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Background:The carbon dioxide (CO 2 ) 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 CO 2 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), CO 2 fractional laser-treated (group FL), and CO 2 fractional laser followed by three times 532 nm LLL-treated (group FG). Hematoxylin-eosin staining (H&E), Massontrichrome 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 CO 2 fractional laser by improving the integrity of skin barrier and allowing for scarless healing. Therefore, How to cite this article: Gong C, Lu Y, Jia C, Xu N. Low-level green laser promotes wound healing after carbon dioxide fractional laser therapy.

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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 β‐galactosidase (SA‐β‐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‐β‐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.

BackgroundThe 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.ResultsEutopic 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.ConclusionOur 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.