Background: Oxidative stress plays a significant role in the progression of periodontal diseases. Hexagonal boron nitride (hBN) nanoparticles have antimicrobial, antiplaque, and antioxidant properties. The aim of this study to evaluate the protective and therapeutic effects of hBN against oxidative stress induced by hydrogen peroxide (H₂O₂) in human gingival fibroblast (HGF) cells. Methods: In this study, a primary cell line of HGFs was used. Oxidative stress was induced by treating the cells with 800 µM H₂O₂. hBN was applied at concentrations of 0.001, 0.005, and 0.01 mg/mL, either 2 h prior to or 2 h following H₂O₂ exposure. Cells were incubated for 24 h post-treatment. Cell viability was assessed using the 2,3-bis-[2-methoxy-4-nitro-5-sulfophenyl]-2 H-tetrazolium-5-carboxyanilide salt (XTT) assay. Additionally, the total oxidant status (TOS) was measured before and after oxidative damage at the 0.01 mg/mL hBN concentration. Results: hBN did not negatively affect cell viability in HGF cells at any concentration. The application of hBN to HGF cells before and after oxidative damage resulted in statistically significant (P < 0.001), albeit modest improvements in cell viability (2-5.5% and 3-6.5%, respectively). No significant differences were observed in TOS (P = 0.234), indicating that the cytoprotective effects were not mediated via alterations in TOS. Conclusions: Within the limitations of this in vitro study, hBN was found to enhance cell viability under H₂O₂-induced oxidative stress in HGF cells. These findings suggest a potential role for hBN in modulating antioxidant responses and supporting periodontal healing processes. However, their clinical relevance remains uncertain. Therefore, further mechanistic studies and clinical investigations are required to validate the potential adjunctive role of hBN in the prevention and treatment of periodontal diseases.

Objectives: Gold nanoparticles are very popular metallic nanomaterials and they have a wide spectrum of biomedical applications. This study was aimed to the production of stable and monodisperse polyethyleneimine (PEI) and polyethylene glycol (PEG) coated gold nanoparticles (AuNP20 and AuNP50), investigation of their in vivo biochemical effects in the BALB/c mice. Methods: Gold nanoparticles were synthesized and their surfaces were modified by PEI and PEG. All the necessary physicochemical characterizations were performed. After the single high dose i.v. injection (5 mg Au/kg animal weight) of the AuNP groups, their in vivo biochemical effects were evaluated multiparametrically in the mice on day 14. Results: Highly monodisperse and stable AuNPs were synthesized successfully. Significant changes in the biochemical hemogram parameters were observed depending on the surface coatings of the AuNPs. PEI and PEG surface coatings increased biocompatibility. No excessive oxidative stress response was observed in all the gold nanoparticle groups. Conclusions: It has been concluded that the surface chemistry of the particles is a more decisive parameter than the size in terms of in vivo biochemical toxicity. The surface functionalization, stability and biocompatibility of the AuNPs are important parameters for the potential biomedical applications of gold nanoparticles in future studies.

Aim: The anti-cancer mechanisms of quercetin have been elucidated in several studies. These mechanisms are controlled by different signalling pathways within the cancer cell. This study examined the lethal effects of commercially available quercetin extracts at different doses on cancer cell lines. Methods: In our study, we used 3 different commercially available supplements and looked at how well they worked against breast cancer. In our study, the presence of cell death was determined by first performing the MTT assay on the 4t1 breast cancer cell line. Additionally, cell mode was applied by staining quercetin extracts in the same commercial forms with Bax antibody to determine death mode at the same doses. Results: The analysis showed that although the highest dose of quercetin (500 µM) induced apoptotic processes in cancer cells, no death was observed at the lower dose in two different supplements. Conclusions: Our study results indicate that quercetin selectively inhibits cancer cell proliferation and likely induces apoptosis, making it a promising candidate for cancer therapy with potentially fewer side effects. We believe that further clinical and experimental studies are needed to elucidate its mechanisms and optimize its therapeutic application.

Objective: This study aimed to establish a reliable protocol for obtaining healthy and long-lived cortical neurons from newborn mice, providing a valuable model for studying neuronal function. Materials and Methods: Cortical regions of P0 mice were isolated and healthy neurons were obtained by enzymatic and mechanical dissociation. On the seventh day of incubation, the presence of neurons was detected by staining with neuron-specific antibodies. Transgenic mice expressing fluorescent proteins specific to neurons, glia and oligodendrocytes were also used for culture. Results: Almost all the neurons had adhered to the petri dish bottom by the second hour of incubation. Most of the neurons were healthy and started to grow extension quickly. Conclusion: Neuron cultures are an important tool in research and are invaluable for studying the behaviour of cells. Nanoparticles facilitate genetic manipulation of these cultures for various biotechnological applications. In particular, they have great potential in areas such as the delivery of genetic material into cells, drug delivery and targeted treatment methods. Such techniques have the potential to open up new avenues for the study and treatment of neurological diseases.

The axolotl ( Ambystoma mexicanum ), a neotenic salamander with remarkable regenerative capabilities, serves as a key model for studying nervous system regeneration. Despite its potential, the cellular and molecular mechanisms underlying this regenerative capacity remain poorly understood, partly due to the lack of reliable in vitro models for axolotl neural cells. In this study, we developed a novel protocol for primary cultures of adult axolotl telencephalon/pallium, enabling the maintenance of viable and functionally active neural cells. Using calcium imaging and immunocytochemistry, we demonstrated the presence of neuronal and glial markers, synaptic connections, and spontaneous calcium activity, highlighting the functional integrity of the cultured cells. Our findings reveal that these cultures can be maintained in both serum and serum-free conditions, with neurons exhibiting robust neurite outgrowth and responsiveness to injury. This protocol addresses a critical gap in axolotl research by providing a controlled in vitro system to study neurogenesis and regeneration. By offering insights into the regenerative mechanisms of axolotl neurons, this work lays the foundation for comparative studies with mammalian systems, potentially informing therapeutic strategies for neurodegenerative diseases and CNS injuries in humans.

Background: Preliminary evidence suggests that astrocytes might contribute to the disease mechanisms of N‐methyl‐D‐aspartate receptor (NMDAR) encephalitis. However, the precise role of astrocytes in the pathogenesis of encephalitis is poorly understood. Methods: To characterize the impact of NMDAR antibodies on the activity of astrocytes, we isolated and purified serum IgG from three patients with NMDAR encephalitis and three healthy controls. Primary cultured mouse astrocytes and neuron–astrocyte cocultures were incubated with 5 μ g patient or control IgG for 12 and 24 h. Cell viability and astrocyte activity were assessed by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl tetrazolium bromide (MTT) and calcium (Ca ²⁺ ) imaging studies (using a vector expressing a genetically encoded indicator under the GFAP promoter), respectively. Supernatant levels of TNF‐ α , a mediator of astrocyte–neuron interactions, were measured by ELISA. Results: Purified serum IgG from N‐methyl‐D‐aspartate receptor‐antibody positive patients (NMDAR‐Ab+ IgG) and healthy controls did not alter the viability of isolated astrocytes and cocultures. NMDAR‐Ab+ IgG suppressed the duration and amplitude of Ca ²⁺ activity of isolated astrocytes at 12 and/or 24 h, whereas all parameters of Ca ²⁺ activity were enhanced by NMDAR‐Ab+ IgG in astrocyte–neuron cocultures at 12 h. TNF‐ α levels were increased in supernatants of NMDAR‐Ab+ IgG–administered astrocyte–neuron cocultures but not isolated astrocytes. Discussion: This study provides the first preliminary evidence on the impact of patient‐derived NMDAR‐Ab+ IgG on astrocytic activity. Our results imply that the interaction of NMDAR‐Abs with neurons and astrocytes creates a positive feedback loop reinforcing the activation of astrocytes. TNF‐ α might be one of the perpetrators of this loop.