RESUMO
RESUMEN La crioterapia es el conjunto de procedimientos que utilizan el frío en la terapéutica médica. Emplea diversos sistemas y tiene como resultado la disminución de la temperatura de la piel; produce una destrucción local de tejido de forma eficaz y controlada. El objetivo de este trabajo fue realizar una actualización para exponer los aspectos esenciales sobre formas de empleos, indicaciones, complicaciones y contraindicaciones. Existen varios métodos de aplicación de la crioterapia, que incluyen las técnicas de congelación de spray o aerosol y con aplicadores, el método criosonda, y el uso de termoacoplador. Está indicada en varias entidades, entre las que se encuentran la queratosis seborreica y actínica, lentigos solares, carcinoma basocelular y espinocelular in situ. Las complicaciones más observadas son vesicoampollas, hiperpigmentación e hipopigmentación, y las contraindicaciones comunes son intolerancia al frío, tumores con bordes no delimitados o con pigmentación muy oscura, en localizaciones cerca de los márgenes de los ojos, párpados, mucosas, alas nasales y el conducto auditivo. El dominio de los métodos de aplicación e indicaciones es indispensable para elegir la conducta adecuada; de esta forma se evitan complicaciones y efectos colaterales (AU).
ABSTRACT Cryotherapy is the whole of procedures that use cold in medical therapy. It uses various systems and results in a decrease in skin temperature, leading to a local destruction of tissue in an effective and controlled way. The objective of this work is to make an update to expose the essential aspects on the ways of use, indications, complications and contraindications. There are several cryotherapy application methods that include spray or spray freezing techniques and applicators, the cryoprobe method, and the thermocoupler use. It is indicated in several entities, and among the most frequent are seborrheic and actinic keratosis, solar lentigo, basal cell and squamous cell carcinomas in situ. The most observed complications are vesical blisters, hyperpigmentation and hypopigmentation, and the most common complications are: cold intolerance, tumors with non-delimited borders or very dark pigmentation, located near the margins of the eyes, on eyelids, mucous membranes, nasal wings, and on the ear canal. The mastery of the signs and application methods are essential to choose the appropriate behavior against the disease: side effects and complications are avoided that way (AU).
Assuntos
Humanos , Masculino , Feminino , Crioterapia/métodos , Dermatologia/métodos , Terapêutica , Ferimentos e Lesões/diagnóstico , Senilidade Prematura/diagnóstico , Nitrogênio/uso terapêuticoRESUMO
Objective To determine the inhibitory effect and mechanism of metformin ( MF) on photo-damage of human skin fibroblasts ( HSF) induced by UVA .Methods Human skin fibroblasts were randomly divided into con-trol group, UVA group and UVA+MF group.The proliferation of HSF was detected by CCK-8 assay kit.SA-β-gal staining was performed to evaluate the senescence state .The level of ROS was examined by fluorescence probe DCF-DA staining using flow cytometry .Real-time PCR was used to determine mRNA expression of senescence -asso-ciated signals of MMP 1 and MMP3.The protein expression of MMP 1, MMP3, SOD1 and SOD2 were measured by Western blot .R esults To the proliferation of HSF , 0.01 mmol/L Metformin had no significant effect , but 0.1 and 1 mmol/L Metformin depressed significantly ( P<0.05 ) .Compared with the Control group , it showed that UVA irradiation increased the positive rate of SA-β-gal staining ( P<0.01 ) , the level of ROS ( P<0.05 ) , mRNA and protein expression of MMP1 and MMP3 significantly(P<0.01);Also decreased the expression of SOD1 and SOD2 ( P<0.01) .Compared with the UVA group , it showed that metformin decreased the positive rate of SA-β-gal staining (P<0.05), the level of ROS(P<0.05), mRNA and protein expression of MMP1 and MMP3 significantly(P<0.05);Also increased the expression of SOD 1 ( P<0.01 ) and SOD2.Conclusions Metfomin can inhibit photo-damage of human skin fibroblasts induced by UVA via decreasing ROS and metal matrix protease generation , also the improvement of cellular antioxidant capacity .
RESUMO
OBJECTIVE: To investigate the protection of aucubin on keratinocyte damaged by Ultraviolet B and explore its possible mechanism. METHODS: The photo damage model of keratinocyte was established by irradiating of UVB (64 mJ · cm-1). The different concentration aucubin were used for damaged cell. The cell viability was detected by MTT, the SOD activity, GSH-Px activity, CAT activity, MDA content were assayed by kit respectively. The mRNA levels of P38, TNF-α and IL-6 were determined by RT-PCR. The secretion levels of TNF-α and IL-6 of cultured keratinocyte were detected by ELISA. RESULTS: After the UVB irradiation, the cell viability, the activities of SOD, GSH-Px and CAT were decreased, the content of MDA, TNF-α and IL-6, the mRNA levels of P38, TNF-α and IL-6 were increased (P < 0.01). The above changes were inhibited by 1 × 10-1 and 1 × 10-1 mol · L-1 aucubin (P < 0.05 or P < 0.01). CONCLUSION: The aucubin could inhibit the injury by UVB for keratinocyte. And its possible mechanism may have relationship with the inhibition of oxidative damage, regulatory P38 signal pathway, adjusting the expression of TNF-α and IL-6.