PMC

Images of calcein-loaded cells treated with 200 μmol/L nystatin. The images were taken using confocal microscopy at different time points after the nystatin addition (indicated on the images).

Forest plots evaluating the efficacy of nystatin (fixed-effect model).
Notes: (A) The overall clinical efficacy of nystatin was significantly superior to the placebo in treating denture stomatitis; (B) the overall mycological efficacy of nystatin was significantly superior to the placebo in treating denture stomatitis; (C) the overall clinical efficacy of nystatin was significantly inferior to fluconazole for treating oral or oropharyngeal candidiasis in infants, children, and HIV/AIDS patients; and (D) the overall mycological efficacy of nystatin was significantly inferior to fluconazole for treating oral or oropharyngeal candidiasis in infants, children, and HIV/AIDS patients.
Abbreviations: CI, confidence interval; OR, odds ratio.

The GUVs show different behavior due to the pore-formation process in vesicles with smaller glucose molecules outside and larger sucrose molecules inside, as seen using phase-contrast microscopy []. Development of typical membrane protrusions (indicated by arrows) due to the nystatin binding to the outer membrane monolayer at low nystatin concentrations (a). Loss of vesicle contrast due to transient tension pores at intermediate nystatin concentrations (b). Slow (c) and fast (d) vesicle ruptures at high nystatin concentrations: GUVs before the rupture (left), during the rupture (middle, tension pore indicated by arrow), and immediately after the rupture (right) are shown. The times after the GUV transfer into the nystatin solution are depicted on the images. The bars represent 20 μm. For more detailed descriptions see Refs. [] and [].

A SW1116 and SW480 were treated with control siRNA or siSOAT1 in the presence or absence of nystatin (20 μM). Cell proliferation activity was detected by CCK-8 after 72 h. B SW1116 and SW480 were treated with DMSO or avasimibe (10 μM) in the presence or absence of nystatin (20 μM). Cell proliferation activity was detected by CCK-8 after 72 h. C SW1116 and SW480 were incubated with DMSO or avasimibe (10 μM) in the presence or absence of nystatin (20 μM) for 5 d, respectively. The cell proliferation ability was detected by the colony formation assay. D SW1116 and SW480 were treated with nystatin (10–30 μM) for 16 h. E SW1116 and SW480 were transfected with negative control siRNA or SOAT1 siRNA for 48 h, respectively. The cells were then incubated with DMSO or nystatin (20 μM) for 16 h. F SW1116 and SW480 were incubated with DMSO or avasimbie (10 μM) in the presence or absence of nystatin (20 μM) for 16 h, respectively. The expression of proteins was detected by Western blot.