Luteolin-7-glucoside inhibits IL-22/STAT3 pathway, reducing proliferation, acanthosis, and inflammation in keratinocytes and in mouse psoriatic model

Cell Death and Disease

Volumn 7, Issue 8, 2016, Pages

  Palombo, R ^a   Savini, I ^a   Avigliano, L ^a   Madonna, S ^b   Cavani, A ^b   Albanesi, C ^b   Mauriello, A ^a   Melino, G ^a,c   Terrinoni, A ^a  

^a UNIVERSITY OF ROME TOR VERGATA   (Italy)

^b LABORATORIO DI PATOLOGIA VASCOLARE   (Italy)

^c UNIVERSITY OF LEICESTER   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

CHOLESTEROL; GLUTATHIONE; GLUTATHIONE DISULFIDE; HEXANOIC ACID; INTERLEUKIN 22; LINOLEIC ACID; LUTEOLIN 7 GLUCOSIDE; OCTANOIC ACID; PALMITIC ACID; PALMITOLEIC ACID; STAT3 PROTEIN; STEARIC ACID; AMINOQUINOLINE DERIVATIVE; GLUCOSIDE; IMIQUIMOD; INTERLEUKIN DERIVATIVE; INTERLEUKIN-22; LIPID; LUTEOLIN; LUTEOLIN-7-GLUCOSIDE;

ACANTHOSIS; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ANTIOXIDANT ACTIVITY; ANTIPROLIFERATIVE ACTIVITY; ARTICLE; CELL AGING; CELL CYCLE REGULATION; CELL DIFFERENTIATION; CELL ENERGY; CELL METABOLISM; CONTROLLED STUDY; DERMATITIS; HUMAN; HUMAN CELL; KERATINOCYTE; LIPOGENESIS; MOUSE; MOUSE MODEL; NONHUMAN; OXIDATION REDUCTION STATE; PHENOTYPE; PRIORITY JOURNAL; PROTEIN EXPRESSION; PSORIASIS; SIGNAL TRANSDUCTION; ACANTHOSIS NIGRICANS; ANIMAL; BIOSYNTHESIS; C57BL MOUSE; CELL CULTURE; CELL NUCLEUS; CELL PROLIFERATION; COMPLICATION; DISEASE MODEL; DRUG EFFECTS; IMMUNOHISTOCHEMISTRY; INFLAMMATION; METABOLISM; OXIDATION REDUCTION REACTION; PATHOLOGY; PROTEIN TRANSPORT;

ACANTHOSIS NIGRICANS; AMINOQUINOLINES; ANIMALS; CELL AGING; CELL DIFFERENTIATION; CELL NUCLEUS; CELL PROLIFERATION; CELLS, CULTURED; DISEASE MODELS, ANIMAL; GLUCOSIDES; HUMANS; IMMUNOHISTOCHEMISTRY; INFLAMMATION; INTERLEUKINS; KERATINOCYTES; LIPIDS; LUTEOLIN; MICE, INBRED C57BL; OXIDATION-REDUCTION; PHENOTYPE; PROTEIN TRANSPORT; PSORIASIS; SIGNAL TRANSDUCTION; STAT3 TRANSCRIPTION FACTOR;

EID: 85014887289     PISSN: None     EISSN: 20414889     Source Type: Journal    
DOI: 10.1038/cddis.2016.201     Document Type: Article

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