Alfredo Grilli

Inflammation plays a key role in various diseases such as pancreatitis, cancer, and rheumatoid arthritis. Acute inflammation involves processes like vasodilation, increased vascular permeability, and leukocyte accumulation, which lead to cellular damage due to reactive oxygen species (ROS). Low-frequency electromagnetic fields (ELF-EMFs) have shown potential in reducing oxidative stress and inflammation. This study assesses the effectiveness of a new wearable device containing graphene quantum dots in reducing inflammation and oxidative stress in Jurkat T cells stimulated by lipopolysaccharide (LPS). The device is evaluated for its impact on ROS production and inflammation. The results show that the device significantly lowers ROS levels and reduces the inflammatory response by decreasing pro-inflammatory cytokines such as IL-6, TNF-α, and IL-1β. Additionally, the device inhibits LPS-induced iNOS and COX-2 activity and modulates NF-κB signaling, indicating its potential as a therapeutic tool for managing inflammation and oxidative stress. These findings highlight the device’s ability to combat inflammation, offering a non-invasive and effective approach for inflammatory diseases.

In this study, a microbial–enzymatic strategy was pursued to address the challenge of degrading thermoplastic and thermosetting polymers. Environmental microorganisms were isolated, and their enzymatic activities were assessed using colorimetric assays to evaluate their potential for producing enzymes capable of degrading these polymers. Microorganisms demonstrating higher activity in the enzymatic assays were selected for a 30-day biodegradation experiment, in which epoxy resins, polyethylene terephthalate, or polystyrene served as the sole carbon source. The effectiveness of biodegradation was assessed through the ATR-FTIR analysis of the chemical composition and the SEM examination of surface characteristics before and after degradation. The results indicated that thermoplastic compounds were more susceptible to microbial degradation, exhibiting greater changes in absorbance. In particular, PET treated with Stenotrophomonas sp. showed the most significant efficacy, achieving a 60.18% reduction in the area under the curve with a standard error of ± 3.42 when analyzed by FTIR spectroscopy. Significant alterations in surface morphology were noticed in thermoplastic compounds. In contrast, thermosetting compounds demonstrated lower reactivity, as evidenced by the absence of band shifts in FTIR spectra and minor changes in bond absorbance and surface morphology.

Many recent studies have explored the healing properties of the extremely low-frequency electromagnetic field (ELF-EMF) to utilize electromagnetism for medical purposes. The non-invasiveness of electromagnetic induction makes it valuable for supportive therapy in various degenerative pathologies with increased oxidative stress. To date, no harmful effects have been reported or documented. We designed a small, wearable device which does not require a power source. The device consists of a substrate made of polyethylene terephthalate and an amalgam containing primarily graphene nanocrystals, also known as quantum dots. This device can transmit electromagnetic signals, which could induce biological effects. This study aims to verify the preliminary effects of the electromagnetic emission of the device on leukemic cells in culture. For this purpose, we studied the best-known effects of magnetic fields on biological models, such as cell viability, and the modulations on the main protagonists of cellular oxidative stress.

Several studies have already demonstrated the biocompatibility of a tooth as a grafting material in the regeneration of bone tissue, showing its osteoconductive potential, while no studies have verified whether the osteoinductive potential of a tooth remains constant or is altered after its treatment with the Tooth Transformer (TT) device. The aim of the study was to demonstrate that the treatment with the TT device did not alter the osteoinductivity of an extracted tooth that was stored dry. Twelve extracted human teeth were collected from real patients. Caries, tartar and filling materials were removed from each tooth; each tooth was coarsely cut and stored at room temperature (RT) until use. Each sample was shredded, demineralized and disinfected, using the TT device. Protein extraction was carried out for each sample, and Western Blot analysis was performed to test the presence of mineralization protein LIM-1 and transforming growth factor-β. The presence of the human Bone Morphogenetic Protein 2 (BMP-2) and human collagen Type I (COL-I) was found in dry tooth samples processed with the TT device and subjected to Enzyme-Linked Immunosorbent Assay (ELISA) testing. The treatment of chemical demineralization using the TT device does not alter the osteoinductive potential of a dry tooth.

Cholesterol accumulation in macrophages leads to the formation of foam cells and increases the risk of developing atherosclerosis. We have verified whether hydroxytyrosol (HT), a phenolic compound with anti-inflammatory and antioxidant properties, can reduce the cholesterol build up in THP-1 macrophage-derived foam cells. We have also investigated the potential mechanisms. Oil Red O staining and high-performance liquid chromatography (HPLC) assays were utilized to detect cellular lipid accumulation and cholesterol content, respectively, in THP-1 macrophages foam cells treated with HT. The impact of HT on cholesterol metabolism-related molecules (SR-A1, CD36, LOX-1, ABCA1, ABCG1, PPARγ and LRX-α) in foam cells was assessed using real-time PCR (RT-qPCR) and Western blot analyses. Finally, the effect of HT on the adhesion of THP-1 monocytes to human vascular endothelial cells (HUVEC) was analyzed to study endothelial activation. We found that HT activates the PPARγ/LXRα pathway to upregulate ABCA1 expression, reducing cholesterol accumulation in foam cells. Moreover, HT significantly inhibited monocyte adhesion and reduced the levels of adhesion factors (ICAM-1 and VCAM-1) and pro-inflammatory factors (IL-6 and TNF-α) in LPS-induced endothelial cells. Taken together, our findings suggest that HT, with its ability to interfere with the import and export of cholesterol, could represent a new therapeutic strategy for the treatment of atherosclerotic disease.

It is well known that soccer sport has the potential for high levels of stress and anxiety and that these are linked to Cortisol (C) variations. To date, much research has been devoted to understanding how Oxytocin (OT) can affect anxiety in response to a challenge. The aim of this study was to investigate, in 56 young male soccer players, the psychophysiological stress response 96 and 24 h before one soccer match of a tournament, in order to establish whether athletes who won or lost, show different levels of C and OT or expressions of competitive state anxiety subcomponents. We found that winners had significantly lower Cognitive anxiety and higher Self-confidence scores than losers. Also, significant differences between winners and losers in C and OT concentrations were observed, with higher OT levels in who has won and higher C levels in who has lost. Our results showed interesting associations between OT, C, anxiety feelings, and the outcome of competition.

The beneficial effects of exercise on the brain are well known. In general, exercise offers an effective way to improve cognitive function in all ages, particularly in the elderly, who are considered the most vulnerable to neurodegenerative disorders. In this regard, myokines, hormones secreted by muscle in response to exercise, have recently gained attention as beneficial mediators. Irisin is a novel exercise-induced myokine, that modulates several bodily processes, such as glucose homeostasis, and reduces systemic inflammation. Irisin is cleaved from fibronectin type III domain containing 5 (FNDC5), a transmembrane precursor protein expressed in muscle under the control of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α). The FNDC5/irisin system is also expressed in the hippocampus, where it stimulates the expression of the neurotrophin brain-derived neurotrophic factor in this area that is associated with learning and memory. In this review, we aimed to discuss the role of irisin as a key mediator of the beneficial effects of exercise on synaptic plasticity and memory in the elderly, suggesting its roles within the main promoters of the beneficial effects of exercise on the brain.

Matrix metalloproteinases (MMPs) play a crucial role in tumor angiogenesis, and metastasis. 4′-geranyloxyferulic acid (GOFA) has anti-tumor and anti-inflammatory proprieties. Herein, we aimed to determine whether this compound affects cell survival, invasion, and migration through reactive oxygen species (ROS)-mediated MMPs activation of extracellular signal-regulated kinases (ERKs) and p38 signaling in lymphocytic histiocytoma (U937) and colorectal cancer (HCT116) cells. We observed that lipopolysaccharide (LPS) stimulated U937 and HCT116 cells presented abnormal cell proliferation and increased metalloproteinase (MMP-9) activity and expression. Non-cytotoxic doses of GOFA blunted matrix invasive potential by reducing LPS-induced MMP-9 expression and cell migration via inhibiting ROS/ ERK pathway. GOFA also attenuated apoptosis and cell senescence. Our findings indicate that GOFA, inhibiting cancer cell proliferation and migration, could be therapeutically beneficial to prevent tumor metastasis.

The L-3,4-dihydroxyphenylalanine (LD) is the gold standard drug currently used to manage Parkinson’s disease (PD) and to control its symptoms. However, LD could cause disease neurotoxicity due to the generation of pro-oxidant intermediates deriving from its autoxidation. In order to overcome this limitation, we have conjugated LD to the natural antioxidant glutathione (GSH) to form a codrug (GSH-LD). Here we investigated the effect of GSH-LD on H₂O₂-induced cellular toxicity in undifferentiated and differentiated lymphoma U-937 and dopaminergic neuroblastoma SH-SY5Y cell lines, used respectively as models to study the involvement of macrophages/microglia and dopaminergic neurons in PD. We analyzed the effect of GSH-LD on apoptosis and cellular oxidative stress, both considered strategic targets for the prevention and treatment of neurodegenerative diseases. Compared to LD and GSH, GSH-LD had a stronger effect in preventing hydrogen peroxide (H₂O₂) induced apoptosis in both cell lines. Moreover, GSH-LD was able to preserve cell viability, cellular redox status, gluthation metabolism and prevent reactive oxygen species (ROS) formation, in a phosphinositide 3-kinase (PI3K)/kinase B (Akt)-dependent manner, in a neurotoxicity cellular model. Our findings indicate that the GSH-LD codrug offers advantages deriving from the additive effect of LD and GSH and it could represent a promising candidate for PD treatment.

Chenopodium quinoa Wild is a “pseudocereal” grain which attracts a lot of attention in the scientific community as it has a positive effect on health. Here, we investigate the presence of biologically active O-prenylated phenylpropanoids in the ethanol extract of commercially available quinoa seeds. We claim that 4′-Geranyloxyferulic acid (GOFA) was the only phytochemical product found that belongs to quinoa’s group secondary metabolites. We studied the changes in the oxidative and inflammatory status of the cellular environment in HCT 116 cell line processed with quinoa extract and its component GOFA; the implementation was done through the analysis of the antioxidant enzymes (SOD and CAT), the pro-inflammatory components (iNOS, IL-6 and TNF-α), and the products of intermediary metabolism (ONOO⁻, O₂⁻). Moreover, the l-arginine uptake was proposed as a target of the tested compounds. We demonstrated that the GOFA, through a decrease of the CAT-2B expression, leads to a reduction of the l-arginine uptake, downregulating the harmful iNOS and restoring the altered redox state. These results propose a new molecular target involved in the reduction of the critical inflammatory process responsible for the cancer progression.