Preparation and evaluation of a highly skin- and nail-permeable efinaconazole topical formulation for enhanced treatment of onychomycosis.

Onychomycosis is a progressive fungal infection of the nails that involves the deeper nail layer and nail bed. It is important to maintain sufficient drug concentration in the diseased tissues after topical application. In this study, a stable topical delivery system for efinaconazole (EFN) was designed to enhance absorption potential through the skin and nail plate by incorporating ethanol, diethylene glycol monoethyl ether (Transcutol P) and isopropyl myristate, and cyclomethicone into the topical solution as a delivery vehicle, permeation enhancers, and a wetting agent, respectively.

Superoxide dismutase 1 inhibits alpha-melanocyte stimulating hormone and ultraviolet B-induced melanogenesis in murine skin.

Background: Over the last decade, the incidence of ultraviolet B (UVB)-related skin problems has increased. Oxidative stress caused by UVB induces the secretion of melanocyte growth and activating factors from keratinocytes, which results in the formation of cutaneous hyperpigmentation. Therefore, increasing the antioxidant abilities of skin cells is thought to be a beneficial strategy for the development of sunscreen agents.

Mixtures of recombinant growth factors inhibit the production of pro-inflammatory mediators and cytokines in LPS-stimulated RAW 264.7 cells by inactivating the ERK and NF-κB pathways.

Growth factors are important for regulating a variety of cellular processes and typically act as signaling molecules between cells. In the present study, we examined the mechanisms underlying the inhibitory effects of mixtures of recombinant growth factors (MRGFs) on nitric oxide (NO) and pro-inflammatory cytokine production in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells.

Functional inactivation of triosephosphate isomerase through phosphorylation during etoposide-induced apoptosis in HeLa cells: potential role of Cdk2.

Up-regulation of cyclin-dependent protein kinase 2 (Cdk2) activity has been suggested to be prerequisite for progression of apoptosis induced by various apoptotic stimuli. In this study, we applied a phospho-proteomic technique to screen target molecules of Cdk2 during etoposide-induced apoptosis. For this purpose, phosphoproteins from the cell lysates were enriched by using Fe³+-IMAC column chromatography and resolved on a high resolution 2D PAGE gel.

Cyclin-dependent protein kinase 2 activity is required for mitochondrial translocation of Bax and disruption of mitochondrial transmembrane potential during etoposide-induced apoptosis.

Previous studies have suggested that upregulation of Cyclin A-dependent protein kinase 2 (Cdk2) activity is an essential event in apoptotic progression and the mitochondrial permeability transition in human cancer cells. Here, we show that upregulated Cyclin A/Cdk2 activity precedes the proteolytic cleavage of PARP and is correlated with the mitochondrial translocation of Bax and the loss of mitochondrial transmembrane potential (Deltapsim) during etoposide-induced apoptosis in human cervical adenocarcinoma (HeLa) cells. Etoposide-induced apoptotic cell death is efficiently prevented in cells that overexpress a dominant negative mutant of Cdk2 (Cdk2-dn) or p21(WAF1/CIP1), a specific Cdk inhibitor.