Αρχειοθήκη ιστολογίου

Παρασκευή 13 Οκτωβρίου 2017

Hypochlorous acid is anti-pruritic and anti-inflammatory in a mouse model of atopic dermatitis

Abstract

Background

It has been reported that topical hypochlorous acid (HOCl) formulations lead to relief of itch in human patients with atopic dermatitis, however the specific anti-pruritic mechanism of action remains unclear.

Objective

To confirm itch relief and reduction of lesions in a mouse model of atopic dermatitis and to elucidate possible HOCl's mode of action.

Methods

In this study, the effects of topical administration of HOCl hydrogel (0.05%) on atopic dermatitis-like lesions in NC/Nga mice model as well as in vitro effects of HOCl on dorsal root ganglia neurons and mouse bone marrow derived dendritic cells (mBMDC) were investigated. NC/Nga mice were sensitized with house dust mite allergen and treated topically with HOCl hydrogel both preventively as well as therapeutically against established lesions. Allergen challenge was continued during HOCl hydrogel application.

Results

Treatment with HOCl hydrogel prevented the development of lesions and scratching bouts during the whole observation period. When administered after full development of lesions, HOCl reduced lesions and scratching behaviour to a similar extent as a positive control 0.1% betamethasone dipropionate ointment. The reduced inflammatory response by HOCl treatment was demonstrated by reduced secretion of inflammatory cytokines in affected skin tissue from NC/Nga mice. In addition, HOCl significantly reduced IL-12 production in mBMDC. The diminished scratching behaviour was confirmed by impaired response to several pruritogens in dorsal root ganglia neurons excised from NC/Nga mice after termination of the studies. The response to the stimuli was also reduced by pre-incubation of sensory neurons from untreated BALB/c mice with 0.0001% HOCl.

Conclusions and Clinical Relevance

These data indicate a direct reduction of sensory response by HOCl, leading to significantly reduced itch and inflammation in vivo.

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