Current Pharmaceutical Design - Volume 31, Issue 35, 2025

Due to increasing antibiotic resistance, researchers are investigating the medicinal potential of nanoparticles, particularly their antibacterial and antiviral properties. Among other things, this concern mandates the journey for novel and more potent antibacterial drugs. The crucial role of nanoparticles in the treatment of various microbial diseases has been demonstrated in several research studies.

This study focuses on the role of Selenium nanoparticles (SeNPs) against infectious diseases, with an emphasis on exploring their probable mechanisms of action.

Nanoparticles have been exploited as delivery mechanisms and broad-spectrum inhibitors in viral and microbial studies. Their significant therapeutic potential stems from their high surface area to volume ratio, which enables diverse applications. Various materials have been employed in the synthesis of nanoparticles, each tailored to meet specific therapeutic requirements. The unique combination of biological relevance, environmental friendliness, and versatile applications makes SeNPs a promising alternative to other nanoparticles in various fields.

The therapeutic potential of nanoparticles, especially Selenium nanoparticles (SeNPs), is significant and warrants further exploration. They have shown promise as delivery agents and potent materials for combating infectious diseases, making them a valuable asset in the fight against antibiotic resistance.

Selenium nanoparticles (SeNPs) are potential biological prospects because of their biocompatibility, bioavailability, and low toxicity. Size, shape, and synthesis affect SeNP uses in biological systems. SeNPs are chemopreventive, anti-inflammatory, and antioxidant medicines that may cure fungal, bacterial, and parasite infections, cancer, and diabetes. They have better absorption, bioavailability, and antibacterial action than micron-size particles. Their large surface area facilitates biological contact and bioactive chemical functionalization. Functionalized SeNPs are less cytotoxic than other seleniums. They prevent DNA oxidation, detoxify heavy metals, and inhibit hydroxyl radicals. In conclusion, selenium nanoparticles have considerable promise for medication delivery, antimicrobials, and cancer and diabetes treatment. They are attractive nanomedicine prospects due to their low toxicity, biocompatibility, and high bioavailability.

Nanomedicine offers immense potential in the field of Central Nervous System (CNS) disorder treatment, encompassing conditions such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, epilepsy, and stroke.

Through the utilization of nanotechnology-driven drug delivery systems, the efficacy of drugs can be amplified, their toxicity minimized, and their bioavailability increased, enabling them to effectively reach the intended site within the CNS. This review aims to examine the therapeutic possibilities that nanomedicine presents in addressing these debilitating disorders. This exploration entails an analysis of diverse nanotechnology-based approaches for CNS drug delivery, including polymeric nanoparticles, liposomes, dendrimers, and carbon nanotubes. Moreover, notable advancements in nanotechnology-based therapeutics for CNS disorders are highlighted, such as the application of nanoparticles for delivering curcumin in Alzheimer's disease, liposomes for delivering L-DOPA in Parkinson's disease, and dendrimers for delivering interferon-beta in multiple sclerosis.

Additionally, the potential of nanotechnology-based approaches in the treatment of epilepsy and stroke is discussed. The review concludes by addressing the challenges faced and emphasizes the significant potential of clinical trials in enhancing drug delivery and future prospects in the development of nanotechnology-based therapeutics for CNS disorders.

Overall, the therapeutic potential of nanomedicine in CNS disorder treatment is vast, instilling optimism for the creation of safe and effective therapies for these devastating conditions.

Pancreatic cancer (PC) remains a formidable challenge in cancer, which requires innovative approaches to identify novel therapeutic strategies. Evodia rutaecarpa, a traditional herbal remedy known for its analgesic and antiemetic properties, has been reported to exhibit anticancer effects.

We employed network pharmacology to elucidate the bioactive ingredients of Evodia rutaecarpa and their potential targets in the context of early-onset pancreatic cancer. By integrating data from public databases, we identified genes associated with PC and developed a protein-protein interaction (PPI) network. Topological analysis of the PPI network facilitated the identification of core targets, which were subsequently subjected to molecular docking with corresponding bioactive ingredients of Evodia rutaecarpa. The computational approach aimed to unveil the pharmacological mechanisms of basic putative crucial proteins and associated pathways implicated in early-onset PC. Pathway and GO analysis highlighted the significant involvement of Evodia rutaecarpa in pathways such as cAMP signaling, cytokine-cytokine receptor interaction, rheumatoid arthritis, interleukin signaling, bladder cancer, IL-17, IL-24 signaling, cytokine-mediated signaling, chemokine, and calcium-mediated signaling.

Further exploration focused on a hub protein module derived from PPIs, with molecular docking emphasizing strong binding interactions between Evodia rutaecarpa and ERBB2, a protein strongly implicated in PC management compared to other identified hub proteins (STAT1, ERBB2, CXCL10, INS, RACK1, FOS, HLA-DRB1, POMC, PRKAA1). Additionally, the pharmacokinetic analysis of Evodia rutaecarpa indicated its efficacy as a therapeutic agent with minimal adverse effects. Rutaecarpine, identified as the main bioactive ingredient, emerged as a potential inhibitor of PC growth through the suppression of ERBB2.

These outcomes provide novel insights into the prevention and treatment of PC, presenting Evodia rutaecarpa as a promising candidate for further experimental validation and clinical exploration. The identified discovery has the potential to reduce the drug resistance of Evodia rutaecarpa by engaging with a new target in a specific manner, thus improving therapeutic effectiveness.

Qu’s formula 6 (QUF6), a patented Chinese herbal medicine, is used to treat hypothyroidism in the context of in vitro fertilization-embryo transfer (IVF-ET). This research aims to identify the potential bioactive components and elucidate the underlying molecular mechanisms by which QUF6 cures hypothyroidism during IVF-ET.

To find the active components of QUF6, the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) and relevant literature were searched. GeneCards and other resources were used to find the targets associated with hypothyroidism and IVF-ET. Using Cytoscape software, the network of interactions was created between the targets and components, the protein-protein interaction (PPI) network was built, and significant targets were verified. Afterward, Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed on crucial targets. Finally, molecular docking and dynamic modeling were carried out to analyze the essential components and core targets of QUF6.

By creating an interaction network, it was discovered that 92 active components in QUF6 can operate on 25 disease-related targets, with quercetin and other components playing important pharmacodynamic roles. Tumor necrosis factor (TNF), interleukin-6 (IL-6), interleukin-1B (IL-1B), apoptosis regulator Bcl-2 (BCL2), prostaglandin G/H synthase 2 (PTGS2), cellular tumor antigen p53 (TP53), and epidermal growth factor (EGF) were the main targets for the therapy of hypothyroidism. The KEGG pathway enrichment study identified 91 signaling pathways, whereas the GO enrichment analysis identified 1608 entries. Through molecular docking and MD simulations, stable binding was identified between the top five active constituents and the top seven potential targets.

Quercetin, beta-sitosterol, kaempferol, 7-ketocholesterol, and rehmapicrogenin were determined to be the active ingredients in QUF6. The potential mechanism of action for QUF6 may involve modulation of TNF, IL6, IL1B, BCL2, PTSG2, TP53, and EGF to regulate oxidative stress levels, inflammation responses, and apoptosis processes associated with hypothyroidism during IVF-ET.