Role of mitochondrial ATP-sensitive potassium channel-mediated PKC-ε in delayed protection against myocardial ischemia/reperfusion injury in isolated hearts of sevoflurane-preconditioned rats

This study aimed to determine the role of mitochondrial adenosine triphosphate-sensitive potassium (mitoKATP) channels and protein kinase C (PKC)-ε in the delayed protective effects of sevoflurane preconditioning using Langendorff isolated heart perfusion models. Fifty-four isolated perfused rat hearts were randomly divided into 6 groups (n=9). The rats were exposed for 60 min to 2.5% sevoflurane (the second window of protection group, SWOP group) or 33% oxygen inhalation (I/R group) 24 h before coronary occlusion. The control group (CON) and the sevoflurane group (SEVO) group were exposed to 33% oxygen and 2.5% sevoflurane for 60 min, respectively, without coronary occlusion. The mitoKATP channel inhibitor 5-hydroxydecanoate (5-HD) was given 30 min before sevoflurane preconditioning (5-HD+SWOP group). Cardiac function indices, infarct sizes, serum cardiac troponin I (cTnI) concentrations, and the expression levels of phosphorylated PKC-ε (p-PKC-ε) and caspase-8 were measured. Cardiac function was unchanged, p-PKC-ε expression was upregulated, caspase-8 expression was downregulated, cTnI concentrations were decreased, and the infarcts were significantly smaller (P<0.05) in the SWOP group compared with the I/R group. Cardiac function was worse, p-PKC-ε expression was downregulated, caspase-8 expression was upregulated, cTnI concentration was increased and infarcts were larger in the 5-HD+SWOP group (P<0.05) compared with the SWOP group. The results suggest that mitoKATP channels are involved in the myocardial protective effects of sevoflurane in preconditioning against I/R injury, by regulating PKC-ε phosphorylation before ischemia, and by downregulating caspase-8 during reperfusion.

Polyphenol (-)-Epigallocatechin Gallate during Ischemia Limits Infarct Size Via Mitochondrial K(ATP) Channel Activation in Isolated Rat Hearts

Polyphenol (-)-epigallocatechin gallate (EGCG), the most abundant catechin of green tea, appears to attenuate myocardial ischemia/reperfusion injury. We investigated the involvement of ATP-sensitive potassium (K(ATP)) channels in EGCG-induced cardioprotection. Isolated rat hearts were subjected to 30 min of regional ischemia and 2 hr of reperfusion. EGCG was perfused for 40 min, from 10 min before to the end of index ischemia. A nonselective K(ATP) channel blocker glibenclamide (GLI) and a selective mitochondrial K(ATP) (mK(ATP)) channel blocker 5-hydroxydecanoate (HD) were perfused in EGCG-treated hearts. There were no differences in coronary flow and cardiodynamics including heart rate, left ventricular developed pressure, rate-pressure product, +dP/dt(max), and -dP/dt(min) throughout the experiments among groups. EGCG-treatment significantly reduced myocardial infarction (14.5+/-2.5% in EGCG 1 micrometer and 4.0+/-1.7% in EGCG 10 micrometer, P<0.001 vs. control 27.2+/-1.4%). This anti-infarct effect was totally abrogated by 10 micrometer GLI (24.6+/-1.5%, P<0.001 vs. EGCG). Similarly, 100 micrometer HD also aborted the anti-infarct effect of EGCG (24.1+/-1.2%, P<0.001 vs. EGCG ). These data support a role for the K(ATP) channels in EGCG-induced cardioprotection. The mK(ATP) channels play a crucial role in the cardioprotection by EGCG.

Acido glicólico: agente despigmentante e rejuvenescedor / Glycolic acid: depigmenting agent and rejuvenating

A pigmentaçäo da pele, causada pela irradiaçäo da luz ultravioleta, como defesa contra a açäo carcinogênica da luz solar, pode levar ao envelhecimento precoce da pele e a uma hipercromia, cujo tratamento requer o uso de fotoprotetores, despigmentantes e rejuvenescedores. Recentemente, têm sido usadas várias substâncias para previnir e/ou tratar o envelhecimento cutâneo, bem como para diminuir a pigmentaçäo da pele. O hidroxiáxido mais comumente empregado em preparaçöes cosméticas e dermatológicas tem sido o ácido glicólico, pelas propriedades despigmentantes e rejuvenescedoras e pela eficácia que apresenta, em diferentes concentraçöes, quando incorporado a vários tipos de excipientes.

Piel y menopausia: efectos de la edad, estado hormonal y tratamientos / Skin and menopause: age effects, hormone state and treatment

El deterioro de la piel con la edad está influido por factores endógenos como el componente genéticos o la situación hormonal; y por exógenos como el tabaco o las radiaciones ultravioletas de la luz solar. Una piel deteriorada impacta fuertemente en la calidad de vida de una mujer, por lo que es relevante tener posibilidades de mejorarla. Los estrógenos actúan en la piel aumentando el ácido hialurónico, lo que produce una mayor hidratación de la dermis; esta edematización, asociada al aumento de la polimerización del colágeno que provocan los estrógenos, aumentan el grosor cutáneo; también estas hormonas inducen mayor formación de vasos en la piel, lo que se traduce en mayor actividad metebólica de la epidermis. Estos efectos explican que la terapia de reemplazo hormonal mejore la calidad de la piel, disminuyendo las arrugas y mejorando las características biomecánicas de la piel. Otras alternativas para atenuar el envejecimiento cutáneo pueden ser algunas terapias no endocrina como los ácidos alfa-hidroxilados y los ácidos retinoicos. La protección de las radiaciones solares y los cambios de hábitos nocivos para la piel, como el consumo de cigarrillo son medidas que deben aconsejarse a todas las pacientes

El lipohidroxiácido y el envejecimiento cutáneo / Lipohydroxiacid and cutaneous aging

El envejecimiento induce marcados cambios de la superficie cutánea y particularmente de la capa córnea. La aplicación de lipo-hidroxi-ácido, un derivado lipofílico del ácido salicílico, aporta una mejoría de ciertas alteraciones asociadas al envejecimiento. Produce una eliminación más uniforme de los corneocitos y un aumento del espesor de las capas basal y de Malpighi, dentro de los límites fisiológicos