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1.
AAPS PharmSciTech ; 25(5): 94, 2024 May 06.
Article in English | MEDLINE | ID: mdl-38710898

ABSTRACT

This study introduces and assesses the potential of a Luliconazole-loaded nanofiber (LUL-NF) patch, fabricated through electrospinning, for enhancing topical drug delivery. The primary objectives involve evaluating the nanofiber structure, characterizing physical properties, determining drug loading and release kinetics, assessing antifungal efficacy, and establishing the long-term stability of the NF patch. LUL-NF patches were fabricated via electrospinning and observed by SEM at approximately 200 nm dimensions. The comprehensive analysis included physical properties (thickness, folding endurance, swelling ratio, weight, moisture content, and drug loading) and UV analysis for drug quantification. In vitro studies explored sustained drug release kinetics, while microbiological assays evaluated antifungal efficacy against Candida albicans and Aspergillus Niger. Stability studies confirmed long-term viability. Comparative analysis with the pure drug, placebo NF patch, LUL-NF patch, and Lulifod gel was conducted using agar diffusion, revealing enhanced performance of the LUL-NF patch. SEM analysis revealed well-defined LUL-NF patches (0.80 mm thickness) with exceptional folding endurance (> 200 folds) and a favorable swelling ratio (12.66 ± 0.73%). The patches exhibited low moisture uptake (3.4 ± 0.09%) and a moisture content of 11.78 ± 0.54%. Drug loading in 1 cm2 section was 1.904 ± 0.086 mg, showing uniform distribution and sustained release kinetics in vitro. The LUL-NF patch demonstrated potent antifungal activity. Stability studies affirmed long-term stability, and comparative analysis highlighted increased inhibition compared to a pure drug, LUL-NF patch, and a commercial gel. The electrospun LUL-NF patch enhances topical drug delivery, promising extended therapy through single-release, one-time application, and innovative drug delivery strategies, supported by thorough analysis.


Subject(s)
Antifungal Agents , Aspergillus niger , Candida albicans , Drug Delivery Systems , Drug Liberation , Imidazoles , Nanofibers , Antifungal Agents/administration & dosage , Antifungal Agents/pharmacology , Antifungal Agents/chemistry , Nanofibers/chemistry , Candida albicans/drug effects , Aspergillus niger/drug effects , Drug Delivery Systems/methods , Imidazoles/chemistry , Imidazoles/administration & dosage , Imidazoles/pharmacology , Delayed-Action Preparations , Microbial Sensitivity Tests/methods , Drug Carriers/chemistry , Drug Stability
2.
Life Sci ; 286: 119989, 2021 Dec 01.
Article in English | MEDLINE | ID: mdl-34597609

ABSTRACT

AIMS: Isoformononetin (IFN), a methoxyl isoflavone present in most of human dietary supplements. However, being a highly potent antioxidant and anti-inflammatory molecule, its activity against neuronal oxidative stress and neuroinflammation has not been explored till now. The present study was inquested to assess the antioxidant, anti-apoptotic and anti-inflammatory activity of IFN against streptozotocin induced neuroinflammation in different brain regions of rat. MAIN METHODS: Four groups of animals were subjected to treatment as control, toxic control (STZ; single intracerebrovascular injection), third group (STZ + IFN; 20 mg/kg p.o.), fourth group (IFN) for 14 days. The different brain regions of rats were evaluated for inflammatory, apoptotic and biochemical antioxidant markers. The brain tissues were further assessed for gene expression, immunohistochemical and western blotting examination for localization of inflammasome cascade expression that plays a pivotal role in neuroinflammation. KEY FINDINGS: The modulation in oxidant/antioxidant status after exposure of STZ was significantly balanced after administration of IFN to rats. Further, IFN was also found to be an apoptotic agent as it modulates the apoptotic gene (Bax) and anti-apoptotic gene (BcL2) expression. IFN significantly curtailed the augmented protein expression of NLRP3, NLRP2, ASC, NFκBP65, IL-1ß and caspase-1 due to STZ administration in cortex and hippocampus rat brain regions. SIGNIFICANCE: The aforementioned results proclaim the neuroprotective functioning of IFN against STZ induced inflammation. IFN significantly prevents the neuroinflammation by decreasing the generation of ROS that reduces the activation of NLRP3/ASC/IL-1 axis thereby exerting neuroprotection as evidenced in rat model of STZ induced neuroninflammation.


Subject(s)
Antioxidants/pharmacology , CARD Signaling Adaptor Proteins/metabolism , Encephalitis/prevention & control , Interleukin-1/metabolism , Isoflavones/pharmacology , NLR Family, Pyrin Domain-Containing 3 Protein/metabolism , Streptozocin/toxicity , Animals , Disease Models, Animal , Encephalitis/chemically induced , Encephalitis/metabolism , Encephalitis/pathology , Gene Expression/physiology , Interferons/physiology , Lipid Peroxidation/drug effects , Nitric Oxide/biosynthesis , Oxidative Stress/drug effects , Rabbits , Rats , Rats, Sprague-Dawley , Reactive Oxygen Species/metabolism , Signal Transduction , Tumor Necrosis Factor-alpha/metabolism
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