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A study was conducted to evaluate the effectiveness and safety of a topical emollient in treating mild-to-moderate atopic dermatitis (AD) in adolescents and adults. The study involved 100 participants and lasted for 24 weeks. The results showed that the group using the emollient had significant improvements in various measures compared to the placebo group. No safety concerns were reported. However, the study had limitations and further research is needed to explore other aspects of AD and the effects of the emollient. Overall, the emollient shows promise as a therapeutic option for long-term care of AD patients. [Extracted from the article]

Skin is an organ having a crucial role in the protection of muscle, bone, and internal organs and undergoing continuous self‐renewal and aged. The growing interest in the prevention of skin aging and rejuvenation has sparked a surge of industrial and research studies focusing on the biological and transcriptional changes that occur during skin development and aging. In this study, the aim is to identify transcriptional differences between two main types of human skin cells: the human dermal fibroblasts (HDFs) and the human epidermis keratinocytes (HEKs) isolated from 30 neonatal and 30 adults (old) skin. Through differentially expressed gene (DEG) profiling using DEseq2, 604 up‐, and 769 down‐regulated genes are identified in the old group. A functional analysis using Metascape Gene Ontology and Reactome pathways revealed systematic transcriptomic shifts in key skin formation and maintenance markers, alongside a distinct difference in HOX gene families crucial for embryonic development and diverse biological processes. Among the 39 human HOX gene family, ten posterior HOX genes (HOXA10, 11, 13, HOXB13, HOXC11, and HOXD9‐13) are significantly downregulated, and anterior 25 genes (HOXA2‐7, HOXB1‐9, HOXC4‐6 and 8–9, and HOXD1,3,4 and 8) are upregulated, especially in the old HDFs. The study successfully demonstrates the correlation between HOX genes and the skin aging process, providing strong evidence that HOX genes are proposed as a new marker for skin aging assessment. [ABSTRACT FROM AUTHOR]

In this study, we investigated the inhibitory mechanisms of resorcinol in B16F10 mouse melanoma cells. We found that resorcinol reduced both the melanin content and tyrosinase activity in these cells. In addition, resorcinol suppressed the expression of melanogenic gene microphthalmia-associated transcriptional factor (MITF) and its downstream target genes tyrosinase, tyrosinase-related protein (TRP)-1, and TRP-2. In addition, we found that resorcinol reduced intracellular cAMP levels and protein kinase A (PKA) activity, and increased phosphorylation of the p38 mitogen-activated protein kinase (MAPK). Resorcinol was also found to directly inhibit tyrosinase activity. However, resorcinol-induced decrease in melanin content, tyrosinase activity, and tyrosinase protein levels were attenuated by SB203580, a p38 MAPK inhibitor. Taken together, these data indicate that anti-melanogenic activity of resorcinol is be mediated through the inhibition of cAMP signaling and activation of p38 MAPK, indicating that resorcinol may be a possible ameliorating agent in the treatment of hyperpigmentation skin disorders. [ABSTRACT FROM AUTHOR]

In this study, caviar (sturgeon eggs) was used to elucidate its roles in adiponectin production and skin anti-aging. Recently, caviar has been largely used not only as a nutritional food, but also in cosmetic products. In particular, it has been reported that docosahexaenoic acid (DHA), as one of the main phospholipid components of caviar extract, induces intracellular lipid accumulation and the expression of adiponectin in adipocytes. Although adipocytes are well known to be associated with the skin dermis by secreting various factors (e.g., adiponectin), the effects of caviar extract and DHA on the skin are not well studied. Here, we demonstrate the effects of caviar extract and DHA on adipocyte differentiation and adiponectin production, resulting in a preventive role in UV-irradiated skin aging. Caviar extract and DHA enhanced adipocyte differentiation and promoted the synthesis of transcription factors controlling adipocyte differentiation and adiponectin. In addition, the mRNA expression levels of matrix metalloproteinase-1 (MMP-1) were decreased in UVB-irradiated Hs68 fibroblasts that were cultured in conditioned medium from caviar extract or DHA-treated differentiated adipocytes. Taken together, these results indicate that caviar extract and DHA induce adipocyte differentiation and adiponectin production, thereby inhibiting UVB-induced premature skin aging via the suppression of MMP-1 production. [ABSTRACT FROM AUTHOR]

Melanogenesis is a physiological process that results in the synthesis of melanin pigments, which play a crucial protective role against skin photocarcinogenesis. We investigated the effects of a Polygoni Multiflori Ramulus extract on melanogenesis and isolated emodin from Polygoni Multiflori as an active compound. In addition, the possible mechanisms of action were examined. We found that emodin inhibited both melanin content and tyrosinase activity concentration and time dependently. Tyrosinase, tyrosinase-related protein (TRP)-1, and TRP-2 mRNA levels decreased following emodin treatment. However, while the mRNA levels of microphthalmia-associated transcription factor (MITF) were not affected by emodin, emodin reduced MITF protein levels. Furthermore, expression of the liver X-receptor (LXR) α gene, but not the LXR β gene was upregulated by emodin. Moreover, emodin regulated melanogenesis by promoting degradation of the MITF protein by upregulating the LXR α gene. The emodin effects on MITF was found to be mediated by phosphorylation of p42/44 MAPK. Taken together, these findings indicate that the inhibition of melanogenesis by emodin occurs through reduced MITF protein expression, which is mediated by upregulation of the LXR α gene and suggest that emodin may be useful as a hyperpigmentation inhibitor. [ABSTRACT FROM AUTHOR]

Melanogenesis plays a critical role in the protection of skin against external stresses such as ultraviolet irradiation and oxidative stressors. This study was aimed to investigate the effects of cannabidiol on melanogenesis and its mechanisms of action in human epidermal melanocytes. We found that cannabidiol increased both melanin content and tyrosinase activity. The mRNA levels of microphthalmia-associated transcription factor (MITF), tyrosinase, tyrosinase-related protein (TRP) 1, and TRP2 were increased following cannabidiol treatment. Likewise, cannabidiol increased the protein levels of MITF, TRP 1, TRP 2, and tyrosinase. Mechanistically, we found that cannabidiol regulated melanogenesis by upregulating MITF through phosphorylation of p38 mitogen-activated protein kinase (MAPK) and p42/44 MAPK, independent of cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) signaling. In addition, the melanogenic effect of cannabidiol was found to be mediated by cannabinoid CB 1 receptor, not by CB 2 receptor. Taken together, these findings indicate that cannabidiol-induced melanogenesis is cannabinoid CB 1 receptor-dependent, and cannabidiol induces melanogenesis through increasing MITF gene expression which is mediated by activation of p38 MAPK and p42/44 MAPK. Our results suggest that cannabidiol might be useful as a protective agent against external stresses. [ABSTRACT FROM AUTHOR]

Melanogenesis refers to synthesis of the skin pigment melanin, which plays a critical role in the protection of skin against ultraviolet irradiation and oxidative stressors. We investigated the effects of afzelin on melanogenesis and its mechanisms of action in human epidermal melanocytes. In this study, we found that afzelin increased both melanin content and tyrosinase activity in a concentration-dependent manner. While the mRNA levels of microphthalmia-associated transcription factor (MITF), tyrosinase, and tyrosinase-related protein (TRP)-1 increased following afzelin treatment, the mRNA levels of TRP-2 were not affected by afzelin. Likewise, afzelin increased the protein levels of MITF, TRP-1, and tyrosinase but not TRP-2. Mechanistically, we found that afzelin regulated melanogenesis by upregulating MITF through phosphorylation of p38 mitogen-activated protein kinase (MAPK), independent of cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) signaling. Taken together, these findings indicate that the promotion of melanogenesis by afzelin occurs through increased MITF gene expression, which is mediated by activation of p38 MAPK, and suggest that afzelin may be useful as a protective agent against ultraviolet irradiation. [ABSTRACT FROM AUTHOR]