Topical application of delphinidin reduces psoriasiform lesions in the flaky skin mouse model by inducing epidermal differentiation and inhibiting inflammation

Abstract

Summary Background Psoriasis is a chronic inflammatory skin disease characterized by hyperproliferation and aberrant keratinocyte differentiation. We have shown that treatment of reconstituted human skin with delphinidin, an anthocyanidin, present in pigmented fruits and vegetables, increased the expression and processing of caspase-14, which is involved in cornification. Delphinidin also increases the expression of epidermal differentiation marker proteins. Objectives To determine whether topical application of delphinidin can modulate pathological markers of psoriasiform lesions in flaky skin mice and if this is associated with increased epidermal differentiation and a reduction in proliferation and inflammation. Methods Five-week-old female homozygous flaky skin mice (fsn/fsn) were treated topically with delphinidin (0.5 mg per cm2 and 1 mg per cm2 skin areas, respectively), five times a week, up to 14 weeks of age. Results Treatment of flaky skin mice with delphinidin resulted in a reduction in (i) pathological markers of psoriasiform lesions; (ii) infiltration of inflammatory cells; and (iii) mRNA and protein expression of inflammatory cytokines. Delphinidin treatment also increased the expression and processing of caspase-14, and expression of filaggrin, loricrin, keratin-1 and keratin-10. Furthermore, there was a decrease in the expression of markers for cell proliferation (proliferating cell nuclear antigen and keratin-14) and modulation of tight junction proteins (occludin and claudin-1). In addition, delphinidin treatment increased the expression of activator protein-1 transcription factor proteins (JunB, JunD, Fra1 and Fra2). Conclusions Delphinidin could be a promising agent for treatment of psoriasis and other hyperproliferative skin disorders.

Anti‑inflammatory effect of delphinidin on intramedullary spinal pressure in a spinal cord injury rat model

“…NF-κB can regulate expression of many cellular factors and regulate inflammatory reactions. Abnormally activated NF-κB may launch the apoptosis of neurons in trauma of central nervous system, excitotoxic injury, ischemic damage and neurodegenerative disease (12). NF-κB is abnormally activated following SCI, activating inducible nitric oxide synthase in neurons (7).…”

“…The expression of various genes in SCI is regulated by NF-κB, including the expression of pro-inflammatory cell factors, such as TNF-α, IL-1β and IL-6, as well as proteases, such as matrix metalloproteinase (7). Pal et al (12) reported that delphinidin reduces psoriasiform lesions by inducing epidermal differentiation and inhibiting inflammation in flaky skin mice. Cho et al (9) suggested that delphinidin inhibited extracellular matrix production in nasal polyp-derived fibroblasts through the MAPK/NF-κB signaling pathway induced by TGF-β1 stimulation.…”

“…Delphinidin has been extensively used as a complementary anti-inflammation and trauma treatment in the form of a food supplement (12,13). The present study investigated whether the anti-inflammatory effect of delphinidin alleviates the SCI-induced inflammation in a rat model through intramedullary spinal pressure.…”

Restoring mitochondrial function and normalizing ROS‐JNK/MAPK pathway exert key roles in glutamine ameliorating bisphenol A‐induced intestinal injury

“…Sos1, as a binding protein of Ras, participates in the promotion of epithelial cell growth via regulating epithelial growth factor receptor signal 41 . Krt10 and Krt76, had been shown to regulate epithelial cell differentiation and proliferation 42 . Ribosome production factor 2 homolog (Rpf2) is a mutual‐action relevant protein of Ki‐67 that is a marker of cell proliferation 43 .…”

Pivotal role of Acitretin nanovesicular gel for effective treatment of psoriasis: ex vivo–in vivo evaluation study

“…In psoriatic skin, lymphocytes may alter the epidermal growth resulting in keratinocyte hyperproliferation and abnormal differentiation of apoptotic cells. 104 Various experimental animal models have been developed for psoriasis, namely, asebia mouse, 105 flaky skin mouse, 106 ultraviolet ray-B induced photodermatitis model, 107 genetically modified models of psoriasiform skin diseases, 108 and mouse tail model. [56][57][58][59][60] In this study, mouse tail model was selected to to avoidance of direct contact of its acidic functional group (−COOH), the trigger factor for irritation episodes, with the SC of the skin.…”