The advent of nanotechnology has brought about revolutionary innovations in biological research techniques and medical practice. In recent years, various “smart” nanocarriers have been introduced to deliver therapeutic agents specifically to the tumor tissue in a controlled manner, thereby minimizing their side effects and reducing both dosage and dosage frequency. A large number of nanoparticles have demonstrated initial success in preclinical evaluation but modest therapeutic benefits in the clinical setting, partly due to insufficient delivery to the tumor site and penetration in tumor tissue. Therefore, a precise understanding of the relationships betweenthe physicochemical properties of nanoparticles and their interaction with the surrounding microenvironment in the body is extremely important for achieving higher concentrations and better functionality in tumor tissues. This knowledge would help to effectively combine multiple advantageous functions in one nanoparticle. The main focus of the discussion in this review, therefore, will relate to the main physicochemical properties of nanoparticles while interacting within the body and their tuning potential for increased performance.

Introduction: This study focuses on the development of dextran-coated iron oxide nanoparticles (Fe₃O₄@Dextran NPs) as carriers for chrysin, a natural flavonoid with recognized anticancer activity.Methods: Fe₃O₄@Dextran NPs were synthesized via co-precipitation and loaded with chrysin at different drug-to-nanoparticle ratios. Structural and physicochemical characterization was performed using X-ray Diffraction (XRD), Fourier Transform Infrared Spectroscopy (FTIR), and Vibrating Sample Magnetometry (VSM). Drug loading efficiency was determined spectrophotometrically. The anticancer efficacy of the drug-loaded samples was assessed in vitro against HCT-116 human colorectal carcinoma cells using the MTT assay, with statistical analysis performed by one-way ANOVA.Results: XRD revealed an average crystallite size of 17 nm for Fe₃O₄@Dextran, which decreased to ∼15 nm upon chrysin loading. FTIR confirmed the successful incorporation of chrysin without compromising structural stability. VSM measurements demonstrated superparamagnetic behavior with a saturation magnetization of 69.2 emu/g. Drug loading efficiencies were 42%, 54%, and 57% at drug-to-nanoparticle ratios of 1:0.5, 1:1, and 1:2, respectively, with evidence of saturation at higher concentrations. The Fe₃O₄@Dextran+D2 formulation exhibited optimal drug loading, maintaining structural integrity and enhanced cytotoxic activity against HCT-116 cells.Conclusion: Fe₃O₄@Dextran+D2 demonstrated favorable structural integrity (as evidenced by XRD and FTIR analyses) along with notable anticancer activity against HCT-116 cells. Its performance is attributed to optimal drug loading without surface saturation, supporting its potential as a structurally stable drug delivery system.

Enhancing nanoparticles’ anti-cancer capabilities as drug carriers requires the careful adjustment of formulation parameters, including loading efficiency, drug/carrier ratio, and synthesis method. Small adjustments to these parameters can significantly influence the drug-loading efficiency of nanoparticles. Our study explored how chitosan and polyethylene glycol (PEG) coatings affect the structural properties, drug-loading efficiency, and anti-cancer efficacy of Fe₃O₄ nanoparticles (NPs). The loading efficiency of the NPs was determined using FTIR spectrometry and XRD. The quantity of chrysin incorporated into the coated NPs was examined using UV–Vis spectrometry. The effect of the NPs on cell viability and apoptosis was determined by employing the HCT 116 human colon carcinoma cell line. We showed that a two-fold increase in drug concentration did not impact the loading efficiency of Fe₃O₄ NPs coated with PEG. However, there was a 33 Å difference in the crystallite sizes obtained from chitosan-coated Fe₃O₄ NPs and drug concentrations of 1:0.5 and 1:2, resulting in decreased system stability. In conclusion, PEG coating exhibited a higher loading efficiency of Fe₃O₄ NPs compared to chitosan, resulting in enhanced anti-tumor effects. Furthermore, variations in the loaded amount of chrysin did not impact the crystallinity of PEG-coated NPs, emphasizing the stability and regularity of the system.

Background: Blue light (BL) irradiation has been shown to induce photobiomodulation (PBM) in cells. Here, we investigate its influence on cell types involved in wound healing. Methods: Cellular responses of immortalized human keratinocytes (HaCaTs), normal human dermal fibroblasts (NHDFs), and human umbilical vein endothelial cells (HUVECs) after light treatment at 450 nm were analyzed by kinetic assays on cell viability, proliferation, ATP quantification, migration assay, and apoptosis assay. Gene expression was evaluated by transcriptome analysis. Results: A biphasic effect was observed on HaCaTs, NHDFs, and HUVECs. Low-fluence (4.5 J/cm²) irradiation stimulated cell viability, proliferation, and migration. mRNA sequencing indicated involvement of transforming growth factor beta (TGF-β), ErbB, and vascular endothelial growth factor (VEGF) pathways. High-fluence (18 J/cm²) irradiation inhibited these cellular activities by downregulating DNA replication, the cell cycle, and mismatch repair pathways. Conclusions: HaCaTs, NHDFs, and HUVECs exhibited a dose-dependent pattern after BL irradiation. These findings broaden the view of PBM following BL irradiation of these three cell types, thereby promoting their potential application in wound healing and angiogenesis. Our data on low-fluence BL at 450 nm indicates clinical potential for a novel modality in wound therapy.

Background: Postthrombotic syndrome (PTS) has a major impact on the quality of life after deep venous thrombosis (DVT). From clinical practice and related trials, anticoagulants show potential for reducing the occurrence and alleviating the symptoms of PTS. Methods: A systematic review and Bayesian network meta-analysis (NMA) were conducted by combing the literature from the databases of MEDLINE, Embase, Web of Science, Cochrane Libraries, and ClinicalTrials, through a variety of medical subject headings (Mesh) and PTS keywords. With regard to PTS prophylaxis, all anticoagulant-related randomized controlled trials (RCTs) and observational studies were assessed. The network model was conducted through the R software, and further comparisons were conducted using the Bayesian hierarchical random effects model. The odds ratio (OR) and the corresponding 95% CI were calculated for analysis. Results: Data from two RCTs and nine non-randomized studies meeting the selection criteria were included in the Bayesian analysis model, which incorporated seven anticoagulants. Edoxaban (OR: 0.42, 95% CI: 0.18–1.0) and rivaroxaban (OR: 0.54, 95% CI: 0.38–0.76) were significantly more effective than warfarin in the prevention of PTS (Villalta score ≥ 5). A subgroup analysis based on the severity of PTS showed that rivaroxaban was more effective than warfarin, with OR: 0.59, 95% CI: 0.41–0.84 (Villalta score 5 to 14) and OR: 0.48, 95% CI: 0.22–0.9 (Villalta score ≥ 15, ulceration), respectively. Edoxaban had the highest probability (80.1%) of providing preventive benefits for PTS. For mild/moderate and severe PTS, rivaroxaban provided the highest benefits in preventing PTS (89.3% and 85.6%, respectively). Conclusion: Edoxaban demonstrated a better prophylactic effect on PTS (Villalta score > 5), while rivaroxaban displayed a better effect against mild/moderate (Villalta score 5 to 14) and severe PTS (Villalta score ≥ 15, ulceration).

Adipose-derived stem cells (ASCs) have been used as a therapeutic intervention for peripheral artery disease (PAD) in clinical trials. To further explore the therapeutic mechanism of these mesenchymal multipotent stromal/stem cells in PAD, this study was designed to test the effect of xenogeneic ASCs extracted from human adipose tissue on hypoxic endothelial cells (ECs) and terminal unfolded protein response (UPR) in vitro and in an atherosclerosis-prone apolipoprotein E-deficient mice (ApoE^−/− mice) hindlimb ischemia model in vivo. ASCs were added to Cobalt (II) chloride-treated ECs; then, metabolic activity, cell migration, and tube formation were evaluated. Fluorescence-based sensors were used to assess dynamic changes in Ca²⁺ levels in the cytosolic- and endoplasmic reticulum (ER) as well as changes in reactive oxygen species. Western blotting was used to observe the UPR pathway. To simulate an acute-on-chronic model of PAD, ApoE^−/− mice were subjected to a double ligation of the femoral artery (DLFA). An assessment of functional recovery after DFLA was conducted, as well as histology of gastrocnemius. Hypoxia caused ER stress in ECs, but ASCs reduced it, thereby promoting cell survival. Treatment with ASCs ameliorated the effects of ischemia on muscle tissue in the ApoE^−/− mice hindlimb ischemia model. Animals showed less muscle necrosis, less inflammation, and lower levels of muscle enzymes after ASC injection. In vitro and in vivo results revealed that all ER stress sensors (BIP, ATF6, CHOP, and XBP1) were activated. We also observed that the expression of these proteins was reduced in the ASCs treatment group. ASCs effectively alleviated endothelial dysfunction under hypoxic conditions by strengthening ATF6 and initiating a transcriptional program to restore ER homeostasis. In general, our data suggest that ASCs may be a meaningful treatment option for patients with PAD who do not have traditional revascularization options.