Background/Objectives: Wound healing is a complex biological process influenced by inflammation, oxidative stress, and cellular regeneration. Plant-derived bioactive compounds have shown potential to accelerate tissue repair through antioxidant and anti-inflammatory mechanisms. This study aimed to develop and evaluate a Platanus orientalis extract-loaded liposomal formulation for potential wound-healing applications. Methods: Four polar extracts (P1–P4) were prepared using different solvent systems and extraction techniques and were characterized by LC-HRMS to determine their phytochemical profiles. Among the identified constituents, quercetin was consistently detected across all extracts and selected as the reference compound due to its well-known wound-healing activity. Liposomes were prepared via thin-film hydration followed by probe sonication and characterized for particle size, polydispersity index (PDI), zeta potential, encapsulation efficiency, and total drug content. In vitro release, cytotoxicity, and wound-healing assays were subsequently conducted to assess performance. Results: The optimized liposome formulation had a mean particle size of 106.6 ± 5.4 nm, a PDI of 0.11 ± 0.04, and a zeta potential of −14.1 ± 0.5 mV. Environmental scanning electron microscopy (ESEM) confirmed the nanosized spherical morphology and homogeneous vesicle distribution, supporting the successful development of the liposomal delivery system. Encapsulation efficiency and total drug content were determined as 72.25 ± 1.05% and 96.15 ± 0.14%, respectively. In vitro release studies demonstrated a biphasic pattern with an initial burst followed by a sustained release, reaching approximately 75% cumulative quercetin release within 24 h. Physical stability testing confirmed that the optimized liposomal formulation remained physically stable at 5 ± 3 °C for at least 60 days. The optimized formulation showed no cytotoxic effects on CDD-1079Sk fibroblast cells and exhibited significantly enhanced wound closure in vitro. Conclusions: These findings indicate that the liposomal delivery of Platanus orientalis extract provides a biocompatible and sustained-release system that enhances wound-healing efficacy, supporting its potential use in advanced topical therapeutic applications.

The rapid expansion of nanotechnology has led to the widespread use of nanomaterials, especially metal-based nanoparticles (NPs), across various industrial and biomedical fields. Due to their superior properties, copper-based nanoparticles are one of the most used metal-based NPs. However, there are very limited data on the toxicological profile of cuprous oxide NPs (Cu2O NPs). This study aimed to evaluate the neurotoxic effects of Cu2O NPs in SH-SY5Y and Neuro-2A cells by characterizing the NPs and assessing cellular uptake, cytotoxicity, genotoxicity, apoptosis/necrosis, and oxidative stress. TEM and SEM NPs characterization confirming the nanoscale size of NPs. ICP-MS analysis revealed significant, dose-dependent, and cell-dependent cellular uptake, with SH-SY5Y cells showing higher uptake levels. Cu2O NPs caused a significant decrease in the cell’s viability. The calculated IC50 values were 20.4 μg/mL and 23.9 μg/mL in SH-SY5Y by NRU and MTT assays, respectively, while it was 34.7 μg/mL and 8.3 μg/mL in Neuro-2A. Comet assay results demonstrated DNA damage in SH-SY5Y, but not in Neuro-2A. An increase in the apoptotic (1.5-fold to 3.3-fold) and necrotic cells was observed in both cell lines, with pronounced necrotic effect in Neuro-2A (6.9-fold at 5 μg/mL). Cu2O NPs increased MDA, GSH, and SOD levels and decreased CAT activity. Indicating oxidative stress in the cells, particularly in SH-SY5Y. In conclusion, our findings indicate that Cu2O NPs exert significant effects in vitro, primarily through oxidative stress-mediated mechanisms. Results highlight the importance of further mechanistic and in vivo studies to better understand the safety – toxicity profile of Cu2O NPs.

1. Topical formulations containing plant-derived extracts continue to attract considerable interest in pharmaceutical research due to their potential to deliver bioactive compounds directly to the ...

Many antiviral agents are known to induce off-target mitochondrial toxicity due to the prokaryotic origin of mitochondria. Mitochondrial dysfunction is frequently linked to cardiotoxicity. We aimed to elucidate the mitochondrial toxicity profile of molnupiravir via focusing on mitochondrial dynamics, biogenesis, and oxidative stress in cardiac cells. Mitochondrial function was evaluated by luminometric measurement of ATP (adenosine triphosphate) content, and flow cytometric analysis of mitochondrial membrane potential, and mitochondrial mass. The expression levels of genes involved in mitochondrial fusion-fission were assessed by RT-PCR. In addition, molecular docking analysis was performed to evaluate the interaction between molnupiravir and the dynamin related-protein DRP1. Protein carbonylation was determined as an oxidative stress parameter. Toxicity evaluation was further investigated in Caenorhabditis elegans to support the in vitro findings at the organismal level. Molnupiravir exposure led to a significant dose-dependent reduction in intracellular ATP level and mitochondrial mass, accompanied by increased protein carbonylation. Mitochondrial membrane potential remained slightly increased. Alterations in the expression of genes regulating mitochondrial dynamics suggested an imbalance between fusion and fission processes, while mitochondrial biogenesis-related signaling was progressively suppressed. C. elegans exposed to higher concentrations of the drug (20-500 µM) exhibited significant lifespan reduction at all doses. Molecular docking analysis demonstrated a moderate binding affinity of molnupiravir to DRP1, supporting a potential direct interaction with mitochondrial fission machinery. In conclusion, our results demonstrate that molnupiravir induces mitochondrial stress through oxidative damage, impaired biogenesis, and altered dynamics, emphasizing the need for careful evaluation of mitochondrial safety of molnupiravir in cardiac tissue.