Silver nanoparticles (AgNP) are one of the most studied nanoparticles due to their anti-bacterial, -fungal, -viral, -parasitic, and -inflammatory properties. This raises the need to evaluate the toxicity and biological effects of AgNP in the immune system in order to develop new safer biomedical products. In this study, an AgNP formulation currently approved for veterinary applications was applied to mouse bone marrow-derived dendritic cells (BMDC), considered important antigen-presenting cells of the immune system, to evaluate cytotoxicity, genotoxicity, and any significant influence on expression of cellular markers associated with BMDC phenotype and maturation status. The results showed that after 12 h of AgNP exposure, a significant decrease in BMDC viability occurred at the highest concentration tested (1.0 µg AgNP/ml) and at lower doses, the cells maintained membrane integrity and metabolic activity. DNA damage was not significant with any AgNP level aside from the 1.0 µg AgNP/ml level. Regarding phenotype, no differences in expression of CD40 (co-stimulatory molecule highly present in mature BMDC) or in CD273 (a marker for inhibitory T-cell response) were observed. The current results showed that the toxicity of this AgNP formulation was dose-related. The findings also suggest BMDC could maintain structural conservation of co-stimulatory/co-inhibitory surface molecules after 12 h of exposure to this AgNP. This work represents the first step in identifying the toxic effects of this AgNP formulation on dendritic cells.

Obesity is an excessive accumulation of fat that exacerbates the metabolic and inflammatory processes. Studies associate these processes with conditions and dysregulation in the intestinal tract, increased concentrations of lipopolysaccharides (LPSs) in the blood, differences in the abundance of intestinal microbiota, and the production of secondary metabolites such as short-chain fatty acids. β-Caryophyllene (BCP) is a natural sesquiterpene with anti-inflammatory properties and with the potential purpose of fighting metabolic diseases. A diet-induced obesity model was performed in 16-week-old C57BL/6 mice administered with BCP [50 mg/kg]. A reduction in the expression of Claudin-1 was observed in the group with a high-fat diet (HFD), which was caused by the administration of BCP; besides BCP, the phylaAkkermansia and Bacteroidetes decreased between the groups with a standard diet (STD) vs. HFD. Nevertheless, the use of BCP in the STD increased the expression of these phyla with respect to fatty acids; a similar effect was observed, in the HFD group that had a decreasing concentration that was restored with the use of BCP. The levels of endotoxemia and serum leptin increased in the HFD group, while in the HFD + BCP group, similar values were found to those of the STD group, attributing the ability to reduce these in conditions of obesity.

Resistin is an adipokine produced in adipose tissue with pro-inflammatory properties, whose elevation has been associated with insulin resistance and diabetes. Over the past years, significant research has explored the pathophysiological mechanisms involving resistin, utilizing various in vitro and in vivo models. Additionally, numerous clinical studies have aimed to establish a correlation between resistin and the development and progression of macrovascular and microvascular complications in type 2 diabetes. This narrative review summarizes in vitro, in vivo, and human studies published in English since the discovery of resistin in 2001 to the present, examining the role of this adipokine in the pathophysiology of macrovascular and microvascular complications in in vivo and in vitro T2D models, as well as the clinical evidence supporting its use as a biochemical marker in patients with these conditions. The results exhibit considerable heterogeneity and appear to be dependent on the experimental model or population studied. While experimental evidence supports resistin’s involvement at the cellular and molecular levels in the pathogenesis of these complications, current clinical evidence remains insufficient to justify its use as a biochemical marker for either diagnosis or prognosis. Therefore, further well-designed studies are required to elucidate resistin’s potential role in the clinical setting.

Silver nanoparticles (AgNPs) are widely studied in oncological nanomedicine, although concerns persist regarding their toxicity, elimination, and tissue accumulation. The biological properties of AgNPs depend on the synthesis method and the reducing agent used, which may influence cytotoxicity and cellular metabolism. This study aimed to evaluate the effect of the reducing agent on the cytotoxicity of AgNPs in leukemia (JURKAT) cell lines and peripheral blood mononuclear cells (PBMCs). AgNPs were synthesized via chemical reduction using glucose (GLU) or polyvinylpyrrolidone (PVP) as reducing agents. Nanoparticles were characterized by UV-Vis, FTIR, DLS, zeta potential, and TEM. Cell viability was assessed using trypan blue exclusion, and cytotoxicity was determined using the MTT assay. UV-Vis analysis showed distinct surface plasmon resonance profiles, and FTIR confirmed characteristic functional groups on the nanoparticle surface. DLS and zeta potential values indicated colloidal stability, with PVP-AgNPs presenting a more negative surface charge. TEM revealed greater size heterogeneity in GLU-AgNPs. GLU-AgNPs induced lower cytotoxicity and higher cell viability in JURKAT and PBMCs compared to PVP-AgNPs (p < 0.05). Leukemia cells were more susceptible to both nanoparticle types than PBMCs, showing a favorable selectivity index for GLU-AgNPs (SI = 2.44). These findings suggest that biocompatible reducing agents may improve the safety profile of AgNPs.

The utilization of food as a therapeutic measure for various ailments has been a prevalent practice throughout history and across different cultures. This is exemplified in societies where substances like Hibiscus sabdariffa have been employed to manage health conditions like hypertension and elevated blood glucose levels. The inherent bioactive compounds found in this plant, namely, delphinidin-3-sambubioside (DS3), quercetin (QRC), and hibiscus acid (HA), have been linked to various health benefits. Despite receiving individual attention, the specific molecular targets for these compounds remain unclear. In this study, computational analysis was conducted using bioinformatics tools such as Swiss Target Prediction, ShinnyGo 0.77, KEGG, and Stringdb to identify the molecular targets, pathways, and hub genes. Supplementary results were obtained through a thorough literature search in PubMed. DS3 analysis revealed potential genetic alterations related to the metabolism of nitrogen and glucose, inflammation, angiogenesis, and cell proliferation, particularly impacting the PI3K-AKT signaling pathway. QRC analysis demonstrated interconnected targets spanning multiple pathways, with some overlap with DS3 analysis and a particular focus on pathways related to cancer. HA analysis revealed distinct targets, especially those associated with pathways related to the nervous system. These findings emphasize the necessity for focused research on the molecular effects of DS3, QRC, and HA, thereby providing valuable insights into potential therapeutic pathways.

Gastric cancer (GC) remains a significant global health challenge, with high mortality rates, especially in developing countries. Current treatments are invasive and have considerable risks, necessitating the exploration of safer alternatives. Quercetin (QRC), a flavonoid present in various plants and foods, has demonstrated multiple health benefits, including anticancer properties. This study investigated the therapeutic potential of QRC in the treatment of GC. We utilized advanced molecular techniques to assess the impact of QRC on GC cells, examining its effects on cellular pathways and gene expression. Our findings indicate that QRC significantly inhibits GC cell proliferation and induces apoptosis, suggesting its potential as a safer therapeutic option for GC treatment. Further research is required to validate these results and explore the clinical applications of QRC in cancer therapy.