RESUMO
Objectives: This double-blind crossover-controlled trial aimed to verify the effect of electrical stimulation therapy on pressure injuries with undermining. Methods: : In this trial, we compared the healing rates between a sham period and a treatment period using monophasic pulsed microcurrent therapy. The participants were randomly assigned to the sham or treatment group and received stimulation for 2 weeks. All the participants, physical therapists, and researchers were blinded to the allocation. For the main analysis, data on the effect of the intervention on changes in weekly healing and contraction rates of the wound areas, including undermining, were analyzed based on a two-period crossover study design. The intervention effect was estimated by examining the mean treatment difference for each period using Wilcoxon's signed-rank test. Results: : The reduction of the entire wound area, including the undermining area, resulted in significantly higher healing and contraction rates in the treatment group (overall wound area reduction rate: contraction rate, P=0.008; period healing rate, P=0.002). Conclusions: : Electrical stimulation therapy for pressure injuries, using conditions based on the findings of an in vivo culture study, was effective in reducing the wound area.
RESUMO
Twin studies, especially those involving monozygotic (MZ) twins, facilitate the analysis of factors affecting skin aging while controlling for age, gender, and genetic susceptibility. The purpose of this study was to objectively assess various features of facial skin and analyze the effects of environmental factors on these features in MZ twins. At the Osaka Twin Research Center, 67 pairs of MZ twins underwent medical interviews and photographic assessments, using the VISIA(®) Complexion Analysis System. First, the average scores of the right and left cheek skin spots, wrinkles, pores, texture, and erythema were calculated; the differences between the scores were then compared in each pair of twins. Next, using the results of medical interviews and VISIA data, we investigated the effects of environmental factors on skin aging. The data were analyzed using Pearson's correlation coefficient test and the Wilcoxon signed-rank test. The intrapair differences in facial texture scores significantly increased as the age of the twins increased (P = 0.03). Among the twin pairs who provided answers to the questions regarding history differences in medical interviews, the twins who smoked or did not use skin protection showed significantly higher facial texture or wrinkle scores compared with the twins not exposed to cigarettes or protectants (P = 0.04 and 0.03, respectively). The study demonstrated that skin aging among Japanese MZ twins, especially in terms of facial texture, was significantly influenced by environmental factors. In addition, smoking and skin protectant use were important environmental factors influencing skin aging.
Assuntos
Meio Ambiente , Envelhecimento da Pele/patologia , Fumar , Protetores Solares , Adulto , Idoso , Idoso de 80 Anos ou mais , Face , Feminino , Humanos , Japão , Masculino , Pessoa de Meia-Idade , Gêmeos MonozigóticosRESUMO
BACKGROUND: Oxidative stress has been suggested as a mechanism underlying skin aging, as it triggers apoptosis in various cell types, including fibroblasts, which play important roles in the preservation of healthy, youthful skin. Catechins, which are antioxidants contained in green tea, exert various actions such as anti-inflammatory, anti-bacterial, and anti-cancer actions. In this study, we investigated the effect of (+)-catechin on apoptosis induced by oxidative stress in fibroblasts. METHODS: Fibroblasts (NIH3T3) under oxidative stress induced by hydrogen peroxide (0.1 mM) were treated with either vehicle or (+)-catechin (0-100 µM). The effect of (+)-catechin on cell viability, apoptosis, phosphorylation of c-Jun terminal kinases (JNK) and p38, and activation of caspase-3 in fibroblasts under oxidative stress were evaluated. RESULTS: Hydrogen peroxide induced apoptotic cell death in fibroblasts, accompanied by induction of phosphorylation of JNK and p38 and activation of caspase-3. Pretreatment of the fibroblasts with (+)-catechin inhibited hydrogen peroxide-induced apoptosis and reduced phosphorylation of JNK and p38 and activation of caspase-3. CONCLUSION: (+)-Catechin protects against oxidative stress-induced cell death in fibroblasts, possibly by inhibiting phosphorylation of p38 and JNK. These results suggest that (+)-catechin has potential as a therapeutic agent for the prevention of skin aging.
Assuntos
Apoptose/efeitos dos fármacos , Catequina/farmacologia , Fibroblastos/citologia , Estresse Oxidativo/efeitos dos fármacos , Extratos Vegetais/farmacologia , Substâncias Protetoras/farmacologia , Animais , Antioxidantes/farmacologia , Caspase 3/metabolismo , Fibroblastos/efeitos dos fármacos , Fibroblastos/enzimologia , Fibroblastos/metabolismo , Peróxido de Hidrogênio/metabolismo , Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo , Camundongos , Células NIH 3T3 , Fosforilação/efeitos dos fármacos , Pele/citologia , Pele/efeitos dos fármacos , Pele/metabolismo , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismoRESUMO
L-arginine is considered a conditionally essential amino acid and has been shown to enhance wound healing. However, the molecular mechanisms through which arginine stimulates cutaneous wound repair remain unknown. Here, we evaluated the effects of arginine supplementation on fibroblast proliferation, which is a key process required for new tissue formation. We also sought to elucidate the signaling pathways involved in mediating the effects of arginine on fibroblasts by evaluation of extracellular signal-related kinase (ERK) 1/2 activation, which is important for cell growth, survival, and differentiation. Our data demonstrated that addition of 6 mM arginine significantly enhanced fibroblast proliferation, while arginine deprivation increased apoptosis, as observed by enhanced DNA fragmentation. In vitro kinase assays demonstrated that arginine supplementation activated ERK1/2, Akt, PKA and its downstream target, cAMP response element binding protein (CREB). Moreover, knockdown of GPRC6A using siRNA blocked fibroblast proliferation and decreased phosphorylation of ERK1/2, Akt and CREB. The present experiments demonstrated a critical role for the GPRC6A-ERK1/2 and PI3K/Akt signaling pathway in arginine-mediated fibroblast survival. Our findings provide novel mechanistic insights into the positive effects of arginine on wound healing.