Infrared radiation is increasingly and uncritically used for cosmetic and wellness purposes, despite the poorly understood biologic effects of such treatments on humans. In the present study, we investigated the effects of infrared radiation on collagen and elastin production in dermal fibroblasts, as well as the clinical and histopathologic effects of infrared radiation on photo-aged facial skin lesions. In order to determine the effects of infrared radiation on collagen and elastin production, dermal fibroblasts were exposed to infrared radiation for varying lengths of time and collagen and elastin contents were subsequently determined. Additionally, 20 patients with mild to moderate facial wrinkles and hyperpigmented lesions received daily treatments of far infrared radiation (900 to 1000micronm) for six-months. During the treatment, patients and a medical observer conducted independent photographic and clinical evaluations every 4 weeks, and skin biopsies were obtained for histological analysis at baseline and one month post-treatment. We found that the content of collagen and elastin produced by the fibroblasts increased after infrared radiation, and that this increase was proportional to the duration of irradiation exposure. Following 6 months of treatment, all patients reported good (51-75%) improvements in skin texture and roughness. Additionally, patients noted fair (25-50%) improvement in color tone of the skin; however, improvements in hyperpigmented lesions were not observed. Objective medical evaluation of the patients indicated that roughness and laxity were fairly improved, but there was no significant improvement in hyperpigmented lesions. Histological examination failed to reveal any differences as well. These results suggest that infrared radiation may have beneficial effects on skin texture and wrinkles by increasing collagen and elastin contents from the stimulated fibroblasts. Therefore, skin treatment with infrared radiation may be an effective and safe non-ablative remodeling method, and may also be useful in the treatment of photo-aged skin.
Time Factors ; Skin Pigmentation/*radiation effects ; *Skin Aging ; Skin/*radiation effects ; Middle Aged ; *Light ; *Infrared Rays ; Humans ; Fibroblasts/metabolism ; Female ; Elastin/metabolism ; Collagen/metabolism ; Biopsy ; Adult

Low-frequency ultrasound can increase the transdermal delivery of many drugs, including macromolecular drugs. The main mechanism is ultrasonic cavitation. Most researchers pointed out that it could change the form-structure of stratum corneum keratinocytes and, in this way, it can improve the permeability of skin. Low-frequency sonophoresis has been in use for in-vitro experiments and in-vivo animal experiments, and so far, both small-molecules transdermal delivery and macromolecules transdermal delivery have been successfully performed in many experiments. However, there are few reports about the real low-frequency sonophoresis for clinical treatment. A large number of clinical trials are necessary to confirm its safety and practicality. Once its safety is confirmed and the suitable low-frequency sonophoresis devices are developed successfully, Low-frequency Sonophoresis will come to be a safe, effective, controllable, and economic new delivery method.
Administration, Cutaneous ; Animals ; Humans ; Skin ; diagnostic imaging ; metabolism ; Skin Absorption ; radiation effects ; Ultrasonography

OBJECTIVETo investigate the effect of static magnetic field on deep wound healing of SD rats and VEGF during the wound healing and different strength static magnetic field on deep wound healing of SD rats.

METHODSDivided forty-eight SD rats into three groups: 0.16 T magnetic disk treatment (0.16 T group), 0.32 T magnetic disk treatment (0.32 T group), control group. General wounds healing situation was observated on the 3, 6, 9, 12 day. The area of every wound was calculated. The tissue of granulation was dyeing by immune tissue chemical decoration method, in which VEGF protein content with its range in tissue was measured.

RESULTSThe healing index of 0.16 T magnetic group wounds were larger than that of control group on 6th and 9th day, there were statistical difference. The healing index of 0.32 T magnetic group wounds were larger than that of control group on 3rd, 6th, 9th and 12th day, there were statistical difference. The healing index of 0.32 T group wounds contrasted to that of 0.16 T group wounds had no statistical significance. Observation of VEGF at the course of wound healing:the expressing of VEGF in magnetic group wounds on 3rd and 6th was stronger than in control group wounds, there were statistical difference. While there were no obvious difference between them on 9th and 12th day (P>0.05). But the contrast between that in 0.32 T group and in 0.16 T group had no statistical difference. The expressing strength of VEGF in magnetic group reached the peak amplitude on the 6th day, and that in control group reached peak amplitude on 9th day. And the peak amplitude of magnetic group was stronger than that of control group.

CONCLUSIONStatic magnetic disc of 0.16T and 0.32 T can promote deep wound of SD rats heal. The mechanism of static magnetic field promoting wound heal may be relative to the expressing highly of VEGF during early and middle time.

Animals ; Magnetic Field Therapy ; Male ; Rats ; Rats, Sprague-Dawley ; Regeneration ; physiology ; radiation effects ; Skin ; radiation effects ; Vascular Endothelial Growth Factor A ; genetics ; metabolism ; Wound Healing ; radiation effects

OBJECTIVETo investigate the mechanism involved in aging process of immortalized human keratinocyte (HaCaT) and primary human epidermis keratinocyte of adults (HEKa) irradiated by ultraviolet B(UVB).

METHODSHEKa and HaCaT were repeatedly exposed to UVB at a subcytotoxic level. SA-beta-Gal staining was performed to evaluate the senescence state; flow cytometry was applied to detect the changes of apoptosis, necrosis and cell cycle. Intracellular levels of superoxide dismutase (SOD) and malondialdehyde (MDA) were measured by ELISA method. Western blot was performed to detect the expression pattern of redox protein p66Shc and RT-PCR was performed to determine the mRNA level of human telomerase reverse transcriptase (hTERT).

RESULTStrong positive SA-beta-Gal staining was observed in both HEKa cell and HaCaT cells after UVB irradiation. Apoptosis rate increased from (1.81 +/-0.25)% to (4.43 +/-0.28)% and necrosis rate increased from (0.05 +/-0.01)% to (0.10 +/-0.03)% in HaCaT cell, but no marked arrest of cell cycle was observed during UVB irradiation. As a contrast, apoptosis rate of in HEKa cells significantly increased from (0.65 +/-0.05)% to (59.53 +/-2.35)%, and the necrosis rate in HEKa cells also reached (3.89 +/-0.24)%(P<0.05). Growth arrest in G0/G1 phase was also found in HEKa cells. In both cell lines, intracellular level of SOD decreased and MDA increased remarkably after UVB exposure, and an increased expression of p66Shc protein was also observed. High level of hTERT mRNA was detected in HaCaT cells and UVB exposure had little effect on its expression.

CONCLUSIONThe stress-induced premature senescence (SIPS) in HaCaT and HEKa cell lines by UVB irradiation might be closely associated with increased intracellular levels of oxidative stress, not related to the telomerase expression.

Apoptosis ; Cell Line ; Cells, Immobilized ; radiation effects ; Cellular Senescence ; physiology ; radiation effects ; Humans ; Keratinocytes ; cytology ; radiation effects ; Malondialdehyde ; metabolism ; Skin ; cytology ; Superoxide Dismutase ; metabolism ; Telomerase ; genetics ; metabolism ; radiation effects ; Ultraviolet Rays ; beta-Galactosidase ; pharmacology

Various kinds of glycosaminoglycans (GAGs) and proteoglycans (PGs) have been known to be involved in structural and space-filling functions, as well as many physiological regulations in skin. To investigate ultraviolet (UV) radiation-mediated regulation of GAGs and PGs in cultured human dermal fibroblasts, transcriptional changes of many types of PGs and GAG chain-synthesizing enzymes at 18 hr after 75 mJ/cm2 of UV irradiation were examined using quantitative real-time polymerase chain reaction methods. Hyaluronic acid synthase (HAS)-1, -2, and -3 and hyaluronidase-2 mRNA expressions were significantly increased by UV irradiation. Expressions of lumican, fibromodulin, osteoglycin, syndecan-2, perlecan, agrin, versican, decorin, and biglycan were significantly decreased by UV irradiation, while syndecan-1 was increased. Expressions of GAG chain-synthesizing glycosyltransferases, xylosyltransferase-1, beta1,3-glucuronyltransferase-1, beta1,4-galactosyltransferase-2, -4, exostosin-1, chondroitin polymerizing factor, and chondroitin sulfate synthase-3 were significantly reduced, whereas those of beta1,3-galactosyltransferase-6, beta1,4-galactosyltransferase-3, -7, beta-1,3-N-acetylglucosaminyltran sferase-2, and -7 were increased by UV irradiation. Heparanase-1 mRNA expression was increased, but that of heparanase-2 was reduced by UV irradiation. Time-course investigation of representative genes showed consistent results. In conclusion, UV irradiation may increase hyaluronic acid production through HAS induction, and decrease other GAG productions through downregulation of PG core proteins and GAG chain-synthesizing glycosyltransferases in cultured human dermal fibroblasts.
Cell Line ; Fibroblasts/metabolism/radiation effects ; Gene Expression Regulation/radiation effects ; Glucuronosyltransferase/genetics/radiation effects ; Glycosaminoglycans/*biosynthesis/chemistry ; Glycosyltransferases/genetics/*metabolism ; Humans ; Hyaluronic Acid/biosynthesis ; Hyaluronoglucosaminidase/genetics/radiation effects ; Polymerase Chain Reaction ; Proteoglycans/*biosynthesis/genetics/radiation effects ; RNA, Messenger/analysis/genetics ; Skin/*metabolism/radiation effects ; Transcription, Genetic/radiation effects ; *Ultraviolet Rays

OBJECTIVETo explore the effect of millimeter wave exposure at low power density on gene expression in human keratinocytes (HaCaT).

METHODSHaCaT keratinocytes were exposed to 30.16 GHz millimeter wave with power densities of 1.0 or 3.5 mW/cm2 for 30 min per day. Gene expression profiles were obtained using the Affymetrix human genome U95A GeneChip. Reverse-transcription polymerase chain reaction (RT-PCR) was performed to confirm the differential expression of genes obtained from Genechip analysis.

RESULTPAR-2 and ERGIC-53 genes in HaCaT cells were up-regulated by 3.5 mW/cm2 millimeter wave exposure for 4 times. ERGIC-53 gene was also up-regulated by 1.0 mW/cm2 millimeter wave exposure for 4 times. However, no significant change for PAR-2 expression was found after the same exposure.

CONCLUSIONMillimeter wave exposure could affect gene expression in human keratinocytes, which might be related to the intensity and the times of exposure.

Cells, Cultured ; Dose-Response Relationship, Radiation ; Electromagnetic Fields ; Gene Expression ; radiation effects ; Humans ; Keratinocytes ; metabolism ; radiation effects ; Mannose-Binding Lectins ; genetics ; metabolism ; Membrane Proteins ; genetics ; metabolism ; Microwaves ; Radiation ; Receptor, PAR-2 ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Skin ; cytology

To determine whether platelet-rich fibrin lysate (PRF-L) could restore the function of chronically ultraviolet-A (UVA)-irradiated human dermal fibroblasts (HDFs), we isolated and sub-cultured HDFs from six different human foreskins. HDFs were divided into two groups: those that received chronic UVA irradiation (total dosages of 10 J cm-2) and those that were not irradiated. We compared the proliferation rates, collagen deposition, and migration rates between the groups and between chronically UVA-irradiated HDFs in control and PRF-L-treated media. Our experiment showed that chronic UVA irradiation significantly decreased (p<0.05) the proliferation rates, migration rates, and collagen deposition of HDFs, compared to controls. Compared to control media, chronically UVA-irradiated HDFs in 50% PRF-L had significantly increased proliferation rates, migration rates, and collagen deposition (p<0.05), and the migration rates and collagen deposition of chronically UVA-irradiated HDFs in 50% PRF-L were equal to those of normal fibroblasts. Based on this experiment, we concluded that PRF-L is a good candidate material for treating UVA-induced photoaging of skin, although the best method for its clinical application remains to be determined.
Blood Platelets/*cytology/*metabolism ; Cell Movement/radiation effects ; Cell Proliferation/radiation effects ; Cells, Cultured ; Collagen/metabolism ; Fibrin/*metabolism ; Fibroblasts/*cytology/metabolism/*radiation effects ; Humans ; Skin/*cytology ; Time Factors ; Ultraviolet Rays/*adverse effects

In the present study, the detrimental effect of beta-emission on pig skin was evaluated. Skin injury was modeled in mini-pigs by exposing the animals to 50 and 100 Gy of beta-emission delivered by 166Ho patches. Clinicopathological and immunohistochemical changes in exposed skin were monitored for 18 weeks after beta-irradiation. Radiation induced desquamation at 2~4 weeks and gradual repair of this damage was evident 6 weeks after irradiation. Changes in basal cell density and skin depth corresponded to clinically relevant changes. Skin thickness began to decrease 1 week after irradiation, and the skin was thinnest 4 weeks after irradiation. Skin thickness increased transiently during recovery from irradiation-induced skin injury, which was evident 6~8 weeks after irradiation. Epidermal expression of nuclear factor-kappa B (NF-kappaB) differed significantly between the untreated and irradiated areas. One week after irradiation, cyclooxygenase-2 (COX-2) expression was mostly limited to the basal cell layer and scattered among these cells. High levels of COX-2 expression were detected throughout the full depth of the skin 4 weeks after irradiation. These findings suggest that NF-kappaB and COX-2 play roles in epidermal cell regeneration following beta-irradiation of mini-pig skin.
Animals ; Cyclooxygenase 2/genetics/*metabolism ; *Holmium ; Male ; NF-kappa B/genetics/*metabolism ; Radiation Injuries, Experimental/metabolism/*veterinary ; Skin/metabolism/*radiation effects ; Swine ; Swine, Miniature

Equol, an isoflavonoid metabolite produced from the dietary isoflavone daidzein by the gut microflora in mammals, has been found to protect not only against ultraviolet (UV) radiation-induced cutaneous inflammation and photoimmune suppression, but also have antiphotocarcinogenic properties in mice. Because the state of DNA damage has been correlated with suppression of the immune system and photocarcinogenesis, we have therefore examined the potential of equol to offer protection from solar-simulated UV (SSUV) radiation-induced DNA damage in hairless mice by the immunohistochemical approach using monoclonal antibody specific for cyclobutane pyrimidine dimers (CPDs; H3 antibody). Topical application of 20 micrometer equol lotion, which was applied both before and after SSUV significantly reduced the number of CPDs. This reduction was evident immediately after SSUV exposure, at 1 h after exposure, and at 24 h after exposure, revealing 54%, 50%, and 26% reduction in CPDs, respectively. When the same concentration was applied for 5 consecutive days after SSUV exposure, there was no significant difference in the reduction of CPDs immediately after SSUV irradiation or at 1 hour afterwards, but there were significant reductions of 23% and 42% at 24 and 48 h after SSUV exposure, respectively. Despite apparently reducing the number of CPDs post-SSUV, topically applied equol did not appear to increase the rate of dimer removal. To conclude, equol applied topically prior to SSUV irradiation offers protection against CPD formation in hairless mice, possibly by acting as a suncreen and thus inhibiting DNA photodamage.
Administration, Topical ; Animals ; DNA/drug effects/radiation effects ; *DNA Damage ; Female ; Immunohistochemistry ; Isoflavones/*pharmacology ; Mice ; Mice, Inbred HRS ; Pyrimidine Dimers/metabolism ; Skin/drug effects/metabolism/*radiation effects ; Sunlight/adverse effects ; Ultraviolet Rays/*adverse effects

Wound combined with total body irradiation (TBI) injury results in impairment of tissue repair and delayed processes of healing, so it has been considered as an important and representative model of impaired wound healing, but the mechanism is not fully clarified. Fibroblasts in wound are the most important cells participating in tissue repair, whereas its radiosensitivity is not high. To understand whether TBI injury has direct damaging effects on fibroblasts in wound, fibroblasts in wound combined with TBI injury and in wound of simple incision injury were isolated and cultured, and parameters associated with tissue repair were determined. The results showed that the abilities of proliferation, attachment and adhesion of fibroblasts isolated from wounds combined with TBI injury significantly decreased as compared with those of simple incision injury, nevertheless, apoptotic ratio of fibroblasts isolated from wounds combined with TBI injury increased significantly. These data suggest that TBI injury may cause direct damaging effects on fibroblasts in wounds, which might be one of the dominant reasons for impairment of wound healing when it is combined with TBI injury.
Animals ; Disease Models, Animal ; Fibroblasts ; metabolism ; physiology ; radiation effects ; Radiation Injuries, Experimental ; metabolism ; Rats ; Rats, Wistar ; Skin ; injuries ; Whole-Body Irradiation ; Wound Healing ; physiology