Our finding demonstrated that LED photomodulation with 585nm wavelength suppressed melanin content in HEMs, and the effect was caused by its dose-dependent inhibition on melanogenesis and the induction of HEMs autophagy. This may provide new insights into the efficacy of LED photomodulation in the treatment of hyperpigmentation disorders.
Autophagy is a process involving the self-digestion of components that participates in anti-oxidative stress responses and protects cells against oxidative damage. However, the role of autophagy in the anti-oxidative stress responses of melanocytes remains unclear. To investigate the role of autophagy in human epidermal melanocytes, we knocked down and overexpressed ATG7, the critical gene of autophagy, in normal human epidermal melanocytes. We demonstrated that ATG7-dependent autophagy could affect melanin content of melanocytes by regulating melanogenesis. Moreover, suppression of ATG7-dependent autophagy inhibits proliferation and promotes oxidative stress-induced apoptosis of melanocytes, whereas enhancement of ATG7-dependent autophagy protects melanocytes from oxidative stress-induced apoptosis. Meanwhile, deficiency of ATG7-dependent autophagy results in premature senescence of melanocytes under oxidative stress. Notably, we verified that ATG7-dependent autophagy could alter oxidative stress homeostasis by regulating reactive oxygen species (ROS) production, nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant pathway, and the activity of several antioxidant enzymes in melanocytes. In conclusion, our study suggested that ATG7-dependent autophagy is indispensable for redox homeostasis and the biological functions of melanocytes, such as melanogenesis, proliferation, apoptosis, and senescence, especially under oxidative stress.
Summary
Background
Up till now, there is no standardized and satisfactory treatment strategy for Riehl’s melanosis.
Objective
In this pilot study, we evaluated the efficacy and safety of a novel combination therapy with oral administration of tranexamic acid (TA) and Glycyrrhizin compound for recalcitrant Riehl’s melanosis.
Methods
Ten patients with Riehl’s melanosis were recruited in this study. After elimination of potential contraindication, all patients were treated with 500 mg TA together with 150 mg Glycyrrhizin compound per day orally for 3 months, followed by 500 mg TA per day orally alone for another 3 months. Lesions were imaged by reflectance confocal microscopy (RCM), dermatoscopy, and VISIA® Complexion Analysis System monthly. Mexameter was adopted to evaluate Melanin Index (MI) and Erythema Index (EI). Clinical outcome scores were given by both physicians and patients.
Results
Seven out of ten patients received “marked improvement”, while two received “moderate improvement” and one “minimal improvement” at the final visit. Both mean MI and EI were significantly decreased compared with baselines. Furthermore, RCM and dermatoscopy analyses confirmed the improvement of pigmentation and erythema with decreased pigment granules and telangiectatic vessels.
Conclusion
Oral administration of TA in combination with Glycyrrhizin compound may be an effective therapy for Asian patients with recalcitrant Riehl’s melanosis.
lhis paper presents a new algorithm deterrnining the K-th best path without any circuit between two specified vertices in a connected, simple and nonoriented graph, The rnethod presented here is based on the well-known fact that the minimum set of ring sum of several Euler graphs and a special path between two vertices consists of all paths between the vertices. Lastly, an illu.strative example is giyen and the effLciency of the algorithn is estimated approxirnately.
Oxidative stress represents an imbalance between the generation of reactive oxygen and nitrogen species and the ability of antioxidant systems to decompose those products. Oxidative stress is implicated in the pathogenesis of hyperpigmentation, hypopigmentation, melanoma, and other skin diseases. Regulatory networks involving oxidative stress and related pathways are widely represented in hypopigmentation diseases, particularly vitiligo. However, there is no complete review into the role of oxidative stress in the pathogenesis of hyperpigmentation disorders, especially regarding associations involving oxidative stress and cellular signaling pathways. Here, we review oxidative and antioxidant systems, oxidative stress-induced signal transduction mechanisms, and effects of antioxidant drugs used in preclinical and clinical settings in hyperpigmentation disorders.
Fibroblast-derived melanogenic paracrine mediators are known to play a role in melanogenesis. To investigate the effect of CCN1 (also called CYR61 or cysteine-rich 61) on melanogenesis, normal human epidermal melanocytes were treated with recombinant CCN1 protein. Our findings show that CCN1 activates melanogenesis through promoting melanosome maturation and up-regulation of MITF, TRP-1, and tyrosinase via the integrin α6β1, p38 MAPK, and ERK signaling pathways. Furthermore, we found that UVB irradiation stimulates the secretion of CCN1 from normal human dermal fibroblasts, and CCN1 knockdown in fibroblasts attenuates melanogenesis in melanocyte-fibroblast co-culture system. Moreover, using immunohistochemistry and immunofluorescence staining, we discovered that CCN1 is overexpressed in the dermis of both solar lentigines and Riehl's melanosis lesions. These findings suggest that CCN1 is a fibroblast-derived melanogenic paracrine mediator that is secreted under UVB irradiation, and it may play an important role in the development of hyperpigmentation diseases such as Riehl's melanosis.
Vitiligo is an acquired disfiguring disorder caused by melanocyte (MC) destruction, clinically featured by depigmented maculae and/ or patches on skin. The incidence of vitiligo is 0.5%-2.0% worldwide (Krüger & Schallreuter, 2012). Although vitiligo does not affect the survival of patients, it can bring social pressure (Salman et al., 2016) and cause mental diseases (Osinubi et al., 2017), which greatly impairs general health and social lives of patients. Thus, it is of great significance to carry out in-depth studies on the pathogenesis of vitiligo and explore new molecular markers and more effective therapeutic targets. Over the past decades, various pathogenesis hypotheses of vitiligo have been proposed including neural theory, oxidative stress theory, autoimmune hypothesis, intrinsic theory, melanocytorrhagy hypothesis (Gauthier et al., 2003), and integrated theory, all of which acknowledged the damage of MCs as
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