Multiple Sclerosis (MS) is a chronic inflammatory disease that affects the brain and spinal cord. Inflammation, demyelination, synaptic alteration, and neuronal loss are hallmarks detectable in MS. Experimental autoimmune encephalomyelitis (EAE) is an animal model widely used to study pathogenic aspects of MS. Autophagy is a process that maintains cell homeostasis by removing abnormal organelles and damaged proteins and is involved both in protective and detrimental effects that have been seen in a variety of human diseases, such as cancer, neurodegenerative diseases, inflammation, and metabolic disorders. This study is aimed at investigating the autophagy signaling pathway through the analysis of the main autophagic proteins including Beclin-1, microtubule-associated protein light chain (LC3, autophagosome marker), and p62 also called sequestosome1 (SQSTM1, substrate of autophagy-mediated degradation) in the hippocampus of EAE-affected mice. The expression levels of Beclin-1, LC3, and p62 and the Akt/mTOR pathway were examined by Western blot experiments. In EAE mice, compared to control animals, significant reductions of expression levels were detectable for Beclin-1 and LC3 II (indicating the reduction of autophagosomes), and p62 (suggesting that autophagic flux increased). In parallel, molecular analysis detected the deregulation of the Akt/mTOR signaling. Immunofluorescence double-labeling images showed co-localization of NeuN (neuronal nuclear marker) and Beclin-1, LC3, and p62 throughout the CA1 and CA3 hippocampal subfields. Taken together, these data demonstrate that activation of autophagy occurs in the neurons of the hippocampus in this experimental model.

In the field of regenerative medicine, acrylated epoxidized vegetable oils are emerging as a promising avenue of exploration. The aim of this study is to evaluate the degradability of two formulations of acrylated epoxidized soybean oil (AESO): pure AESO and AESO diluted with soybean oil (SO) for potential bioprintability applications. The comprehensive investigation of these two polymeric formulations included optimization of polymerization conditions, confirmation of cytocompatibility, and, most importantly, the study of their degradability. The results reveal that AESO, used as a biomaterial for biomedical applications, undergoes a distinctive degradation process, combining both enzymatic and oxidative degradation (AESO/SO samples lose 29.45% of their weight after 60 days). This phenomenon is the result of a complex interplay of factors, including the chemical composition and physical characteristics of the polymer, the unique tissue environment in which it is implanted, and the duration of implantation.

The development of reusable and biocompatible biomaterial-based culture substrates is increasingly relevant for improving sustainability in biomedical research workflows. In this study, polyethylene terephthalate glycol-modified (PETG) was evaluated as a potential alternative to conventional polystyrene (PS) for in vitro cell culture applications. PETG substrates were fabricated through laser cutting and tested for their ability to support cell adhesion, viability, proliferation, and lineage-specific differentiation across multiple human cell models, including calvarial mesenchymal stromal cells (CMSCs), bone marrow-derived mesenchymal stromal cells (hBM-MSCs), dermal fibroblasts, LHCN-M2 myoblasts, and SH-SY5Y neuroblastoma cells. Morphological and immunofluorescence analyses demonstrated that PETG supported cell attachment and focal adhesion formation, comparable to standard PS surfaces. Cell viability and proliferation assays confirmed metabolic activity and growth over time. Furthermore, PETG substrates supported osteogenic, adipogenic, myogenic, and neuronal differentiation, as demonstrated by histological staining, myotube formation, neurite outgrowth, and lineage-specific gene expression analyses. Finally, PETG maintained CMSC morphology and metabolic activity after repeated recovery, ethanol/UV treatment, and gelatin re-coating, with comparable results between new substrates and those reused for up to three cycles. These findings support PETG as a biocompatible culture substrate with preliminary short-term reuse potential and possible sustainability benefits for laboratory workflows.

Endothelial VEGFR-2 plays a central role in vascular remodeling during intestinal inflammation, yet its activation during the early stages of colitis remains poorly characterized. Because Akt is a major downstream effector of VEGFR-2 signaling and a key mediator of endothelial responses, we investigated whether VEGFR-2 phosphorylation and Akt activation occur during the early phase of TNBS-induced colitis before the development of extensive mucosal injury. Acute colitis was induced in adult female Wistar rats by intracolonic administration of TNBS. Colonic tissues were collected on days 2, 4, and 6 after induction. Histological analyses and macrophage (CD68⁺ cells) infiltration were performed to characterize disease progression. VEGFR-2 expression and phosphorylation at Tyr1175 were evaluated on day 4 by Western blot, immunoprecipitation, and immunofluorescence. Akt activation was also assessed. TNBS-induced colitis is characterized by histological injury and increased CD68⁺ macrophage infiltration on day 4, with severe tissue damage observed on day 6. On day 4, colitis is associated with increased endothelial VEGFR-2 expression, enhanced VEGFR-2 phosphorylation at Tyr1175, and Akt activation. Early TNBS-induced colitis is associated with endothelial VEGFR-2 phosphorylation and Akt activation before the onset of extensive mucosal destruction on day 6. These findings support activation of the VEGFR-2/Akt signaling axis as an early vascular response during intestinal inflammation and suggest its potential contribution to disease progression.