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In this study, we performed a patch test by applying Bariderm Shield Cream MD in patients with facial dermatitis or sensitive skin with weakened skin barrier function and investigated whether it had an effect in relieving clinical symptoms and improving skin barrier function. We also want to find out the safety of whether new dermatitis will not occur. Methods: 15 pruritus patients (average age 33.07 ± 11.57) applied this twice daily for 8 weeks. Effectiveness was evaluated using SS-10 (Sensitive scale-10), severity by area, TEWL (transepidermal water loss), and SCH (skin corneum hydration). We performed repeated measures ANOVA and post hoc analysis using Python statistics. Results: Fifteen pruritus patients (average age 33.07 ± 11.57) applied this twice daily for 8 weeks. Effectiveness was evaluated using SS-10 (Sensitive scale-10), severity by area, TEWL (transepidermal water loss), and SCH (skin corneum hydration). SS-10 showed a significant difference at week 8. TEWL decreased after 8 weeks, while moisture increased after 4 weeks of application. Severity scores for erythema, scales, papules, and pustules on both cheeks notably decreased compared to baseline at week 4 and 8 after application. Conclusion: This study shows that Barriederm Shield Cream MD® is safe for patients with sensitive skin. It suggests that it is suitable for sensitive skin, with the result of improving the skin barrier, and addresses safety and efficacy issues. [ABSTRACT FROM AUTHOR]

Obesity can induce chronic low-grade inflammation via oxidative stress. Tetrahydrocurcumin (THC) is a major curcumin metabolite with anti-inflammatory and antioxidant effects, but little is known about its effects on the skin of obese individuals. Thus, the aim of this study was to investigate the effects of THC on inflammatory cytokine production, oxidative stress, and autophagy in the skin of mice with high-fat diet- (HFD-) induced obesity. Eight-week-old C57BL/6J mice were fed a regular diet, HFD (60% of total calories from fat), or HFD supplemented with THC (100 mg/kg/day orally) for 12 weeks. We measured their body weights during the experimental period. After 12-week treatments, we performed western blotting and real-time polymerase chain reaction analyses on skin samples to evaluate the expression of inflammatory cytokines, oxidative stress markers, and autophagy markers. We observed higher tumor necrosis factor-α (TNF-α), NADPH oxidase 2 (Nox2), Nox4, and phosphorylated p65 levels; lower nuclear factor erythroid 2-related factor 2 (Nrf2) expression; and higher light chain 3 (LC3), autophagy-related 5 (Atg5), and Beclin 1 expression in the skin of HFD mice compared to the corresponding levels in the skin of mice fed with regular diet. THC administration decreased TNF-α, Nox2, Nox4, and phosphorylated p65 levels and activated the Nrf2 pathway. Interestingly, THC administration suppressed the expression of the autophagy markers LC3, Atg5, and Beclin 1. Overall, HFD-fed mice exhibited an elevation in inflammation, oxidative stress, and autophagy in their skin. THC ameliorated obesity-related skin pathology, and therefore, it is a potential therapeutic agent for obesity-related inflammatory skin diseases. [ABSTRACT FROM AUTHOR]

Polychlorinated biphenyls (PCBs) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) are major environmental pollutants, and their effects on the human body critically depend on the aryl hydrocarbon receptor ( Ah R). The aim of this study was to evaluate the significance of the Ah R and its ligands in chronic inflammatory skin diseases such as atopic dermatitis (AD) and psoriasis. Expression of Ah R-related mRNA was increased in lesional skin from patients with AD and psoriasis compared to those of normal skin from healthy controls. The AhR and aryl hydrocarbon receptor nuclear translocator were colocalized in the nuclei of keratinocytes at the lower epidermis of psoriatic lesions, which suggested activation of the AhR pathway. After treatment of normal human epidermal keratinocytes with TCDD or PCBs, IL-6 and IL-8 production were increased. The results of this study suggest that Ah R is highly expressed in the acute lesional skin of patients with AD and psoriasis, and the Ah R pathway is activated especially in psoriasis. [ABSTRACT FROM AUTHOR]

Recently, the mTOR signaling has emerged as an important player in the pathogenesis of psoriasis. We previously found that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced psoriatic skin inflammation was related to the inhibition of autophagy in keratinocytes. However, the effects and detailed molecular mechanisms of the mTOR inhibitor rapamycin and TCDD on psoriasis in vivo remain to be elucidated. In this study, we aimed to evaluate the effects of rapamycin and TCDD on skin lesions in imiquimod (IMQ)-induced psoriasis using a mouse model. TCDD aggravated skin inflammation in an IMQ-induced psoriatic mouse model. Furthermore, TCDD increased the expression of aryl hydrocarbon receptor (AHR), CYP1A1, proinflammatory cytokines, oxidative stress markers (NADPH oxidase (Nox) 2, Nox4), and phosphorylated P65NF-ĸB, whereas the expression of autophagy-related factors and the antioxidant marker nuclear factor-erythroid 2-related factor 2 (NRF2) decreased. Rapamycin reduced the aggravated skin inflammation induced by TCDD and restored TCDD-induced autophagy suppression and the increase of AHR expression, oxidative stress, and inflammatory response in the skin lesions of a psoriatic mouse model. In conclusion, we demonstrated that rapamycin alleviates TCDD-induced aggravated dermatitis in mice with imiquimod-induced psoriasis-like dermatitis through AHR and autophagy modulation. [ABSTRACT FROM AUTHOR]

Aryl hydrocarbon receptor (AhR) and autophagy reportedly regulate immune responses in the skin. This study explored the effects of AhR activation on autophagy in human keratinocytes, and the relevance of AhR and autophagy in psoriasis pathogenesis. AhR activation by 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) repressed autophagy, while autophagy inhibition induced AhR activation in HaCaT cells and normal human epidermal keratinocytes (NHEKs). A particularly strong interaction between AhR and autophagy was observed in proinflammatory cytokines-stimulated keratinocytes, an in vitro model of psoriasis. In skin biopsies from psoriasis patients, a similar impact of AhR on autophagy and inflammation was observed. AhR inhibition blocked TCDD- and chloroquine-induced p65NF-κB and p38MAPK phosphorylation in proinflammatory cytokines-stimulated HaCaT cells. Moreover, higher expression of AhR and CYP1A1, and lower expression of LC3, were detected in psoriatic skin tissues, compared to the controls. These data demonstrated that AhR modulated autophagy leads to skin inflammation in human keratinocytes via the p65NF-κB/p38MAPK signaling pathways, suggesting that AhR signaling and autophagy might be involved in the pathogenesis of chronic inflammatory disorders such as psoriasis. [ABSTRACT FROM AUTHOR]

A eutectic mixture of lidocaine and prilocaine ( EMLA) is used topically to provide local anesthesia for a variety of painful superficial procedures. Although the side effects of EMLA are usually mild and transient local reactions, potentially life-threatening complications can occur. We report a case of generalized seizures and methemoglobinemia after topical application of EMLA for curettage of molluscum contagiosum lesions in a 3.5-year-old girl with atopic dermatitis. [ABSTRACT FROM AUTHOR]