@article {1314, title = {Enhanced Antifungal Efficacy of KZ-β/γ-CD Capped Silver Nanoparticles against Trichophyton rubrum}, journal = {Pharmacognosy Research}, volume = {16}, year = {2024}, month = {October 2024}, pages = {879-886}, type = {Original Article}, chapter = {879}, abstract = {

Background: The present medications are inefficient in treating fungal infections, so there is a need to develop an efficient antifungal treatment with minimal side effects and rapid healing. Ketoconazole (KZ) is frequently prescribed for managing fungi-related skin infections However, it is a poorly soluble with low absorption, making it less effective. Objectives: The study aims to enhance the absorption and effectiveness of the antifungal medication KZ by complexing it with β and γ Cyclodextrins (CD) coated with silver nanoparticles (AgNps). Materials and Methods: KZ inclusion complexes with AgNps capped β- and γ-CD (β/γ-CD-KZ-AgNp) were prepared and analysed by UV-vis spectroscopy, FTIR, SEM and XRD. The antifungal efficacy of these complexes against Trichophyton rubrum was assessed by Minimum Inhibitory Concentration (MIC) and Disc-Diffusion assay. Results: The drug KZ was successfully loaded into the AgNp-capped β-CD and γ-CD inclusion complexes, as indicated by a UV peak at 293 nm. The FTIR spectra of the complexes (β/γ-CD-KZ-AgNp) showed peaks for aldehyde, CH stretching and-OH stretching for AgNp, CDs and KZ. The crystalline nature and AgNp coating were confirmed by the X-ray diffraction. Scanning electron microscope images revealed that the complexes were less agglomerated, spherical and embedded with AgNps. The minimum inhibitory concentration of the complexes against Trichophyton rubrum was much higher than that of the drug alone, with 0.5 μg/mL MIC for β-CD-KZ-AgNp and 1 μg/mL for γ-CD-KZ-AgNp in comparison to the control drug KZ (2 μg/mL). The complexes also demonstrated excellent antifungal activity against T. rubrum, with inhibition zone of 29.7 mm for β-CD-KZ-AgNp and 29.1 mm for γ-CD-KZ-AgNp compared to 14.74 mm for the drug alone. Conclusion: The inclusion complexes show great potential as a treatment against fungal infections.

}, keywords = {Fungal Infection, inclusion complexes, Ketoconazole, Silver Nano-particles, β and γ Cyclodextrin}, doi = {10.5530/pres.16.4.100}, author = {Bhargavi Kumaraswamy and Sunil More and Aneesa Fasim and Raju Koneri} } @article {1134, title = {Possible Involvement of Cellular Pathway and Cytokines in Manganese Induced Neurotoxicity in Neuroblastoma Cells via KH{\textendash}Type Splicing Regulatory Protein}, journal = {Pharmacognosy Research}, volume = {15}, year = {2023}, month = {February 2023}, pages = {307-314}, type = {Original Article }, chapter = {307}, abstract = {

Background: Manganese is a toxic essential trace element and too high concentration instigates the neurodegenerative disease known as parkinsonism. Effects of manganese may lead to apoptosis. However, a detailed mechanism of manganese toxicity has not been fully elucidated. Previous published articles have highlighted the augmentation of KHSRP expression following Mn exposure. Objectives: In this work, the importance of KHSRP in Mn{\textendash}induced toxicity was checked along with the impact of other known neurotoxicity inhibitors on KHSRP. Materials and Methods: KHSRP expression, pro and anti-inflammatory cytokines, chemokines, and pharmacological inhibitors (SAHA, Quercetin, and MCC950) were determined by exposing N2a cells to various MnCl2 concentrations. ANOVA and Dunnett{\textquoteright}s test were used to decide on the significance. Results: MnCl2 treatment led to the augmentation of the KHSPR mRNA expression and protein increase in N2a cell line. The MnCl2 treatment of N2a cells also showed an elevated liberation of IL-6, TNF-α, MCP{\textendash}1, and IL-1β. Pharmacological agents like quercetin inhibiting PI3K, MAPK, and WNT pathways, MCC950 blocking NLRP3 pathways, and SAHA showed a decrease in KHSRP expression post Mn treatment. With the inhibition of KHSRP, a decline in the release of IL-1β, IL-6, MCP{\textendash}1, and TNF-α was also observed. Conclusion: These results suggested that MnCl2 treatment of N2a cells induce the expression of KHSRP via the PI3K{\textendash}or NLRP3 pathway. Furthermore, this elevated expression of KHSRP is responsible for an increment in the liberation of pro-inflammatory markers in N2a cells. More exploration is needed to throw light on the pathway driving the KHSRP.

}, keywords = {KH{\textendash}type Splicing Regulatory Protein, Manganese Neurotoxicity, Neuroblastoma, Neurodegeneration, Neuroinflammation.}, doi = {10.5530/pres.15.2.033}, author = {Sharad Singh and Sunil More and G. S. Latha and Himanshu Agrawal and Veena S M and Francois Niyonzima} }