antiallergic activity of kaempferol in BALB/c mice sensitized with ovalbumin (OVA) and challenged with a single dose of OVA. Oral administration of kaempferol attenuated OVA challenge-elevated expression of eotaxin-1 and eosinophil major basic protein via the blockade of NF-κB transactivation, thereby blunting eosinophil accumulation in airway and lung tissue. Therefore, dietary kaempferol is effective in ameliorating allergic and inflammatory airway diseases through disturbing NF-κB signaling.

Flavones have been classified as anti-atherogenic agents that inhibit monocyte adhesion to stimulated endothelium, possibly by blocking induction of cell adhesion molecules (CAM). This anti-atherogenic feature of these flavonoids appears to be related to their chemical structures. Flavones may interfere with key signaling events involved in endothelial cell activation by inflammatory mediators. This study examined the effects of flavones on the induction of CAM and the translocation and DNA binding of nuclear factor-kappa B (NF-kappa B) in TNF-alpha-activated human umbilical vein endothelial cells (HUVEC). The effects of flavones, luteolin and apigenin, on adhesion of THP-1 monocytes to the TNF-alpha-activated HUVEC, protein expression and mRNA levels of vascular cell adhesion molecule-1 (VCAM-1), intracellular cell adhesion molecule-1 (ICAM-1) and E-selectin, and nuclear appearance and DNA binding activity of NF-kappa B were determined. Flavanols, flavonols, and flavanones were used for comparison. TNF-alpha significantly induced HUVEC protein expression of VCAM-1, ICAM-1, and E-selectin with increasing mRNA levels. Luteolin and apigenin inhibited the TNF-alpha-induced upregulation of THP-1 adhesion and VCAM-1 expression; these inhibitory effects were dose-dependent. The flavones at doses of > or =25 micromol/L almost completely abolished the increased CAM protein and mRNA regardless of their anti-oxidative activity. With the exception of the flavonol quercetin, flavonoids had no such effect; quercetin substantially attenuated the CAM induction. The flavones inhibited nuclear translocation and DNA binding activity of the NF-kappa B-containing binding site in the promoter region of the CAM genes in TNF-alpha-activated HUVEC. The inhibition of endothelial CAM induction by flavones is mediated by their interference with the NF-kappa B-dependent transcription pathway. Thus, the flavones may hamper initial atherosclerotic events involving endothelial CAM induction.