Today, hydrogel dressings that can protect injury sites and effectively promote healing have become highly desirable in wound management. Therefore, multifunctional silver-poli(N-isopropylacrylamide/itaconic acid) (Ag-P(NiPAAm/IA)) hydrogel nanocomposites were developed for potential application as topical treatment dressings. The radiolytic method, used for the crosslinking of the polymer matrix as well as for the in situ incorporation of silver nanoparticles (AgNPs) into the polymer matrix, enables the preparation of hydrogel nanocomposites without introducing harmful and toxic agents. Moreover, materials produced using γ-irradiation are simultaneously sterilized, thus fulfilling one of the basic requirements regarding their potential biomedical applications. The NiPAAm/IA ratio and the presence of AgNPs influenced the microstructural parameters of the investigated systems. Increasing the IA content leads to the formation of a more porous polymer matrix with larger pores, while the incorporated AgNPs act as additional junction points, decreasing the porosity and pore size of the resulting nanocomposite hydrogels. Swelling studies showed that most investigated systems uptake the fluids from their surroundings by non-Fick diffusion. Further, the Ag⁺ ion release, antibacterial activity, and cytotoxicity of Ag-P(NiPAAm/IA) hydrogel nanocomposites were examined to evaluate their biomedical potential. All hydrogel nanocomposites showed an initial burst release of Ag⁺ ions (useful in preventing bacteria adherence and biofilm formation), followed by a slower release of the same (ensuring sterility for longer use). An antibacterial activity test against Escherichia coli and Staphylococcus aureus showed that Ag-P(NiPAAm/IA) hydrogel nanocomposites, with silver concentrations around 10 ± 1 ppm, successfully prevent bacterial growth. Finally, it was shown that the investigated hydrogel nanocomposites do not exhibit a cytotoxic effect on human keratinocyte HaCaT cells. Therefore, these multifunctional hydrogel nanocomposites may promote wound repair and show promising potential for application as functional wound dressing.

Aims: Glioblastomas are aggressive and usually incurable high grade gliomas without adequate treatment. In this study we aimed to investigate the potential of desloratadine to induce apoptosis/autophagy as genetically regulated processes that can seal cancer cell fates.Materials and methods: All experiments were performed on U251 human glioblastoma cell line and primary human glioblastoma cell culture. Cytotoxic effect of desloratadine was investigated using MTT and CV assays while oxidative stress, apoptosis and autophagy were detected by flow cytometry and immunoblot.Results: Desloratadine treatment decreased cell viability of U251 human glioblastoma cell line and primary human glioblastoma cell culture (IC50 value 50 µM) trough an increase of intracellular reactive oxygen species and caspase activity. Also, desloratadine decreased the expression of main autophagy repressor mTOR and its upstream activator Akt and increased the expression of AMPK. Conclusion: Desloratadine exerted dual cytotoxic effect inducing both, apoptosis and mTOR/AMPK dependent cytotoxic autophagy in glioblastoma cells and primary glioblastoma cell culture

Metamizole is a pyrazolone-derived drug with analgesic, antipyretic and spasmolytic activity. The available literature data on metamizole effects on tumor cell lines is limited. Modulation of oxidative stress is considered to be an important mechanism through which different drugs may influence tumor cell survival. Objective of this study was to evaluate the effect of metamizole on viability and oxidative stress levels in the C6 rat glioma cell line. C6 cells were treated with metamizole and N-acetylcysteine (NAC) for 24h and 48h. Cell viability was determined using crystal violet and MTT assays. Viability of C6 cells was also determined after combined treatment with metamizole and NAC. Combined treatment doses were determined based on IC ₅₀ values. To assess oxidative stress, levels of malondialdehyde and reduced glutathione were measured in cell culture media. Our results showed that metamizole reduced C6 cell viability in a dose- and time-dependent manner, especially after 48h, with significant reduction of viability, even at lower concentrations. The reduced cell viability and pro-oxidative effects were mainly observed at high metamizole concentrations - 40μg/mL and 80μg/mL. NAC alone, in low concentrations, did not significantly impair cell viability and had slightly improved antioxidant status. In combined treatments, 1mM NAC was partially able to counteract metamizole-induced cell death of C6 cells. Therefore, we can conclude that metamizole reduces viability of the C6 cell line, especially after long-term exposure with significant changes of malondialdehyde and glutathione levels, influencing the C6 cell viability at least partially via oxidative stress.