BACKGROUND: Psoriasis is a chronic inflammatory disorder of skin and joints for which conventional treatments that are effective in clearing the moderate-to-severe disease are limited due to long-term safety issues. This necessitates exploring the usefulness of botanical agents for treating psoriasis. We previously showed that delphinidin, a diet-derived anthocyanidin endowed with antioxidant and anti-inflammatory properties, induces normal epidermal keratinocyte differentiation and suggested its possible usefulness for the treatment of psoriasis [1]. OBJECTIVES: To investigate the effect of delphinidin (0-20 μM; 2-5 days) on psoriatic epidermal keratinocyte differentiation, proliferation and inflammation using a three-dimensional reconstructed human psoriatic skin equivalent (PSE) model. METHODS: PSEs and normal skin equivalents (NSEs) established on fibroblast-contracted collagen gels with respective psoriatic and normal keratinocytes and treated with/without delphinidin were analyzed for histology, expression of markers of differentiation, proliferation and inflammation using histomorphometry, immunoblotting, immunochemistry, qPCR and cultured supernatants for cytokine with a Multi-Analyte ELISArray Kit. RESULTS: Our data show that treatment of PSE with delphinidin induced (1) cornification without affecting apoptosis and (2) the mRNA and protein expression of markers of differentiation (caspase-14, filaggrin, loricrin, involucrin). It also decreased the expression of markers of proliferation (Ki67 and proliferating cell nuclear antigen) and inflammation (inducible nitric oxide synthase and antimicrobial peptides S100A7-psoriasin and S100A15-koebnerisin, which are often induced in psoriatic skin). ELISArray showed increased release of psoriasis-associated keratinocyte-derived proinflammatory cytokines in supernatants of the PSE cultures, and this increase was significantly suppressed by delphinidin. CONCLUSIONS: These observations provide a rationale for developing delphinidin for the management of psoriasis.
BACKGROUND:Psoriasis is a chronic inflammatory disorder of skin and joints for which conventional treatments that are effective in clearing the moderate-to-severe disease are limited due to long-term safety issues. This necessitates exploring the usefulness of botanical agents for treating psoriasis. We previously showed that delphinidin, a diet-derived anthocyanidin endowed with antioxidant and anti-inflammatory properties, induces normal epidermal keratinocyte differentiation and suggested its possible usefulness for the treatment of psoriasis [1]. OBJECTIVES: To investigate the effect of delphinidin (0-20 μM; 2-5 days) on psoriatic epidermal keratinocyte differentiation, proliferation and inflammation using a three-dimensional reconstructed humanpsoriatic skin equivalent (PSE) model. METHODS: PSEs and normal skin equivalents (NSEs) established on fibroblast-contracted collagen gels with respective psoriatic and normal keratinocytes and treated with/without delphinidin were analyzed for histology, expression of markers of differentiation, proliferation and inflammation using histomorphometry, immunoblotting, immunochemistry, qPCR and cultured supernatants for cytokine with a Multi-Analyte ELISArray Kit. RESULTS: Our data show that treatment of PSE with delphinidin induced (1) cornification without affecting apoptosis and (2) the mRNA and protein expression of markers of differentiation (caspase-14, filaggrin, loricrin, involucrin). It also decreased the expression of markers of proliferation (Ki67 and proliferating cell nuclear antigen) and inflammation (inducible nitric oxide synthase and antimicrobial peptides S100A7-psoriasin and S100A15-koebnerisin, which are often induced in psoriatic skin). ELISArray showed increased release of psoriasis-associated keratinocyte-derived proinflammatory cytokines in supernatants of the PSE cultures, and this increase was significantly suppressed by delphinidin. CONCLUSIONS: These observations provide a rationale for developing delphinidin for the management of psoriasis.
Authors: Esther Hoste; Geertrui Denecker; Barbara Gilbert; Filip Van Nieuwerburgh; Leslie van der Fits; Bob Asselbergh; Riet De Rycke; Jean-Pierre Hachem; Dieter Deforce; Errol P Prens; Peter Vandenabeele; Wim Declercq Journal: J Invest Dermatol Date: 2012-09-27 Impact factor: 8.551
Authors: L Eckhart; W Declercq; J Ban; M Rendl; B Lengauer; C Mayer; S Lippens; P Vandenabeele; E Tschachler Journal: J Invest Dermatol Date: 2000-12 Impact factor: 8.551
Authors: Jean Christopher Chamcheu; Farrukh Afaq; Deeba N Syed; Imtiaz A Siddiqui; Vaqar M Adhami; Naghma Khan; Sohinderjit Singh; Brendan T Boylan; Gary S Wood; Hasan Mukhtar Journal: Exp Dermatol Date: 2013-05 Impact factor: 3.960
Authors: Geertrui Denecker; Esther Hoste; Barbara Gilbert; Tino Hochepied; Petra Ovaere; Saskia Lippens; Caroline Van den Broecke; Petra Van Damme; Katharina D'Herde; Jean-Pierre Hachem; Gaetan Borgonie; Richard B Presland; Luc Schoonjans; Claude Libert; Joël Vandekerckhove; Kris Gevaert; Peter Vandenabeele; Wim Declercq Journal: Nat Cell Biol Date: 2007-05-21 Impact factor: 28.824
Authors: Jean Christopher Chamcheu; Vaqar M Adhami; Stephane Esnault; Mario Sechi; Imtiaz A Siddiqui; Kenneth A Satyshur; Deeba N Syed; Shah-Jahan M Dodwad; Maria-Ines Chaves-Rodriquez; B Jack Longley; Gary S Wood; Hasan Mukhtar Journal: Antioxid Redox Signal Date: 2016-10-04 Impact factor: 8.401
Authors: Jean Christopher Chamcheu; Imtiaz A Siddiqui; Vaqar M Adhami; Stephane Esnault; Dhruba J Bharali; Abiola S Babatunde; Stephanie Adame; Randall J Massey; Gary S Wood; B Jack Longley; Shaker A Mousa; Hasan Mukhtar Journal: Int J Nanomedicine Date: 2018-07-20