This study investigates the fabrication and characterization of polymeric nanoparticles based on polyhydroxyalkanoates (PHAs) loaded with curcumin for biomedical applications. PHAs, biodegradable and biocompatible polymers, were synthesized via bacterial fermentation and used to encapsulate curcumin using the nanoprecipitation method. The resulting nanoparticles were characterized for their particle size, polydispersity index, and encapsulation efficiency, achieving high entrapment rates (above 80%) and nanometric size distribution. Stability assessments demonstrated prolonged structural integrity under storage conditions. In vitro release studies conducted in phosphate-buffered saline at pH 5 and 7.4 revealed sustained drug release profiles. Biocompatibility and cytotoxicity assays using human astrocytes and fibroblasts confirmed the nanoparticles’ safety, while antiproliferative tests on glioblastoma and colon cancer cell lines indicated potential therapeutic efficacy. Additionally, skin irritation and corrosion tests using the EpiDerm™ model classified the formulations as non-irritant and non-corrosive. These findings suggest that PHA-based nanoparticles offer a promising nanocarrier system for curcumin delivery, with potential applications in cancer treatment and regenerative medicine. Future research should focus on optimizing the formulation and evaluating in vivo therapeutic effects.

Background: Cervical cancer is among the highest-ranking types of cancer worldwide, with human papillomavirus (HPV) as the agent driving the malignant process. One aspect of the infection’s evolution is given by epigenetic modifications, mainly DNA methylation and chromatin alteration. These processes are guided by several chromatin remodeling complexes, including NuRD. The purpose of this study was to evaluate the genome-wide binding patterns of the NuRD complex components (MBD2 and MBD3) in the presence of active HPV16 E6 and E7 oncogenes and to determine the potential of identified genes through an experimental model to differentiate between cervical precursor lesions, with the aim of establishing their utility as biomarkers. Methods: The experimental model was built using the CaSki cell line and shRNA for E6 and E7 HPV16 silencing, ChIP-seq, qRT-PCR, and Western blot analyses. Selected genes’ expression was also assessed in patients. Results: Several genes have been identified to exhibit altered transcriptional activity due to the influence of HPV16 E6/E7 viral oncogenes acting through the MBD2/MBD3 NuRD complex, linking them to viral infection and cervical oncogenesis. Conclusions: The impacted genes primarily play roles in governing gene transcription, mRNA processing, and regulation of translation. Understanding these mechanisms offers valuable insights into the process of HPV-induced oncogenesis.

Background/Objectives: Glioblastoma is the most common malignant primary brain tumor, characterized by necrosis, uncontrolled proliferation, infiltration, angiogenesis, apoptosis resistance, and genomic instability. Epigenetic modifiers hold promise as adjuvant therapies for gliomas, with synergistic combinations being explored to enhance efficacy and reduce toxicity. This study aimed to evaluate the effects of single or combined treatments with various anticancer drugs (Carboplatin, Paclitaxel, Avastin), natural compounds (Quercetin), and epigenetic modulators (suberoylanilide hydroxamic acid and 5-Azacytidine) on the expression of some long noncoding RNAs and methylation drivers or some functional features in the U87-MG cell line. Methods: Treated and untreated U87-MG cells were used for the evaluation of drug-induced cytotoxicity, apoptotic events, and distribution in cell cycle phases, detection of cytokine release, and assessment of gene expression and global methylation. Results: Cytotoxicity assays led to the selection of drug concentrations to be used in further experiments. Expression analysis revealed distinct downregulation of nearly all investigated genes and long noncoding RNAs following treatments. All treatments resulted in a higher percentage of global methylation compared to untreated controls. All treatments effectively increased levels of apoptosis, while the epigenetic modulators exhibited a lower proliferation profile, with combined treatments showing elevated values of cell lysis. Conclusions: The results indicate a link between Carboplatin and Avastin treatments and DNA methylation mechanisms involving EZH2, DNMT3A, and DNMT3B, with Avastin’s direct impact on these enzymes warranting further study. This research underscores the promise of platinum-based therapies combined with epigenetic drugs to reactivate silenced tumor suppressor genes and optimize methylation profiles.

This study explores an innovative delivery strategy for the management of skin conditions: lipid nanosystems incorporated into a gel matrix. Echinacea purpurea extract, known for its antibacterial, antioxidant, and wound-healing properties, was encapsulated into lipid-based nanosystems and subsequently incorporated into a Carbopol-based gel. The extract, rich in chicoric and caftaric acids, exhibited strong antioxidant activity (IC50 = 56.89 µg/mL). The resulting nanosystems showed nanometric size (about 200 nm), high entrapment efficiency (63.10% –75.15%), and excellent short-term stability. Superior biocompatibility of the nanosystems, compared to the free extract, was demonstrated using an MTS assay on L-929 fibroblasts. Moreover, the cytoprotective potential of the lipid carriers was evident, as pre-treatment significantly increased cell viability under H2O2-induced oxidative stress. These findings suggest that lipid-based encapsulation enhances the therapeutic profile of Echinacea purpurea. The optimal lipid formulation was incorporated into a Carbopol-based gel, which demonstrated an appropriate pH (5.15 ± 0.75), favorable textural properties, sustained polyphenol release, and overall good stability. This research highlights the potential of plant-derived bioactives in the development of dermatocosmetic products, aligning with current trends in eco-conscious and sustainable skincare.

This study explores an innovative delivery strategy for the management of skin conditions: lipid nanosystems incorporated into a gel matrix. Echinacea purpurea extract, known for its antibacterial, antioxidant, and wound-healing properties, was encapsulated into lipid-based nanosystems and subsequently incorporated into Carbopol-based gel. The extract, rich in chicoric and caftaric acids, exhibited strong antioxidant activity (IC₅₀ = 56.9 µg/mL). The resulting nanosystems showed nanometric size (about 200 nm), high entrapment efficiency (63.10–75.15%), and excellent short-term stability. Superior biocompatibility of the nanosystems, compared to the free extract, was demonstrated using an MTS assay on L-929 fibroblasts. Moreover, the cytoprotective potential of the lipid carriers was evident, as pre-treatment significantly increased cell viability under H₂O₂-induced oxidative stress. These findings suggest that lipid-based encapsulation enhances the therapeutic profile of E. purpurea. The optimal lipid formulation was incorporated into a Carbopol-based gel, which demonstrated an appropriate pH (5.15 ± 0.75), favorable textural properties, sustained polyphenol release, and overall good stability. This research highlights the potential of plant-derived bioactives in the development of dermatocosmetic products, aligning with current trends in eco-conscious and sustainable skincare.

Thyroid carcinomas are phenotypically heterogeneous malignancies. Advances in molecular and cellular technologies have revealed genetic, epigenetic, and nongenetic factors underlying this heterogeneity. Our study aimed to assess the impact of single and combined treatments with anticancer agents (Carboplatin, Doxorubicin, Paclitaxel, Avastin), natural compounds (Quercetin), and epigenetic modulators (suberoylanilide hydroxamic acid and 5-Azacytidine) on the expression of long noncoding RNAs, methylation regulators, and functional features in the human thyroid cancer cell line K1. Methods: Treated and untreated K1 cells were used throughout experiments to evaluate the drug-induced cytotoxicity, apoptosis, cell cycle distribution, cytokine release, gene expression, and global DNA methylation levels. Results: Some single- and combined-drug treatments modulated both cell cycle progression and apoptotic events, demonstrating anti-tumor activity of the tested compounds. Gene expression analysis showed treatment-specific regulation of target genes and lncRNAs, including both upregulation and downregulation across different drug combinations. All treatments resulted in increased global DNA methylation levels compared to the untreated controls. Several combinations significantly upregulated DNMT1 and DNMT3B, while concomitantly decreased EZH2 levels. Conclusions: These coordinated epigenetic changes highlight the therapeutic potential of combining epigenetic modulators with chemotherapeutic agents, suggesting a strategy to prevent or reverse treatment resistance and improve outcomes in thyroid cancer patients.