Skin Pharmacology and Physiology最新文献

Introduction: Sensitive eyes are commonly reported by patients, but there are very few epidemiological studies on this disorder. The aim of this study was the evaluation of the self-reported frequency of sensitive eyes and the association with sensitive skin.

Methods: A survey was performed on a representative sample of the population aged more than 18 years in five different countries (Brazil, China, France, Russia, and the USA). All participants answered a questionnaire on sociodemographic characteristics; skin phototype; eye color; tobacco consumption; exposure to sunlight, air pollution, or having pets; and sleep disorders. The presence of sensitive eyes, eyelids, or skin and their triggering factors were assessed with specific questions.

Results: A total of 10,743 individuals (5,285 men and 5,458 women) were included in the study. Among them, 48.2% reported having sensitive skin and 46.0% reported having sensitive eyes. Sensitive eyes were more frequently reported by women (46.5%) than men (39.4%) in all countries, with the exception of China. The presence of sensitive eyes was more frequent if skin was very sensitive. More than half of subjects with sensitive eyes declared that their triggering factors were exposure to sunlight, dust, touch pad screens, or computer screens or dry air. They were more exposed to pollution and tobacco. Their phototype (including eye color) was lighter.

Discussion/conclusion: This large study shows that self-declared sensitive eyes are very frequent and commonly associated with sensitive skin. Triggering factors of sensitive eyes are more specific.

Background: Studies on mice and aging human hair follicles provide compelling evidence that graying of hair results from premature differentiation of melanocyte stem cells in the niche/bulge.

Objective: The aim of this study was to analyze whether differentiation of melanocyte stem cells is responsible for premature graying of hair (PGH).

Methods: Twenty-five patients with PGH (n = 25) attending the dermatology department were recruited. Five unpigmented and 5 pigmented hairs were obtained per patient by separating individual follicles after 1 mm punch biopsies. The hairs were dissected at a distance of 2 mm from the bulb to separate the stem cells (upper segment - US) from the melanocytes (lower segment - LS). RNA was extracted from hair follicle US and LS, and expression of GP100, tyrosinase (TYR), and tyrosinase-related protein-1 (TYRP1) genes was quantified using Qiagen one-step RT-PCR kit.

Results: We found melanogenesis gene expression in both temporary (US) and permanent (LS) segments of unpigmented and pigmented hair follicles. When compared between the US and LS of white hair, the expression of TYR and GP100 was much higher in US than LS, suggestive of melanogenesis in the bulge. Similarly, when compared between white and black US, the expression of all 3 genes was higher in white US than black US, although not statistically significant.

Limitations: Low samples size and lack of data pertaining to the expression of genes at protein level are the limitations of current study.

Conclusion: Even though this pilot study data yielded key information about the expression of GP100, TYR, and TYRP-1 at the mRNA level, further studies quantifying the expression of these genes at protein level are needed to provide additional clues to further address the results in detail.

Background: The growing use of electronic devices and other artificial light sources in recent decades has changed the pattern of exposure to blue light (400-500 nm). Although some progress has been made in the study of the biological effects of blue light on the skin, many questions in this field remain unexplored. The aim of this article was to review the currently available evidence on the deleterious effects of blue light on the skin as well as the methods and strategies designed to protect from the detrimental effects of blue light. The PubMed and ProQuest databases were searched in January 2022. Search results were supplemented by articles considered relevant by the authors.

Summary: The results of in vitro, in vivo, and clinical studies show that blue light produces direct and indirect effects on the skin. The most significant direct effects are the excessive generation of reactive oxygen and nitrogen species, and hyperpigmentation. Reactive oxygen and nitrogen species cause DNA damage and modulate the immune response. Indirect effects of blue light include disruption of the central circadian rhythm regulation via melatonin signaling and local circadian rhythm regulation via direct effects on skin cells. Antioxidants and sunscreens containing titanium dioxide, iron oxides, and zinc oxide can be used to protect against the detrimental effects of blue light as part of a strategy that combines daytime protection and night-time repair.

Key messages: Blue light produces a wide variety of direct and indirect effects on the skin. As exposure to blue light from artificial sources is likely to continue to increase, this area warrants further investigation.

The relationships between the reversed-phase thin layer chromatographic retention parameters obtained on octadecyl-modified silica (RP-18) sorbent for mobile phases containing water and one of six water-miscible organic modifiers (acetone, methanol, acetonitrile, tetrahydrofurane, N,N-dimethylformamide, 1,4-dioxane) and skin permeability coefficients were studied for a group of 21 cosmetic raw materials, mainly organic sunscreens and preservatives. The correlations between the skin permeability coefficients log Kd calculated in silico using EpiSuite software and the RP-18 thin layer chromatographic retention parameters are mostly linear, especially for compounds of lower-to-medium lipophilicity. It was established that skin permeability coefficient models based on retention parameters collected for mobile phases containing acetone or dioxane (75% v/v), proposed for structurally unrelated cosmetic raw materials are also applicable to other actives, as shown using a test set of compounds whose in vivo log Kd data are available. Skin permeability models developed in this study have the benefit of being based on easily obtained, chromatographic descriptors and their applicability extends beyond cosmetic chemistry.

Introduction: The stratum corneum (SC) is a skin barrier that consists of corneocytes, intercellular lipids, and corneodesmosomes. Ceramides are composed of sphingoid bases linked with various types of fatty acids (FAs), and they are an essential constituent of SC intercellular lipids. Among their subtypes, ceramide NP with a phytosphingosine base is especially important. Most of the previous studies on barrier recovery have focused on a specific ceramide with a single chain FA, not with diverse chain lengths. Skin barrier function is impaired by various factors, including topical corticosteroid.

Objective: We evaluated whether a lipid mixture enriched by ceramide NP with FAs of diverse chain lengths (CER [NP]*) can restore the skin barrier function impaired by topical corticosteroid.

Methods: Twenty-seven healthy adult male volunteers were recruited. Topical corticosteroid was applied on both volar forearms of volunteers. Then, the test cream containing a lipid mixture with CER (NP)* was applied on the left forearm, and a vehicle cream without a lipid mixture was applied on the right forearm of each subject. The functional parameters of the skin barrier were compared before and after the treatment. Epidermal differentiation markers, hyaluronic acid synthase 3 (HAS3), cytokine levels, and the lipid profiles in the SC were analyzed.

Results: The functional parameters of the skin barrier, such as barrier recovery rate, SC integrity, and SC hydration were significantly improved in the test cream-applied site compared to the vehicle cream-applied sites. Filaggrin and HAS3 levels were significantly higher in the sites applied with the test cream. Interleukin (IL)-1α levels were also significantly increased in these sites. IL-2, IL-6, IL-10, and IL-13 levels were significantly decreased in the test cream-applied sites. Lipid analyses showed that C18, C20, and total ceramide NP levels significantly increased in the sites where the test cream was applied. Also, C16, C18, C20, C24, and total ceramide NP levels were significantly elevated in the test cream-applied sites after acute barrier disruption.

Conclusion: Our results demonstrate that a lipid mixture enriched by CER (NP)* could recover the barrier function impaired by topical corticosteroid.

Background: The altered balance between oxidants/antioxidants and inflammation, changes in nitric oxide (NO) release, and mitochondrial function have a role in skin aging through fibroblast modulation. Tocopherol is promising in counteracting the abovementioned events, but the effective mechanism of action needs to be clarified.

Objective: The aim of this study was to examine the effects of α-tocopherol on cell viability/proliferation, NO release, mitochondrial function, oxidants/antioxidants, and inflammation in human dermal fibroblasts (HDF) subjected to oxidative stress.

Methods: HDF were treated with H2O2 in the presence or absence of 1-10 μM α-tocopherol. Cell viability, reactive oxygen species (ROS), NO release, and mitochondrial membrane potential were measured; glutathione (GSH), superoxide dismutase (SOD)-1 and -2, glutathione peroxidase-1 (GPX-1), inducible NO synthase (iNOS), and Ki-67 were evaluated by RT-PCR and immunofluorescence; cell cycle was analyzed using FACS. Pro- and anti-inflammatory cytokine gene expression was analyzed through qRT-PCR.

Results: α-Tocopherol counteracts H2O2, although it remains unclear whether this effect is dose dependent. Improvement of cell viability, mitochondrial membrane potential, Ki-67 expression, and G0/G1 and G2/M phases of the cell cycle was observed. These effects were accompanied by the increase of GSH content and the reduction of SOD-1 and -2, GPX-1, and ROS release. Also, iNOS expression and NO release were inhibited, and pro-inflammatory cytokine gene expression was decreased, confirming the putative role of α-tocopherol against inflammation.

Conclusion: α-Tocopherol exerts protective effects in HDF which underwent oxidative stress by modulating the redox status, inflammation, iNOS-dependent NO release, and mitochondrial function. These observations have a potential role in the prevention and treatment of photoaging-related skin cancers.

Introduction: Constantly increasing air pollution (AP) poses a concern affecting not only our health but also our skin. A typical manifestation of the skin damage induced by AP is its premature aging, irritation, skin barrier impairment, pigmentation disorders, and development or exacerbation of various skin diseases. For these reasons, it is crucial to protect the skin from the negative effects of AP. In this study, we evaluated the ability of some compounds commonly used in dermatological or cosmetic preparations with various biological activities to reduce AP-induced skin damage.

Methods: We established a new experimental model using porcine skin explants exposed to cigarette smoke (CS) in which we determined the level of reactive oxygen species (ROS) in the stratum corneum, skin barrier lipids peroxidation, and gene expression of the pro-inflammatory cytokine interleukin 6 in the epidermis. Then, we tested several polysaccharides and their derivatives such as sodium hyaluronate (SH) of different molecular weight (MW, 1.6 MDa, 300 kDa, 15 kDa, 5 kDa), yeast glucomannan, schizophyllan, and carboxymethyl β-glucan, then vitamin C derivative sodium ascorbyl phosphate, niacinamide, and D-panthenol for their ability to prevent CS-induced skin damage. For the evaluation and comparison of their mechanism of action, film-forming effect was determined by TEWL and gloss measurements and the antioxidant properties were assessed by DPPH assay.

Results: In the skin samples exposed to CS, we observed significant negative changes such as the presence of large amount of ROS in the stratum corneum, high level of skin barrier lipids peroxidation and upregulated IL6 gene expression. Pretreatment of the skin samples with all the tested substances significantly prevented CS-induced skin damage. The most effective were high MW SH probably due to its best film-forming effect and sodium ascorbyl phosphate with the best antioxidant properties.

Conclusion: AP leads to a significant skin damage which can be effectively prevented using some conventional cosmetic and dermatological ingredients with various mechanisms of action.

Introduction: Skin surface proteins are potential biomarkers in psoriasis and can be measured noninvasively with the transdermal analysis patch (TAP). This study aimed to assess markers measured by TAP over time in daily clinical practice, explore their correlation with disease severity in pediatric psoriasis, and compare the TAP and tape stripping detection capability.

Methods: In this prospective observational daily clinical practice study, pediatric psoriasis patients (aged >5 to <18 years) were followed during 1 year. At each visit, TAPs were applied to lesional (n = 2), peri-lesional (n = 2), and non-lesional (n = 1) sites. Post-lesional skin was sampled if all lesions on the arms, legs, or trunk cleared. Treatment and psoriasis severity data were collected. IL-1RA, hBD-2, IL-1α, IL-8, VEGF, CXCL-1/2, CCL-27, IL-23, hBD-1, IL-22, IL-17A, KLK-5, and IL-4 levels were quantified by spot-ELISA. For the statistical analysis, Wilcoxon signed rank tests, Mann-Whitney U tests, and Spearman correlations were used. Detection capability of the TAP was compared to tape stripping in a separate cohort of adult psoriasis patients.

Results: 32 patients (median age 15.0 years, median Psoriasis Area and Severity Index [PASI] 5.2) were followed for a mean of 11.3 (±3.4) months with a total of 104 visits. In lesional skin (n = 197), significantly higher IL-1RA, hBD-2, IL-8, VEGF, CXCL-1/2, IL-23, hBD-1, IL-22, CCL-27, and IL-17A levels were found compared to non-lesional skin (n = 104), while IL-1α was higher in non-lesional skin. Marker levels were highly variable over time and did not correlate with disease severity measured by PASI or SUM scores. Comparison of the TAP and tape strip detection capability in adult psoriasis patients (n = 10) showed that lesional hBD-2, IL1-α, IL-8, and VEGF and non-lesional IL-1RA, hBD-2, IL-8, and VEGF were more frequently detected in tape extracts than TAPs.

Conclusion: Due to the lack of correlation with clinical disease severity and the current detection capability of the markers measured by TAP in psoriasis, its use in regular practice is still a bridge too far.

Background: Psoriasis is a chronic inflammatory skin disease. Sinomenine (SIN) has anti-inflammatory and antioxidant effects.

Objective: The objective of this study was to confirm the anti-inflammatory effects and mechanism of SIN in imiquimod (IMQ)-induced psoriasis-like mouse model and IMQ-induced differentiated human keratinocytes (HaCaT) cells.

Methods: BALB/c mice were treated with IMQ to construct a psoriasis-like mice model. PASI score and HE staining were used to observe pathology injury of skin tissue. The secretion of inflammatory factors and the oxidative stress level were detected by ELISA. HaCaT cells after induction of differentiation were treated with IMQ (100 μM) and SIN (10 μg/mL or 50 μg/mL), cell viability, the secretion of inflammatory factors, and the oxidative stress level were detected by MTT assay, ELISA, respectively. The expression of lncRNA XIST was detected by RT-qPCR. The relationship between XIST and EIF4G2 protein was detected by RNA immunoprecipitation (RIP) assay and ubiquitination experiment.

Results: SIN significantly reduced PASI score, epidermal thickness, inflammatory response, and oxidative stress levels that increased by IMQ in vivo. SIN inhibited IMQ-induced HaCaT cell proliferation, inflammatory response, and oxidative stress levels and decreased the expression of XIST. Overexpression of XIST negated the protective effect of SIN on HaCaT cells. XIST interacted directly with EIF4G2 and regulated EIF4G2 expression via K48 ubiquitin. Knockdown of XIST reduced the half-life of EIF4G2 and decreased EIF4G2 protein stability. In addition, the E3 ubiquitin protein ligase MDM2 interacted with EIF4G2 and downregulated EIF4G2 expression. XIST reduced the interaction between MDM2 and EIF4G2, which mediated EIF4G2 K48 ubiquitination. Overexpression of XIST negated the protective effect of SIN on the inflammation of HaCaT cells through activating the NF-κB signaling pathway, while NF-κB pathway inhibitor PDTC reversed this result.

Conclusion: SIN had a protective effect on psoriasis and could inhibit HaCaT cell proliferation and inflammatory response via XIST/MDM2/EIF4G2/NF-κB axis.