Rimonabant reduces keratinocyte viability by induction of apoptosis and exerts topical anti-inflammatory activity in mice. (Articolo in rivista)

Type
Label
  • Rimonabant reduces keratinocyte viability by induction of apoptosis and exerts topical anti-inflammatory activity in mice. (Articolo in rivista) (literal)
Anno
  • 2010-01-01T00:00:00+01:00 (literal)
Alternative label
  • Malfitano AM, Sosa S, Laezza C, De Bortoli M, Tubaro A, Bifulco M. (2010)
    Rimonabant reduces keratinocyte viability by induction of apoptosis and exerts topical anti-inflammatory activity in mice.
    in British journal of pharmacology
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Malfitano AM, Sosa S, Laezza C, De Bortoli M, Tubaro A, Bifulco M. (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 28 (literal)
Rivista
Note
  • ISI Web of Science (WOS) (literal)
Titolo
  • Rimonabant reduces keratinocyte viability by induction of apoptosis and exerts topical anti-inflammatory activity in mice. (literal)
Abstract
  • Background and purpose: There is growing evidence that the cannabinoid CB(1) receptor antagonist, rimonabant (SR141716) exerts potential anti-proliferative and anti-inflammatory actions. Here, we have assessed the effects of rimonabant in vitro in murine immortalized keratinocytes and in vivo by assaying the topical anti-inflammatory activity. Experimental approach: Cell viability and death in a keratinocyte cell line (C5N cells) were measured by Trypan blue exclusion and cytotoxicity by sulforhodamine B assays. Cell cycle progression was assessed by flow cytometry and the expression of apoptotic and anti-apoptotic markers, cyclins, pathways of signal transduction and CB(1) receptor levels were evaluated by Western blot. The topical anti-inflammatory properties of rimonabant were analysed by inhibition of croton oil-induced ear dermatitis in mice. Key results: Rimonabant reduced cell viability and induced apoptosis as shown by the enhanced number of cells in the subG0 phase of the cell cycle, the expression of Bax and reduced levels of Bcl-2 and XIAP. In addition, reduced levels of phosphorylated Akt and NF-kB were detected associated with regulation of total NF-kB and IkB±, phosphorylated IkB±, cyclins D1, E and A. In croton oil-induced ear dermatitis, rimonabant significantly reduced oedema and leukocyte infiltrate. Conclusions and Implications: Rimonabant reduced cell viability, inducing cell death in keratinocytes and decreased croton oil-induced ear dermatitis. Our findings suggest a potential application of rimonabant as a topical anti-inflammatory drug. We did not assess the involvement of CB(1) receptors in these effects of rimonabant. (literal)
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