Treatment with a red-laser-based wound therapy device exerts positive effects in models of delayed keratinocyte and fibroblast wound healing.

BACKGROUND: Light therapy is widely used in medicine. Specifically, photobiomodulation has been shown to exert beneficial effects in wound healing disorders, which present a major challenge in health care. The study's aim was providing information on the effect of a novel, red-laser-based wound therapy device (WTD) on keratinocytes and fibroblasts during wound healing under optimal and non-optimal conditions. METHODS: The scratch wound assay was employed as a wound healing model for mechanical damage with readjustment of specific cell milieus, explicitly chronic TH1 inflammation and TH2-dominant conditions. Furthermore, gene expression analysis of pro-inflammatory cytokines (IL1A, IL6, CXCL8), growth factors (TGFB1, PDGFC), transcription factors (NFKB1, TP53) and heat shock proteins (HSP90AA1, HSPA1A, HSPD1) as well as desmogleins (DSG1, DSG3) in keratinocytes and collagen (COL1A1, COL3A1) in fibroblasts was performed after WTD treatment. RESULTS: It was shown that WTD treatment is biocompatible and supports scratch wound closure under non-optimal conditions. A distinct enhancement of desmoglein and collagen gene expression as well as induction of early growth factor gene expression was observed under chronic inflammatory conditions. Moreover, WTD increased HSPD1 transcript levels in keratinocytes and augmented collagen expression in fibroblasts during wound healing under TH2 conditions. WTD treatment also alleviated the inflammatory response in keratinocytes and induced early growth factor gene expression in fibroblasts under physiological conditions. CONCLUSION: Positive effects described for wound treatment with WTD could be replicated in vitro and seem to be to be conferred by a direct influence on cellular processes taking place in keratinocytes and fibroblasts during wound healing.

Potentiating cutaneous wound healing in young and aged skin with nutraceutical collagen peptides.

BACKGROUND: Chronic wounds continue to be a burden to healthcare systems, with ageing linked to increased prevalence of chronic wound development. Nutraceutical collagen peptides have been shown to reduce signs of skin ageing, but their therapeutic potential for cutaneous wound healing remains undefined. AIM: To determine the potential for nutraceutical collagen peptides to promote cutaneous wound healing in vitro in the context of age. METHODS: The potential for bovine- or porcine-derived nutraceutical collagen peptides to promote wound healing of primary cutaneous fibroblasts and keratinocytes derived from young and aged individuals in vitro was assessed by two-dimensional scratch and cell-viability assays and by immunofluorescence for the cell proliferation marker, Ki67. The achievement of peptide concentrations in vivo, equivalent to those exerting a beneficial effect on wound healing in vitro, was confirmed by pharmacokinetic studies of hydroxyproline, a biomarker for collagen peptide absorption, following peptide ingestion by healthy individuals over a wide age range. RESULTS: Results demonstrated significant nutraceutical collagen peptide-induced wound closure of both young and aged fibroblasts and keratinocytes, mediated by enhanced cellular proliferation and migration. Analysis of blood levels of hydroxyproline in young and aged individuals following porcine collagen peptide ingestion revealed peak serum/plasma levels after 2 h at similar concentrations to those exerting beneficial effects on wound healing in vitro. CONCLUSION: These data demonstrate the capacity for nutraceutical collagen peptides to promote cutaneous wound closure in vitro, at pharmacologically achievable concentrations in vivo, thereby offering a potential novel therapeutic strategy for the management of cutaneous wounds in young and aged individuals.

The therapeutic potential of cannabinoids for integumentary wound management.

The increasing legalization of Cannabis for recreational and medicinal purposes in the United States has spurred renewed interest in the therapeutic potential of cannabinoids (CBs) for human disease. The skin has its own endocannabinoid system (eCS) which is a key regulator of various homeostatic processes, including those necessary for normal physiologic wound healing. Data on the use of CBs for wound healing are scarce. Compelling pre-clinical evidence supporting the therapeutic potential of CBs to improve wound healing by modulating key molecular pathways is herein reviewed. These findings merit further exploration in basic science, translational and clinical studies.

Regulation of Anti-Oxidative, Anti-Inflammatory, and Anti-Apoptotic Activity of Advanced Cooling Composition (ACC) in UVB-Irradiated Human HaCaT Keratinocytes.

We recently demonstrated that advanced cooling composition (ACC) has effective ingredients that exhibit anti-inflammatory effects in RAW 264.7 cells stimulated with lipopolysaccharide (LPS) and exhibit strong antimicrobial effects on Pseudomonas aeruginosa, Staphylococcus aureus, MRSA (methicillin-resistant Staphylococcus aureus), Candida albicans, and Streptococcus mutans. To further investigate whether ACC has beneficial effects in ultraviolet B (UVB)-irradiated human keratinocytes (HaCaT cells), HaCaT cells were pretreated with ACC prior to UVB irradiation. Our data showed that ACC, which is effective at 100 µg/mL, is nontoxic and has an antioxidative effect against UVB-induced intracellular reactive oxygen species (ROS) in HaCaT cells. In addition, ACC exerts cytoprotective effects against UVB-induced cytotoxicity in HaCaT cells by inhibiting abnormal inflammation and apoptosis through the regulation of mitogen-activated protein kinase (MAPK) signals, such as jun-amino-terminal kinase (JNK), p38, and extracellular signal-regulated kinase (ERK). Therefore, these results indicate that ACC is a potentially beneficial raw material that possesses antioxidative, anti-inflammatory, and antiapoptotic effects against UVB-induced keratinocytes and may have applications in skin health.

Anti-psoriatic properties of paeoniflorin: suppression of the NF-kappaB pathway and Keratin 17.

BACKGROUND: Psoriasis is a common inflammatory skin disease characterized by hyperproliferation of epidermal keratinocytes, however, there is still no curative therapy for psoriasis. Paeoniflorin (PF), a Chinese herbal medicine, has shown anti-inflammatory effects. OBJECTIVES: We aimed to illustrate the effect and associated mechanism of PF on keratinocyte proliferation using the IMQ-induced psoriasis mouse model. MATERIALS AND METHODS: The anti-psoriatic effect of PF in vivo and in vitro was assessed by western blot, RT-PCR, immunofluorescence, cell counting kit-8 and haematoxylin/eosin staining. RESULTS: In vivo, epidermal thickness, dermal infiltrated lymphocytes and the level of several antimicrobial peptides, pro-inflammatory cytokines, and K17 were significantly reduced in mice with topical application of PF. In vitro, PF inhibited the proliferation of HaCaT cells in a dose-dependent manner, down-regulated K17 expression, and suppressed NF-kappaB activation. CONCLUSION: Our findings indicate that PF may inhibit the proliferation of keratinocytes by targeting K17, suggesting that PF might be a potential target in the treatment of psoriasis.

Baicalin Inhibits Cell Proliferation and Inflammatory Cytokines Induced by Tumor Necrosis Factor α (TNF-α) in Human Immortalized Keratinocytes (HaCaT) Human Keratinocytes by Inhibiting the STAT3/Nuclear Factor kappa B (NF-κB) Signaling Pathway.

BACKGROUND Baicalin is a flavone isolated from the root of Scutellaria baicalensis and is used in traditional Chinese medicine. Psoriasis is a persistent and recurrent chronic inflammatory skin disease that is characterized by inflammation and increased proliferation of keratinocytes. This study aimed to investigate the effects of baicalin on HaCaT immortalized human keratinocytes in vitro and the molecular mechanisms involved. MATERIAL AND METHODS HaCaT keratinocytes were cultured in increasing concentrations of baicalin at 6.25 µM, 12.5 µM, and 25 µM. The in vitro model of psoriasis was established using HaCaT cells treated with tumor necrosis factor-alpha (TNF-alpha). The MTT assay was used to asses cell viability and apoptosis. Western blot was used to measure the expression of Bcl-2, Bax, pro-caspase-3, and cleaved caspase-3, and enzyme-linked immunosorbent assay (ELISA) was performed to detect inflammatory cytokines. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to detect the levels of STAT3 and p65 mRNA. RESULTS Baicalin reduced cell viability and induced apoptosis of HaCaT human keratinocytes in a dose-dependent manner. Increased cell viability and the expression of inflammatory cytokines by HaCaT cells induced by TNF-alpha were significantly inhibited by baicalin. Baicalin significantly inhibited the activation of the STAT3/NF-kappaB pathway in HaCaT cells stimulated by TNF-alpha. CONCLUSIONS Baicalin inhibited the proliferation and expression of inflammatory cytokines in HaCaT immortalized human keratinocytes in vitro through the inhibition of the STAT3/NF-kappaB signaling pathway.

Emerging Pathophysiological Targets of Psoriasis for Future Therapeutic Strategies.

Psoriasis is a chronic autoimmune skin disorder which involves complex interactions between genes, keratinocytes, T-cells and inflammatory cells. It affects 2-3% population worldwide. Molecular biology and cellular immunology of psoriasis, when linked with biotechnology and genetic studies can help researchers to understand the pathophysiology of psoriasis. T-cells activation, keratinocyte hyperproliferation, and angiogenesis are the core mechanisms entailed in the development of psoriasis lesion. Investigators are trying to overcome the challenges of complex pathophysiology pathways involved in this disorder. The different possible hypotheses for its pathophysiology such as growth factors, enzymes, inflammation, and genetic factors mediated pathophysiology have been described in the present review paper in detail. Clinically available drugs only control the symptoms of psoriasis but are not effective for the treatment of the disorder completely and are also associated with some side effects such as itching, renal disorders, hematologic, nonmelanoma skin cancer, pulmonary, gastrointestinal toxicity, etc. This paper made an effort to understand the pathophysiological targets, discuss the research done so far and the treatments available for the effective management of psoriasis.

Ar-Turmerone Exerts Anti-proliferative and Anti-inflammatory Activities in HaCaT Keratinocytes by Inactivating Hedgehog Pathway.

Psoriasis, a common skin inflammatory disorder, is characterized by the aberrant growth and differentiation of keratinocytes. Ar-Turmerone, a main bioactive ingredient of Curcuma longa, has been found to alleviate skin inflammation in psoriasis-like mice. However, the effects and underlying mechanism of ar-turmerone on keratinocytes remain unknown. The effects of ar-turmerone alone or combined with recombinant human sonic hedgehog (rhShh) on cell proliferation, apoptosis, and inflammatory cytokine secretion were explored by MTT, flow cytometry analysis, and ELISA, respectively. The mRNA and protein levels of Shh, glioblastoma-1 (Gli1), and smoothened (SMO) were determined by RT-qPCR and western blot analysis, respectively. Results disclosed that ar-turmerone dose-dependently suppressed proliferation, facilitated apoptosis, and reduced TNF-α-mediated production of interleukin (IL)-1ß, IL-6, and IL-8 in HaCaT cells. Ar-turmerone blocked Hedgehog pathway in HaCaT cells, as evidenced by the reduced expression of Shh, Gli1, and SMO. Moreover, activation of the Hedgehog pathway by rhShh abolished the effects of ar-turmerone on the proliferation, apoptosis, and TNF-α-mediated inflammatory cytokine expression in HaCaT cells. In conclusion, ar-turmerone suppressed cell proliferative ability and attenuated inflammatory cytokine expression by inactivating Hedgehog pathway in HaCaT cells, contributing to better understanding the potential anti-psoriasis effects of ar-turmerone on psoriasis.

Carbon Nanomaterials and LED Irradiation as Antibacterial Strategies against Gram-Positive Multidrug-Resistant Pathogens.

BACKGROUND: Due to current antibiotic resistance worldwide, there is an urgent need to find new alternative antibacterial approaches capable of dealing with multidrug-resistant pathogens. Most recent studies have demonstrated the antibacterial activity and non-cytotoxicity of carbon nanomaterials such as graphene oxide (GO) and carbon nanofibers (CNFs). On the other hand, light-emitting diodes (LEDs) have shown great potential in a wide range of biomedical applications. METHODS: We investigated a nanotechnological strategy consisting of GO or CNFs combined with light-emitting diod (LED) irradiation as novel nanoweapons against two clinically relevant Gram-positive multidrug-resistant pathogens: methicillin-resistant Staphylococcus aureus (MRSA) and methicillin-resistant Staphylococcus epidermidis (MRSE). The cytotoxicity of GO and CNFs was studied in the presence of human keratinocyte HaCaT cells. RESULTS: GO or CNFs exhibited no cytotoxicity and high antibacterial activity in direct contact with MRSE and MRSA cells. Furthermore, when GO or CNFs were illuminated with LED light, the MRSE and MRSA cells lost viability. The rate of decrease in colony forming units from 0 to 3 h, measured per mL, increased to 98.5 ± 1.6% and 95.8 ± 1.4% for GO and 99.5 ± 0.6% and 99.7 ± 0.2% for CNFs. CONCLUSIONS: This combined antimicrobial approach opens up many biomedical research opportunities and provides an enhanced strategy for the prevention and treatment of Gram-positive multidrug-resistant infections.

Apoptotic or Antiproliferative Activity of Natural Products against Keratinocytes for the Treatment of Psoriasis.

Natural products or herbs can be used as an effective therapy for treating psoriasis, an autoimmune skin disease that involves keratinocyte overproliferation. It has been demonstrated that phytomedicine, which is used for psoriasis patients, provides some advantages, including natural sources, a lower risk of adverse effects, and the avoidance of dissatisfaction with conventional therapy. The herbal products' structural diversity and multiple mechanisms of action have enabled the synergistic activity to mitigate psoriasis. In recent years, the concept of using natural products as antiproliferative agents in psoriasis treatment has attracted increasing attention in basic and clinical investigations. This review highlights the development of an apoptotic or antiproliferatic strategy for natural-product management in the treatment of psoriasis. We systematically introduce the concepts and molecular mechanisms of keratinocyte-proliferation inhibition by crude extracts or natural compounds that were isolated from natural resources, especially plants. Most of these studies focus on evaluation through an in vitro keratinocyte model and an in vivo psoriasis-like animal model. Topical delivery is the major route for the in vivo or clinical administration of these natural products. The potential use of antiproliferative phytomedicine on hyperproliferative keratinocytes suggests a way forward for generating advances in the field of psoriasis therapy.

Shikonin induces apoptosis and suppresses growth in keratinocytes via CEBP-δ upregulation.

Shikonin is an active compound of the oriental medicinal plant, Leptospermum erythrorhizon, which has been previously shown to inhibit psoriasis-like inflammation. However, the underlying mechanism is unclear. In the present study, the mechanisms of keratinocyte proliferation and apoptosis in psoriasis in response to shikonin were explored both in vitro and in vivo. Our results showed that shikonin significantly inhibits cell proliferation and induces apoptosis in both HaCaT and LV-STAT3 HaCaT cells by targeting CEBPD, while a decrease in cell survival, proliferation and viability were found through flow-cytometry and MTS assay. Furthermore, gavage with shikonin markedly alleviated psoriasis-like manifestations in IMQ-induced BALB/c mice clinically (PASI Score) and histopathologically. Immunohistochemistry revealed that shikonin potently suppresses the JAK/STAT3 signaling pathway in local skin lesions and increases CEBPD expression. These results imply that shikonin inhibits keratinocyte proliferation and induces apoptosis, which results in psoriasis treatment through the JAK/STAT3 dependent pathway. In addition, the activation of JAK/STAT3 downregulates CEBPD in HaCaT cells and IMQ-induced BALB/c mice. However, shikonin can reverse these effects, suggesting that CEBPD may be a potential therapeutic target for psoriasis.

Natural dietary antioxidants containing flavonoids modulate keratinocytes physiology: In vitro tri-culture models.

ETHNOPHARMACOLOGICAL RELEVANCE: Several traditional medicinal herbs are widely used for dermatologic and cosmetic preparations. The beneficial skin repair activity is detected in various phases of wound-healing process, such as cell-cell, cell-matrix interactions or collagen synthesis. AIM OF THE STUDY: The study assessed the effects of Opuntia ficus-indica (L.) Mill. (Opuntia) and Milk Thistle (MT) (Silybum marianum (L.) Gaerth) on adult keratinocytes (HaCaT) functioning under basal condition or in the presence of mechanical damage (wounded cells). MATERIALS AND METHODS: The role of the natural compounds was tested on HaCaT grown in mono-culture and tri-culture configurations. In tri-cultures models, HaCaT were treated with the conditioned media (CM) obtained by Human Normal Dermal Fibroblast (NHDF) and Human Dermal Microvascular Endothelial cells (HMVEC) co-cultures. Specifically, were tested cell viability, oxidative stress mechanisms (cytokines release and lipid peroxidation) and cellular remodelling (growth factors release or metalloproteinase modulation). Moreover, the migratory potential of HaCaT was analysed by the use of wound healing in vitro assay. RESULTS: Opuntia and MT differently modified the metabolism (EGF, MMP-9), and the migratory properties of HaCaT both under physiological conditions or upon mechanical damage (wounded cells). Moreover, both compounds modulated HaCaT response to oxidative stress. The response to the natural compounds were modified, and in some cases potentiated, in tri-culture configuration systems. CONCLUSIONS: The data demonstrated that in vitro tri-culture approach is suitable to characterize the role of natural compounds on the complex communication between dermal-epidermal cellular components and microvascular endothelium. Specifically, Opuntia and MT are good alternatives to synthetic compounds in skin repair promotion.

R. nukuhivensis acts by reinforcing skin barrier function, boosting skin immunity and by inhibiting IL-22 induced keratinocyte hyperproliferation.

Rauvolfia nukuhivensis is a well-known plant used for its wide range of beneficial effects in Marquesas islands. It is made up of diverse indole alkaloids and is used as traditional medicine for skin application. The actual mechanism behind the virtue of this plant is still unknown. Hence, in this study we aimed at deciphering the impact of R. nukuhivensis on skin immune system in context of (1) homeostasis, (2) pathogen infection and (3) inflammation. Here we show that R. nukuhivensis enhances cellular metabolic activity and wound healing without inducing cellular stress or disturbing cellular homeostasis. It reinforces the epithelial barrier by up-regulating hBD-1. Nevertheless, in pathogenic stress, R. nukuhivensis acts by preparing the immune system to be reactive and effective directly. Indeed, it enhances the innate immune response by increasing pathogens sensors such as TLR5. Finally, R. nukuhivensis blocks IL-22 induced hyperproliferation via PTEN and Filaggrin up-regulation as well as BCL-2 downregulation. In conclusion, this study provides evidence on the several cutaneous application potentials of R. nukuhivensis such as boosting the immune response or in restoring the integrity of the epithelial barrier.

Genistein suppresses psoriasis-related inflammation through a STAT3-NF-κB-dependent mechanism in keratinocytes.

Psoriasis is a chronic recurrent skin inflammatory disease, and inhibition of inflammation may be an effective means of treating psoriasis. The flavonoid genistein has a clear anti-inflammatory effect. However, the anti-psoriatic effects of genistein and their underlying mechanisms remain unclear. In this study, we investigated the effects of genistein on imiquimod (IMQ)-induced psoriasis-like skin lesions in vivo and explored the mechanisms underlying those effects in vitro. It was found that genistein can significantly improve IMQ-induced pathological scores of cutaneous skin lesions in mice, reduce epidermal thickness, and inhibit the expression of inflammatory factors，including interleukin (IL)-1ß, IL-6, tumour necrosis factor-alpha (TNF-α), chemokine ligand 2 (CCL2), IL-17 and IL-23. In vitro studies, genistein inhibited the proliferation of human keratinocyte HaCaT cells and inhibited the expression of inflammatory factors in a dose-dependent manner which induced by TNFα. Further researches showed that genistein could also significantly inhibit phosphorylated STAT3 (pSAT3) expression in IMQ mice dorsal skin and in TNF-α-induced HaCaT cells. The inhibitory effect of genistein on the expression of IL-6, IL-23 and TNF-α was weakened after Stat3 siRNA in HaCaT cells. Genistein could also significantly inhibit TNF-α induced the nuclear translocation of NF-κB, and inhibit the phosphorylation of I-kBα (pI-kBα). After combining with NF-κB blocker BAY 11-7082, the effect of genistein down-regulate the expression of TNF-α and VEGFA was attenuated in HaCaT cells. The results suggest that genistein may be developed for the treatment of psoriasis lesions.

In Vitro Wound Healing Activity of Wheat-Derived Nanovesicles.

Triticum aestivum plant extracts are often used as a natural healer in traditional medicine but which particles mainly have role in these processes are not scientifically proven. In other words, no attempts have been made to investigate the effects of wheat exosomes in regenerative medicine applications or drug development up to now. The current study was first time performed to demonstrate the activity of wheat exosomes in wound healing process using in vitro approaches. Although its fundamental wound healing process remains a mystery, in the current study, the efficiency of wheat grass juice-derived exosomes on cell viability and migration was examined. Increasing concentrations up to 200 µg/mL of the wheat exosome have yielded astonishing proliferative and migratory effects on endothelial, epithelial, and dermal fibroblast cells. RT-PCR analysis also showed collagen type I; mRNA levels were approximately twofold higher in expression after treating with 200 µg/mL wheat exosome. Additionally, Annexin V staining of apoptotic cells accompanied with the cell cycle analysis resulted with the reduction of the apoptotic cell number with no dispersion to the cell cycle analysis while plant exosomes have also increased tube-like structure formation of the endothelial cells. All in all, this research suggests a brand-new opening for skin wound healing therapy strategy by using wheat-derived exosomes due to its proliferative and migratory characteristics. Plant exosomes require a further research both clinically and in in vivo for wound healing drug development. Moreover, plant exosome therapy strategies would be safer and economical alternative for clinical wound healing.

Improvement of skin barrier dysfunction by Scutellaria baicalensis GEOGI extracts through lactic acid fermentation.

BACKGROUND: The development of an alternative medicine to treat atopic dermatitis (AD) from natural sources is necessary. AIMS: To improve skin barrier dysfunction by enhancing the differentiation of human keratinocytes with the fermented Scutellaria baicalensis. METHODS: Scutellaria baicalensis was fermented with Lactobacillus plantarum and extracted with 70% ethanol (FE). Antioxidant activities and the regulation of the gene expression related to keratinocyte differentiation were measured as well as its proliferation. RESULT: This work first proved that the FE had multiple activities, both increasing keratinocyte differentiation and proliferation: The FE greatly up-regulated expression of the genes of keratinocyte differentiation such as involucrin, keratin 10, and transglutaminase-1 (TG-1) up to 4.06-fold, which was 3 times higher than the 2 other extracts. The effect of baicalein on keratinocyte differentiation was also first found; however, its efficacy was lower than that of the fermented extract. The FE proved to effectively accelerate keratinocyte differentiation, rather than to initiate the differentiation, and also showed an ability of stimulating keratinocyte proliferation up to 2.8 × 106 viable cells/mL as well as 70.24 ng/mL of collagen production in fibroblasts. High efficacy of the FE was confirmed by synergistic effects of large amounts of various bioactive substances in the extracts as baicalein alone did not show remarkable effects and even positive controls had not much better activities than the FE. CONCLUSION: The fermented extract was able to improve skin barrier dysfunction, and the ointment with 1%-5% (v/v) of the extract be directly used for skin clinical trials to treat AD.

Mild hyperbaric oxygen activates the proliferation of epidermal basal cells in aged mice.

The proliferation of epidermal basal cells decreases with age. This study examined the effects of exposure to mild hyperbaric oxygen on the proliferative activity of epidermal basal cells in aged mouse skin. Hairless mice aged 5, 34 and 55 weeks were exposed to mild hyperbaric oxygen at 1266 hPa with 36% oxygen for 6 h/day for 1 or 2 weeks. Skin samples were then collected from the back area to evaluate epidermal thickness and the number and proliferative activity of epidermal basal cells. Exposure to mild hyperbaric oxygen had no effect on the epidermal thickness, irrespective of age, but accelerated the proliferative activity of epidermal basal cells in aged mouse skin.

Mild electrical stimulation with heat shock reduces inflammatory symptoms in the imiquimod-induced psoriasis mouse model.

Psoriasis is a chronic skin disease caused by immune disorder. The chronic skin inflammation involves inflammatory molecules that are released from T lymphocytes and keratinocytes. Therefore, developing an anti-inflammatory therapy that is suitable for long-term treatment is needed. Electrical stimulation induces biological responses by modulating intracellular signaling pathways. Our previous studies showed that the optimized combination treatment of mild electrical stimulation (MES, 0.1-millisecond; ms, 55-pulses per second; pps) and heat shock (HS, 42°C) modulates inflammatory symptoms of metabolic disorders and chronic kidney disease in mice models and clinical trials. Here, we investigated the effect of MES+HS treatment on imiquimod-induced psoriasis mouse model. Topical application of imiquimod cream (15 mg) to mice ear induced keratinocyte hyperproliferation and psoriasis-like inflammation. In MES+HS-treated mice, imiquimod-induced skin hyperplasia was significantly decreased. MES+HS treatment reduced the protein expression of IL-17A and the infiltration of CD3-positive cells in lesioned skin. In addition, MES+HS-treated mice had decreased mRNA expression level of antimicrobial molecules (S100A8 and Reg3γ) which aggravate psoriasis. In IL-17A-stimulated HaCaT cells, MES+HS treatment significantly lowered the mRNA expression of aggravation markers (S100A8, S100A9 and ß-defensin2). Taken together, our study suggested that MES+HS treatment improves the pathology of psoriasis via decreasing the expression of inflammatory molecules.

Enzyme-Treated Asparagus Extract (ETAS) Facilitates the Turnover of UV-B-Irradiated Keratinocytes.

Enzyme-treated asparagus extract (ETAS) is prepared from the lower, residual parts of asparagus, and some functionalities, such as anti-oxidative and neuroprotective activities, have been suggested. The purpose of the present study was to investigate the effects of ETAS on photoaging in the epidermal layer of the skin using cultured keratinocytes. Normal human epidermal keratinocytes were irradiated or left unirradiated with UV-B (10 mJ/cm2) and incubated with ETAS (0.5 or 2 mg/mL) or vehicle. After 3 or 13 h, molecular examinations were performed, and after 24 or 48 h, cell viabilities were determined by a CCK-8 assay. ETAS addition may induce keratinocyte migration and proliferation as well as apoptosis under molecular examination. These results suggest that ETAS might accelerate turnover of keratinocytes.