Capecitabine is recommended as one of the first-line chemotherapy treatments for advanced or metastatic colorectal cancer. Researches have been conducted on capecitabine’s impact on the viability of human colon cancer cells and its potential to induce apoptosis. However, even in cases initially responsive to treatment, the development of acquired resistance significantly limits its efficacy. Challenges still exist in effectively treating patients with chemotherapy, and developing new cytotoxic drugs is hindered by drug resistance. Fisetin alters the cell cycle, inducing apoptosis, inhibiting cancer cell proliferation, and enhancing the therapeutic effectiveness of chemotherapy drugs. This work aims to create a plan for reversing capecitabine resistance. For this purpose, the role of capecitabine and/or fisetin combinations in cell proliferation and apoptosis has been determined in both wild-type and capecitabine-resistant HT29 cells (CR/HT29). We developed capecitabine-resistant cell line from wild-type HT29 cells. This study demonstrated the effects of capecitabine, fisetin, and their combinations on both resistant and wild-type cells through experiments including cell survival skills, cell proliferation, wound healing, colony formation, hoechst staining, and western blot analysis. We established capecitabine-resistant cell lines. P-gp expression increased in CR/HT29 cells. Capecitabine effects on a CR/HT29 cells less than wild-type HT29 cells. The combination of fisetin and capecitabine in cell proliferation caused greater reductions in wild-type HT29 cells than in capecitabine-resistant cells. Fisetin has also additive effects on the apoptotic pathway in CR/HT29 cells. This study provides new perspectives on the combination of capecitabine and/or flavonoid treatment in resistant cells. Graphical abstract

In this study, we created multifunctional bone tissue engineering scaffolds that combine prophylactic antifungal action with structural support. We produced PVA/CS/HA/BA nanofiber matrices via a specifically designed electrospinning technique to stop early cross-linking. Through SEM, our examination of fiber shape revealed diameters ranging from 178 ± 53 nm to 330 ± 69 nm. We discovered that this variation was closely correlated with the Boric Acid (BA) level. Our EDS and FTIR studies further showed that HA and BA were effectively mixed, with a specific focus on the production of borate-ester linkages inside the network. Mechanical examination revealed that 0.25 wt.% BA maximizes the tensile strength at 9.15 MPa, thereby closely matching HA-reinforced standards, while HA incorporation improved thermal stability. Moreover, in vitro hFOB experiments showed sustained cytocompatibility at 0.25 wt.% BA. While 0.5 wt.% BA showed strong antifungal action against Candida albicans, it sadly harmed cell viability. The 0.25 wt.% BA concentration ultimately offers a better balance between mechanical integrity and antibacterial action, therefore presenting a potential method for scaffold generation for bone regeneration in immunocompromised patients.

Encapsulating antiepileptic drugs (AEDs), including ethosuximide (Etho), into nanoparticles shows promise in treating epilepsy. Nanomedicine may be the most significant contributor to addressing this issue. It presents several advantages compared to traditional drug delivery methods and is currently a prominent area of focus in cancer research. Incorporating Etho into bismuth ferrite (BFO) nanoparticles within diverse controlled drug delivery systems is explored to enhance drug efficacy. This approach is primarily desired to aid in targeted drug delivery to the brain’s deepest regions while limiting transplacental permeability, reducing fetal exposure, and mitigating associated adverse effects. In this investigation, we explored Etho, an antiepileptic drug commonly employed for treating absence seizures, as the active ingredient in BFO nanoparticles at varying concentrations (10 and 15 mg). Characterization of the drug-containing BFO nanoparticles involved scanning electron microscopy (SEM) and elemental analysis. The thermal properties of the drug-containing BFO nanoparticles were evaluated via differential scanning calorimetry (DSC) analysis. Cytotoxicity evaluations using the MTT assay were conducted on all nanoparticles, and human neuroblastoma cell line cultures (SH-SY5Y) were treated with each particle over multiple time intervals. Cell viability remained at 135% after 7 days when exposed to 15 mg of Etho in BFO nanoparticles. Additionally, in vitro drug release kinetics for Etho revealed sustained release lasting up to 5 hours with a drug concentration of 15 mg.

Melanoma excision procedures frequently result in complex wounds that require simultaneous tumor suppression and tissue regeneration. However, current post-surgical care heavily relies on synthetic drugs, facing challenges like antibiotic resistance and delayed healing. To address this notable gap, this study introduces a novel “mineral-botanical” hybrid nanofibrous dressing to reduce reliance on conventional synthetic agents. The nanofiber surfaces were subsequently functionalized with a supercritical CO₂ extract of Inula helenium, thereby introducing a highly bioactive botanical agent not previously explored in this hybrid wound-care context. Comprehensive physical and structural characterizations demonstrated that the bioactive coating serves as a resilient physical barrier, significantly enhancing the dressing’s structural integrity in fluidic environments. In vitro biological evaluations revealed a dual-action mechanism: the biomaterial exhibited excellent biocompatibility and accelerated migration in human dermal fibroblasts (HDFs), achieving nearly 100% in vitro wound closure at 24 h. Conversely, the Inula helenium-coated nanofibers demonstrated distinct, selective cytotoxicity against A375 melanoma cells, effectively restricting their proliferation and reducing their viability. Furthermore, the hybrid platform exhibited significant antioxidant potential and achieved 94% antibacterial inhibition against Staphylococcus aureus. In conclusion, this study presents a sustainable, dual-function wound dressing that suppresses residual cancer cells while promoting healthy tissue regeneration, offering a promising alternative to conventional synthetic oncological dressings.

Background: Allium sativum (Garlic), is one of the oldest cultivated plants in the Liliaceae family. It has been used as a medicine for thousands of years. Garlic is one of the most important ampoule vegetables used as a spice and flavoring agent for food. White and black garlic contain a variety of beneficial minerals, vitamins and many other substances used for human health. In addition to vitamins, it contains sugar, protein, fat, calcium, potassium, phosphorus and sulfur. It is also used to treat a wide range of diseases including blood pressure and cholesterol, cancer, anti-inflammatory, antioxidant, fungal and wound healing, asthma, arthritis, chronic fever, tuberculosis, rhinitis, malaria, severe skin diseases, digestive disorders, diabetes, kidney stones, anemia, jaundice, epilepsy, cataract, and night blindness. The aim was to investigate the effects of garlic extract on irradiated colon cancer, neuroblastoma cancer cells and fibroblasts. Material and methods: In the study, colon, brain cancer, and fibroblast cells were replicated in a culture environment and treated for 24 hours with white garlic and fermented black garlic extracts. Cell viability was determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) test. All results were statistically analyzed with GraphPad Prism (Version 8.0.3). Results: According to the results, the determined doses of garlics were treated with 24-hour garlic doses, after which the cells were first given 2 Gray radiation doses for combined radiation therapy. The MTT test determined cell vitality and evaluated the results through statistical analysis. Conclusion: According to our study, we have concluded that white garlic has a protective effect on radiation damage, while black garlic increases cancer cell death.