Plasmonic gold and silver nanoparticles have attracted considerable interest for cancer theragnostic owing to their unique optical and physicochemical properties. However, their therapeutic application is often limited by poor cancer selectivity, necessitating post-synthetic conjugation of targeting ligands to achieve tumour-specific activity. Here, we demonstrate that biological synthesis using phytochemicals from the medicinal plant Tinospora cordifolia intrinsically functionalizes plasmonic nanoparticles with selective anticancer activity. Reduction of gold and silver salts by T. cordifolia phytoconstituents produced discoid plasmonic nanoparticles (TCPNPs) with an average diameter of ∼20 nm. TCPNPs elicited rapid and potent cytotoxicity against lung and breast cancer cells while sparing non-cancerous cells. Mechanistically, TCPNPs disrupted the actin cytoskeleton organization, compromised nuclear membrane integrity, and selectively perturbed mitochondrial homeostasis, resulting in structural remodeling, membrane hyperpolarization, excessive mitochondrial reactive oxygen species generation, and apoptotic cell death. Importantly, these effects were undetected in non-cancer cells, highlighting the intrinsic selectivity of TCPNPs. At sublethal concentrations, TCPNPs significantly inhibited cancer cell migration and clonogenic growth. In contrast, chemically synthesized plasmonic Au and Ag nanoparticles exhibited negligible anticancer activity at equivalent concentrations, indicating that the enhanced bioactivity of TCPNPs originates predominantly from the phytochemical corona acquired during biological synthesis rather than the plasmonic core itself. Collectively, our findings establish that phytochemical synthesis can endow plasmonic nanoparticles with intrinsic tumour-selective functionality, providing a simple strategy to engineer multifunctional nanomedicines without post-synthetic surface modification.
In this study, nifedipine-loaded egg white protein nanoparticles (Nif-EWP NPs) were developed using a simple protein-based method without synthetic surfactants or crosslinking agents, and their exploratory wound-healing potential was evaluated. The nanoparticles were characterized using standard analytical methods, including UV-Vis spectroscopy, dynamic light scattering (DLS), Fourier-transform infrared (FTIR) spectroscopy, and differential scanning calorimetry (DSC). In addition, in vitro release studies supported by mathematical kinetic modeling and in vivo studies using rat models and histological examinations were performed. The selected formulation exhibited a nanoscale hydrodynamic particle size in the range of approximately 150–200 nm and a zeta potential of approximately +20 mV. Comparative FTIR and DSC analyses of nifedipine-loaded EWP NPs (Nif-EWP NPs), EWP NPs alone, and free nifedipine revealed distinct physicochemical characteristics and suggested possible interactions between nifedipine and the nanoparticle matrix. The formulation showed a gradual release profile over 24 h, and kinetic modeling was consistent with diffusion-dominated or near-Fickian release behavior. In the exploratory in vivo study, the Nif-EWP NP group showed the highest numerical wound-area contraction among the experimental groups and significantly greater overall wound contraction than the untreated control group; however, superiority over nifedipine ointment, raw EWP, or blank EWP NPs was not demonstrated. These macroscopic findings were qualitatively consistent with histological observations, including more advanced re-epithelialization, more organized collagen deposition, and reduced scab persistence. Overall, these findings support further investigation of Nif-EWP NPs as a potential topical formulation for wound-healing applications.
Objectives: Tumor cells produce and release significant amounts of lactic acid (LA) via glucose glycolysis, creating an acidic, high-LA tumor microenvironment. This microenvironment promotes the M2 polarization of tumor-associated macrophages (TAMs) and leads to immunosuppression. This study aims to reprogram TAM metabolism and boost antitumor immunity by synergistically reducing extracellular LA levels using a dual-liposome formulation strategy.Methods: We prepared phenylboronic acid (PBA)-modified α-cyano-4-hydroxycinnamate (CHC) liposomes (PBA-CHC-LIP) to target 4T1 tumor cells and inhibit monocarboxylate transporter 4 (MCT4), thereby suppressing LA efflux. Concurrently, gefitinib lactate (GFB-LA) was synthesized to construct high-loading gefitinib liposomes (GFB-LIP) via an active loading method. In vitro experiments were conducted using 4T1 and RAW264.7 cells, and in vivo experiments were performed using a 4T1 tumor-bearing mouse model to evaluate the synergistic effects of the combined therapy on LA efflux, cell apoptosis, macrophage polarization, and tumor progression.Results: PBA-CHC-LIP effectively targeted 4T1 cells and significantly inhibited LA efflux. GFB-LIP achieved an ideal drug loading of 5.3% and an encapsulation efficiency of 94%, promoting 4T1 cell apoptosis and further reducing LA production. The synergistic treatment significantly decreased LA concentrations in the tumor microenvironment both in vitro and in vivo, thereby inhibiting the M2 polarization of TAMs (evidenced by decreased CD206, IL-10, Arg-1, and TGF-β1) and enhancing the M1-TAM-mediated immune response (indicated by elevated IL-12, iNOS, and TNF-α). The combined therapy also effectively inhibited the growth of tumor volume and weight in vivo.Conclusions: The synergistic therapy of PBA-CHC-LIP and GFB-LIP successfully reduced LA levels in the tumor microenvironment and achieved the metabolic reprogramming of tumor-associated macrophages. This provides a novel and effective strategy for reshaping the tumor immune microenvironment and enhancing antitumor therapy.
In this study, spray pyrolysis was employed to fabricate pristine NiO and a CNT@NiO composite electrode at 350 °C for supercapacitor electrodes. The structural and morphological properties of both materials were characterized by X-ray diffraction, Fourier-transform infrared spectroscopy, Brunauer-Emmett-Teller analysis, and scanning electron microscopy. Electrochemical performance was evaluated by cyclic voltammetry, galvanostatic charge-discharge, and electrochemical impedance spectroscopy in 2 M KOH over a potential window of 0 to 0.7 V vs. SCE. BET analysis showed that CNT incorporation increased the specific surface area from 29.55 to 46.51 m2 g-1 and the mean pore diameter from 6.10 to 27.37 nm. The 350-CNT@NiO electrode delivered a specific capacitance of 472.4 F g-1 at 2 A g-1, exceeding that of 350-NiO (18.92 F g-1), with a rate capability of 68.8% compared to 13.6% for 350-NiO. After 1,000 cycles at 2 A g-1, 350-CNT@NiO retained 93.3% of its initial capacitance compared to 81.5% for 350-NiO, with both electrodes maintaining 100% Coulombic efficiency. The results demonstrate that 350-CNT@NiO is a promising electrode material for supercapacitor applications and that spray pyrolysis is a low-cost, scalable fabrication route suitable for energy storage electrode preparation.
Glioblastoma is one of the most aggressive primary brain tumors, and it is difficult to treat since the blood-brain barrier restricts the transport of many therapeutic medicines to the tumor site. Kaempferol (KMP), a naturally occurring flavonoid, has exhibited promising anticancer action, but its therapeutic applicability is restricted by low bioavailability and water solubility. This study demonstrated systematic Box–Behnken design-based optimization of KMP-loaded poly(lactic-co-glycolic acid)-nanoparticles (PLGA-NPs) and the integrated evaluation of their physicochemical and biological performance against glioblastoma cells. The effect of sonication time, concentration of polyvinyl alcohol (PVA), and PLGA, and on NP size and entrapment efficiency was assessed. The optimized formulation resulted in NPs of an average particle size of 103.7 ± 2.08 nm, entrapment efficiency of 75.73 ± 0.39%, polydispersity index value of 0.184, and zeta potential of −21.1 mV, showing that the particles were uniform and stable. FE-SEM micrographs showed that the NPs were spherical in shape. FTIR and XRD studies confirmed the incorporation of KMP into the PLGA matrix without undergoing any chemical reaction. In contrast to free KMP, the optimized formulation demonstrated sustained KMP release, enhanced antioxidant activity, greater cytotoxicity toward U87 glioblastoma cells, and comparatively better compatibility with normal L929 fibroblasts, highlighting the potential of PLGA nanoencapsulation to improve the therapeutic performance of KMP. All these results reveal the significant effect of PLGA nanoencapsulation on the physicochemical and biological characteristics of KMP.
