アンジェス(株)【4563】の掲示板 2023/04/11〜2023/04/14

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Topical application of nuclear factor-κB (NF-κB) decoy appears to provide a novel therapeutic potency in the treatment of inflammation and atopic dermatitis. However, it is difficult to deliver NF-κB decoy oligonucleotides (ODN) into the skin by conventional methods based on passive diffusion because of its hydrophilicity and high molecular weight. In this study, we evaluated the in vitro transdermal delivery of fluorescein isothiocyanate (FITC)-NF-κB decoy ODN using a pulse depolarization (PDP) iontophoresis. In vitro iontophoretic experiments were performed on isolated C57BL/6 mice skin using a horizontal diffusion cell. The apparent flux values of FITC-NF-κB decoy ODN were enhanced with increasing the current density and NF-κB decoy ODN concentration by iontophoresis. Accumulation of FITC-NF-κB decoy ODN was observed at the epidermis and upper dermis by iontophoresis. In

>>1019

Objective: Insulin-resistant hyperglycemia is commonly observed in septic patients and may actually lead to some of adverse outcomes. We examined the changes in insulin signaling and glucose uptake regulation in sepsis and the involvement of the nuclear factor-κB pathway. Design: Controlled animal study. Setting: University research laboratory. Subjects: One hundred fifty-four BALB/c mice (8-12 wks of age). Interventions: The following four experimental groups were studied: sham-operated control, cecal ligation and puncture-induced sepsis, sepsis + nuclear factor-κB decoy oligodeoxynucleotide treatment, and sepsis + scrambled decoy oligodeoxynucleotide treatment. Measurements and Main Results: Septic mice were markedly hyperinsulinemic with apparently normal blood glucose levels in the fasted state, suggesting they are insulin-resistant. In fact, glucose clearance in response to insulin was markedly impaired in septic mice. They had impaired GLUT4 membrane translocation resulting from impaired insulin signaling as indicated by the decreased amount of insulin receptor substrate protein

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