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Luteolin inhibits human cultured keratinocyte inflammatory cytokine release and proliferation
Author(s) -
Weng Zuyi,
Theoharides Theoharis C
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.lb564
Subject(s) - hacat , luteolin , keratinocyte , cytokine , tumor necrosis factor alpha , mapk/erk pathway , chemistry , vascular endothelial growth factor , microbiology and biotechnology , cell growth , kinase , cancer research , immunology , biology , biochemistry , vegf receptors , in vitro , flavonoid , antioxidant
Psoriasis is characterized by keratinocyte hyperproliferation and chronic inflammation, with increased skin expression of tumor necrosis factor (TNF) and vascular endothelial growth factor (VEGF). Flavonoids, such as luteolin, are potent anti‐inflammatory compounds, but their actions on keratinocytes are unknown. The study objective was to examine the effect of luteolin, and its structural derivative methoxyluteolin, on keratinocyte cytokine production and proliferation. Human HaCaT keratinocytes preincubated with luteolin or methoxyluteolin (1–100 μM for up to 24 h) were stimulated with TNF (50 ng/mL, 6 or 24 h). IL‐6, IL‐8 and VEGF mRNA and protein expression were assayed by PCR and ELISA, as well as cell proliferation by XTT. Luteolin and methoxyluteolin (10–100 μM) significantly reduced TNF‐triggered mRNA and protein expression of IL‐6, IL‐8 and VEGF, as well as keratinocyte proliferation. Luteolin and methoxyluteolin also inhibited TNF‐induced activation of nuclear factor‐kappa B (NF‐κB) and mitogen‐activated protein kinase (MAPK). In conclusion, luteolin and methoxyluteolin are promising candidates for treatment of inflammatory skin diseases, such as psoriasis. Supported by NIH grant AR47652.