69 research outputs found
Development and optimisation of spironolactone nanoparticles for enhanced dissolution rates and stability
Stable solid lipid nanoparticles (SLNs) and nanostructured lipid carriers (NLCs) formulations to enhance the dissolution rates of poorly soluble drug spironolactone (SP) were being developed. Probe ultra-sonication method was used to prepare SLNs and NLCs. All NLCs contained stearic acid (solid lipid carrier) and oleic acid (liquid lipid content), whereas, SLNs were prepared and optimised by using the solid lipid only. The particles were characterised in terms of particle size analysis, thermal behaviour, morphology, stability and in vitro release. The zeta sizer data revealed that the increase in the concentration of oleic acid in the formulations reduced the mean particle size and the zeta potential. The increase in concentration of oleic acid from 0 to 30% (w/w) resulted in a higher entrapment efficiency. All nanoparticles were almost spherically shaped with an average particle size of about âŒ170 nm. The DSC traces revealed that the presence of oleic acid in the NLC formulations resulted in a shift in the melting endotherms to a higher temperature. This could be attributed to a good long-term stability of the nanoparticles. The stability results showed that the particle size remained smaller in NLC compared to that of SLN formulations after 6 months at various temperatures. The dissolution study showed about a 5.1- to 7.2-fold increase in the release of the drug in 2 h compared to the raw drug. Comparing all nanoparticle formulations indicated that the NLC composition with a ratio of 70:30 (solid:liquid lipid) is the most suitable formulation with desired drug dissolution rates, entrapment efficiency and physical stability
Itraconazol-Loaded Nanostructured Lipid Carriers (NLC) for Pulmonary Application
Introduction: Aspergillosis is a common fungal infection in falcons. Standard treatment, systemic application of Itraconazol, is limited due to hepatotoxicity. [...
In Vitro Characterisation of Vancomycin Loaded Glyceryl Monooleate-Water Liquid Crystalline Gel/Implants for Ocular Application
In the present investigation, vancomycin was incorporated in liquid crystalline gel made of glyceryl monooleate and water, with the aim to achieve a sustained-release and to deliver locally sufficient concentrations of vancomycin to the eye, improving its efficacy against bacterial infections [1â3]. [...
Secretory phospholipase a2 inhibitor px-18 preserves microvascular reactivity after cerebral ischemia in piglets.
Cerebral ischemia/reperfusion (I/R) results in cellular energy failure and dysfunction of the neurovascular
unit that contribute to subsequent neuronal cell death in the neonate. PX-18 is a putative neuroprotective
inhibitor of secretory phospholipase A2 (sPLA2) but its in vivo testing has been limited by its poor solubility.
Our purpose was to assess whether PX-18 preserved neuronalâvascular reactivity to I/R-sensitive
endothelium-dependent (hypercapnia, bradykinin) and/or neuron-dependent (N-methyl-D-aspartate;
NMDA) stimuli. To make the drug available for in vivo studies, PX-18 was formulated as a 3% nanosuspension
applying high pressure homogenization. Newborn piglets (1-day old, n=40) were anesthetized and ventilated,
and cerebrovascular reactivity to the above stimuli was determined by measuring changes in pial
arteriolar diameters using the closed cranial window/intravital videomicroscopy technique. Intravenous
infusion of PX-18 nanosuspension (6 mg/kg, 20 min) did not affect baseline arteriolar diameters, or
hypercapnia-, bradykinin-, or NMDA-induced pial arteriolar vasodilation under normoxic conditions. Global
cerebral ischemia (10 min) followed by 1 h of reperfusion significantly attenuated hypercapnia-, bradykinin-,
and NMDA-induced vasodilation in untreated or vehicle-treated controls. However, PX-18 resulted in nearly
full preservation of cerebrovascular reactivity to all these stimuli. In conclusion, inhibition of sPLA2 by PX-18
improves neurovascular function both at the neuronal and the microvascular level following I/R. This effect of
PX-18 likely contributes to its neuroprotective effect
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