The histone deacetylase inhibitor, trichostatin A, inhibits the development of 2,4-dinitrofluorobenzene-induced dermatitis in NC/Nga mice

Belinostat resolves skin barrier defects in atopic dermatitis by targeting the dysregulated miR-335:SOX6 axis

“…53 Two independent studies have demonstrated that trichostatin A may suppress the development of AD-like symptoms in mice. 33,34 Recently, it was demonstrated that blocking HDAC activity by using JNJ-26481585, a broad-spectrum HDACI, is crucial to restore nasal mucosal function by promoting tight junction expression. 54 This led us to hypothesize that HDACIs may be effective in treating AD, partly by upregulating miR-335 expression, which can induce differentiation-associated transcriptional signature and restore barrier function.…”

“…Z-stack images were acquired and a phenotypes in mouse models. 33,34 We observed that treating N/ TERT-1 keratinocytes with sodium butyrate (NaB), a broadspectrum HDACI, caused significant miR-335 upregulation (Fig 5, B). NaB treatment also significantly increased MEST expression, supporting our hypothesis that miR-335 is transcribed in tandem with its host gene (Fig 5, C).…”

Oral administration of ginsenoside Rh1 inhibits the development of atopic dermatitis-like skin lesions induced by oxazolone in hairless mice

“…Various murine models have been used to study the mechanisms of human AD and investigate preventive measures [20,23,24,26,[33][34][35]. Since oxazolone-induced skin lesions in hairless mouse exhibited structural, immunologic and biochemical similarities with human AD [25], we induced AD-like skin lesions in SKH1 mice by repeated challenges of oxazolone.…”

“…Various murine models has been used to research mechanisms or treatments of AD: spontaneous model using Nc/Nga mouse in conventional environment [16,17]; transgenic models that express abnormal cytokine levels in mice [18,19]; and induced AD-like models by repeated challenges with allergens (mite extracts [20][21][22] or haptens [23][24][25][26]). Of these models, hapten-induced mice models are advantageous with convenience, reproducibility and low cost [25], but are not characterized by immunologic, epidermal structural and biochemical abnormalities.…”

Effects of the Histone Deacetylase Inhibitor, Trichostatin A, in a Chronic Allergic Airways Disease Model in Mice

“…In addition, in one study TSA was shown to enhance lipopolysaccharide-stimulated IL-8 and block attenuation of IL-8 transcription (Adcock et al 2007). However, most animal studies suggest HDACi possess anti-inflammatory effects via different mechanisms such as the acetylation of non-histone proteins or the up-regulation of Tregs (Kim et al 2010b). In general, the effect of HDACi on pro-inflammation or anti-inflammation is likely to be cell-type dependent.…”