Molybdenum nanoparticles as a potential topical medication for alopecia treatment through antioxidant pathways that differ from minoxidil.

BACKGROUND: Hair loss is a common dermatological condition including various types such as alopecia areata, androgenetic alopecia, etc. Minoxidil is a topical medication used for treating hair loss, which is effective for various types of alopecia. However, minoxidil has limitations in treating hair loss, such as slow onset of action and low efficacy, and it cannot effectively inhibit one of the major pathogenic factors of hair loss - excessive oxidative stress. METHODS: Transition metal elements with rapid electron transfer, such as molybdenum, have been extensively studied and applied for inhibiting oxidative stress. We established a mouse model for hair growth and intervened with nano-sized molybdenum, minoxidil, and a combination of both. The physicochemical properties of nano-sized molybdenum enabled it to mediate oxidative stress more quickly. RESULTS: The results showed that nano-sized molybdenum can accelerate hair growth, increase the number of local hair follicles, and reduce the expression of oxidative stress-related molecules such as iNOS, COX2, and androgen receptors. The combination of nano-sized molybdenum and minoxidil showed an additive effect in promoting hair growth. CONCLUSION: Our findings suggest that nano-sized molybdenum might be a potential topical medication for treating hair loss by inhibiting the oxidative stress pathway. Nano-sized molybdenum, alone or in combination with minoxidil, could be a promising therapeutic approach for patients with hair loss, particularly those who do not respond well to current treatments. Further clinical studies are warranted to confirm the efficacy and safety of this novel treatment.

Integrated analysis of genome-wide gene expression and DNA methylation profiles reveals candidate genes in ovary endometriosis.

Background: The incidence of endometriosis (EMs), a common disease in gynecology, has increased over the years. Women suffer from the symptoms caused by EMs, such as chronic pelvic pain, dysmenorrhea, and infertility. However, the etiology and pathophysiology of EMs remain unclear. This study aimed to identify candidate genes of endometriosis through integrated analysis of genome-wide gene expression and DNA methylation profiles. Results: Eutopic and ectopic endometrial tissues were collected from patients who were diagnosed as ovarian EMs. Genome-wide methylation profiling identified 17551 differentially methylated loci, with 9777 hypermethylated and 7774 hypomethylated loci. Differentially methylated loci were mainly concentrated in the gene body and intergenic regions. Genome-wide gene expression profiling identified 1837 differentially expressed genes (DEGs), with 1079 genes upregulated and 758 downregulated in ectopic groups. Integrated analysis revealed that DNA methylation was negatively correlated to gene expression in most genomic regions, such as exon, 3'UTR, 5'UTR, and promoter. We also identified promoter-related (53 downregulated and 113 upregulated) and enhancer-related DMGs (212 downregulated and 232 upregulated), which were significantly correlated to the gene expression. Further validation of the top-ranked genes belonging to differentially methylated genes (DMGs) and DEGs revealed that TMEM184A, GREM2, SFN, KIR3DX1, HPGD, ESR1, BST2, PIK3CG and RNASE1 were significant candidate genes in ovarian endometriosis. Conclusion: Our study revealed the significance of DNA methylation in the gene expression in ovary endometriosis, which provides new insights and a molecular foundation for understanding the underlying mechanisms of endometriosis.

Low-energy green light alleviates senescence-like phenotypes in a cell model of photoaging.

BACKGROUND: Ultraviolet B (UVB) affects diverse pathways in skin cells, resulting in skin photoaging. Skin fibroblasts internalize and degrade elastin and collagen, playing prominent roles in photoaging. Green light is used in many fields of dermatology, but few studies have examined its role in photoaging. The present work aimed to assess low-energy green light for its effects in a previously proposed cell model of photoaging and to explore the possible anti-photoaging mechanism. METHODS: The stress-induced premature senescence (SIPS) model was constructed via repeated treatment of MDFs with UVB. Senescence-like phenotypes were compared among normal, low-energy green light pretreatment and UVB groups, for example, cell morphological properties, senescence-associated ß-galactosidase (SA-ß-gal) amounts, extracellular matrix (ECM) biosynthesis and degradation, and autophagy. RESULTS: In comparison with the UVB group, the green light pretreatment group showed significantly decreased number of senescent mast cells and markedly declined signal intensity and amounts of SA-ß-gal-positive cells. Furthermore, green light pretreatment directly affected ECM by increasing type I and type III collagen production and decreasing MMP-1 amounts. Moreover, changes in autophagy levels induced by green light pretreatment provided a potential mechanism underlying its anti-aging property. CONCLUSIONS: Low-energy green light pretreatment improves senescence-like phenotypes in vitro, indicating a possible application for anti-aging in clinic after future research has uncovered the potential mechanism.

Low-level green laser promotes wound healing after carbon dioxide fractional laser therapy.

BACKGROUND: The carbon dioxide (CO2 ) fractional laser resurfacing has become one of the hottest therapies for dermatoses. However, complications such as skin swelling, prolonged erythema, post-inflammatory hyperpigmentation, and scar formation remain. Low-level laser (LLL) therapy is accepted to promote skin wound healing and regeneration, decrease inflammation and pain, and modulate immunoreaction with low-dose laser of different wavelength. 532 nm laser therapy is commonly used to remove pigmented spots and to tender skin, but not utilized in wound care. OBJECTIVE: We aimed to determine the efficacy of the low-level 532 nm green laser in wound healing after CO2 fractional laser. METHODS: Six adult male mice (C57BL/6, 8 weeks old) were prepared for animal experiments. The dorsum of each mouse was divided into four parts that, respectively, received designed treatments, as controlled (group Ctrl), 532 nm LLL-treated (group GL), CO2 fractional laser-treated (group FL), and CO2 fractional laser followed by three times 532 nm LLL-treated (group FG). Hematoxylin-eosin staining (H&E), Masson-trichrome staining, CD31 immunohistochemical staining were performed to evaluate the efficacy of wound healing after treated by different irradiations. Western blotting was used to detect the expression of related proteins. Mouse skin fibroblasts (MSFs) were treated with LLL using a wavelength of 532 nm once. Cellular responses were observed and analyzed after 48 hours. Cell viability and migration of different groups were assessed by scratch and the Cell Counting Kit-8 (CCK8) assays, respectively. RESULTS: Collagen remodeling and epidermis thickness were significantly enhanced in group FG than that in group FL in morphology. Besides, CD31 immunohistochemical staining indicated prominently increased angiogenesis in both groups FL and FG than non-irradiation group. The expression of extracellular matrix (ECM)-related protein (Col1, Col3 and MMP1) showed a remarkable improvement in wound healing in group FG than that in group FL. Irradiated MSFs showed a better migration ability compared with non-irradiated controls. LLL enhanced the secretion function of MSFs on Collagen I and III. CONCLUSIONS: Low-level green laser promotes wound healing after CO2 fractional laser by improving the integrity of skin barrier and allowing for scarless healing. Therefore, low-level green laser therapy might serve as a sequential therapy of invasive laser surgery to ensure a better wound care.

Effects of anthocyanins on the prevention and treatment of cancer.

Anthocyanins are a class of water-soluble flavonoids, which show a range of pharmacological effects, such as prevention of cardiovascular disease, obesity control and antitumour activity. Their potential antitumour effects are reported to be based on a wide variety of biological activities including antioxidant; anti-inflammation; anti-mutagenesis; induction of differentiation; inhibiting proliferation by modulating signal transduction pathways, inducing cell cycle arrest and stimulating apoptosis or autophagy of cancer cells; anti-invasion; anti-metastasis; reversing drug resistance of cancer cells and increasing their sensitivity to chemotherapy. In this review, the latest progress on the anticancer activities of anthocyanins and the underlying molecular mechanisms is summarized using data from basic research in vitro and in vivo, from clinical trials and taking into account theory and practice. LINKED ARTICLES: This article is part of a themed section on Principles of Pharmacological Research of Nutraceuticals. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.11/issuetoc.