Structure

Diosgenin

CAS
512-04-9
Catalog Number
ALC-FP-512049
Category
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Specification

Melting Point
≥ 193.0°C
Appearance
White or almost white crystalline powder
Assay
≥ 98%
Drying Loss
≤ 0.50%
Sample Lot No.
240723
Specific Rotation
≥ -115°

Diosgenin for Inhibiting Protein Aggregation in Neurodegenerative Models

Molecular insights into diosgenin's role in preventing protein aggregation in neurodegenerative diseases Parveen N, et al. Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics, 2026, 1874(1), 141116.

Diosgenin was experimentally applied as an anti-aggregation agent using human serum albumin (HSA) as a model protein. Aggregation was induced and quantified through ThT fluorescence and turbidity assays, where diosgenin treatment reduced signals by over 60%, demonstrating significant inhibition. Circular dichroism spectroscopy showed that diosgenin partially restored the α-helix structure of denatured HSA. Molecular docking revealed a binding energy of -11.0 kcal/mol, supported by van der Waals, hydrophobic, and hydrogen-bond interactions. Advanced molecular dynamics simulations further verified reduced β-sheet formation, diminished intermolecular hydrogen bonding, and increased solvent accessibility in HSA and Aβ oligomers. These integrated experimental and computational methods collectively highlight diosgenin's role in stabilizing protein conformation and suppressing aggregation.

Diosgenin for Protecting Intestinal Barrier Integrity in a CLP-Induced Sepsis Model

Diosgenin ameliorates CLP-induced sepsis in mice via suppressing inflammatory responses and preserving intestinal mucosal barrier integrity Li Y, et al. Molecular Immunology, 2025, 187, 210-220.

Diosgenin was experimentally applied in a murine cecal ligation and puncture (CLP) model to evaluate its protective effects against sepsis-induced intestinal injury. In this study, diosgenin treatment improved survival and significantly reduced systemic inflammation, as evidenced by lowered serum TNF-α and IL-6 measured via ELISA. Intestinal barrier integrity was assessed through H&E staining, serum D-lactic acid quantification, and Western blot detection of Claudin-1 and Occludin, revealing marked preservation of mucosal structure. qRT-PCR and immunohistochemistry further demonstrated that diosgenin enhanced mCRAMP expression while suppressing TLR4/MyD88 signaling. Molecular docking confirmed favorable binding of diosgenin to LL-37, TLR4, and MyD88, supporting its mechanistic involvement in attenuating inflammation and barrier dysfunction.

Diosgenin for Modulating Th17 Differentiation via SIRT1 Inhibition in Experimental Arthritis

Diosgenin exerts dual impacts on Th17 cell differentiation in adjuvant-induced arthritis rats by impairing SIRT1-mediated deacetylation Yin Q, et al. Phytomedicine, 2025, 148, 157384.

Diosgenin was experimentally applied as a functional SIRT1 inhibitor to dissect its regulatory effects on Th17 differentiation in adjuvant-induced arthritis (AIA) models. In vivo, AIA rats received graded diosgenin doses, followed by ELISA-based cytokine profiling, flow-cytometric quantification of Th17 cells, and histological evaluation of joint inflammation. Molecular mechanisms were examined using Jurkat T cells, where diosgenin impaired SIRT1-mediated deacetylation and altered the transcriptional activities of NF-κB p65 and RORγt. These effects were validated using siRNA knockdown, SIRT1 overexpression plasmids, immunoprecipitation, ITC binding assays, and reporter gene analysis. The study demonstrates diosgenin's concentration-dependent immune modulation, highlighting its experimental utility in probing SIRT1-dependent inflammatory pathways.

Diosgenin for Enhanced Brain Delivery in Cerebral Ischemia Treatment

Formulation of a novel diosgenin-loaded nanoemulsion and its evaluation for improved brain bioavailability in the management of cerebral ischemia Ahmad N, et al. Journal of Drug Delivery Science and Technology, 114(A), 107468.

A diosgenin-loaded nanoemulsion (DGN-NE) was formulated to overcome the compound's poor solubility and limited brain penetration in cerebral ischemia therapy. Using a Box-Behnken design, diosgenin was dissolved in medium-chain triglycerides and incorporated with Tween-80 and PEG-400, followed by controlled aqueous titration and ultrasonication to generate a uniform nanoemulsion. The optimized formulation achieved a globule size of ~195 nm, narrow PDI, and high transmittance, enabling efficient oral administration. Experimental evaluations demonstrated rapid initial release and sustained permeation, while a validated LC-MS/MS protocol quantified diosgenin in ischemic rat brains with high accuracy. In vivo application of DGN-NE in MCAO rodent models significantly increased AUC and Cmax and produced marked neuroprotection, supported by biochemical, neurobehavioral, and histological analyses. These findings highlight diosgenin's experimental application in nanoemulsion-based delivery to improve brain bioavailability and therapeutic efficacy in ischemic injury.

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