Search Results (11,584)

Background/Objectives: Obesity increases reactive oxygen species (ROS), thereby triggering oxidative stress. Coriander seeds contain polyphenolic compounds that act as natural antioxidants to reduce oxidative stress. Coriander seed ethanolic extract has been proven to decrease malondialdehyde and increase catalase activity in the liver of high-fat-diet-fed rats. Thus, coriander seeds are thought to protect against obesity-induced oxidative liver damage; however, their molecular mechanism has not been revealed. Nuclear factor erythroid 2-related factor 2 (Nrf2) and Forkhead Box O3 (FOXO3) are transcription factors involved in cellular antioxidant regulation (e.g., superoxide dismutase/SOD, glutathione peroxidase/GPx expression, and reduced glutathione/GSH) that are negatively regulated by Kelch-like ECH-associated Protein 1 (Keap1) and 14-3-3 protein to maintain cellular homeostasis. This study aimed to analyze the regulation of antioxidant expression through in silico and in vivo experiments. Methods: The in silico study assessed the potential of coriander seed ethanolic extract to inhibit Keap1 and 14-3-3 using molecular docking. Then, the drug-likeness, pharmacokinetics, and toxicity of the top three compounds were analyzed. Meanwhile, the in vivo study investigated how the coriander seed ethanolic extract impacted the level of Nrf2, FOXO3, and their downstream effectors (T-SOD, MnSOD, GPx, and GSH). The in vivo study involved five groups of rats with obesity induced by a high-fat diet that were fed with 100 mg/kgBW coriander seed ethanolic extract for 12 weeks. Results: The in silico tests revealed that shionoside b had the highest potential to inhibit Keap1 (ΔG = −8.90 kcal/mol; Ki = 298.01 nM) and 14-3-3 protein (ΔG = −6.85 kcal/mol; Ki = 9.46 µM). The in vivo tests showed that the Nrf2, FOXO3, MnSOD, and GPx mRNA expression was significantly different between the groups (p < 0.05). Meanwhile, T-SOD, MnSOD, GPx, and GSH activity were not significantly different between the groups (p > 0.05). Nrf2 was significantly correlated with FOXO3 as well as the T-SOD, MnSOD, and GPx activity, and FOXO3 was significantly correlated with the T-SOD, MnSOD, GPx, and GSH activity. Conclusions: In obese rats, coriander seeds tend to increase Nrf2 and FOXO3 expression, which is positively correlated with their downstream enzymatic and nonenzymatic antioxidant activity. This is possibly due to the interaction between the coriander seed phytoconstituents and protein inhibitors (Keap1 and 14-3-3), which contribute to the stability and nuclear mobilization of Nrf2 and FOXO3. Full article

In 3.5 wt% NaCl solution used to simulate seawater, the individual (self-corrosion) and coupled (galvanic) corrosion behaviors of TA22 titanium alloy and 304 stainless steel were systematically investigated at 25 °C, 35 °C, 45 °C and 55 °C. Post-corrosion surfaces were characterized by scanning electron microscopy (SEM), three-dimensional profilometry and X-ray photoelectron spectroscopy (XPS). The results demonstrated that elevating temperature decreased the compactness and protective quality of the passive film on both alloys, as indicated by increasing donor densities and positive shifts in flat-band potentials. Distinct pitting corrosion occurred on 304 SS above 45 °C. Upon galvanic coupling, the passive film on TA22 was modified in both structure and composition, exhibiting a decreased TiO₂ content and increased lower valence oxides (Ti₂O₃, TiO). The galvanic effect intensified with temperature, leading to progressively aggravated corrosion of 304 SS, characterized by increased pit density, diameter, and depth compared to its self-corrosion state. Full article

Cryopreservation and transplantation of intact ovaries offer a promising approach to fertility restoration in cancer patients. However, ischemia–reperfusion injury following transplantation significantly impairs graft function. This study aimed to evaluate the protective effects of melatonin and elucidate its underlying mechanisms of action, including antioxidant and anti-inflammatory properties. Intact ovaries from 8 to 12-week-old LEWIS rats were cryopreserved and subsequently transplanted. Melatonin (25 mg/kg and 50 mg/kg) was administered daily from day 1 to day 4 postoperatively. Estrous cycle recovery and ovarian histology were examined, along with measurements of hormone concentrations, antioxidant activity, and inflammatory mediators. The oxidative stress response, particularly the nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response elements (ARE) signaling pathway—including Nrf2, Kelch-like ECH-associated protein 1 (Keap1), and sMafg—was investigated to elucidate melatonin’s protective mechanisms. The roles of melatonin receptors and Nrf2 were investigated using specific receptor antagonists (Luzindole, 4P-PDOT) and an inhibitor (ML385) to confirm the involvement of the MT1/Nrf2/ARE pathway. As a result, rats treated with high-dose melatonin (50 mg/kg) exhibited accelerated estrous cycle recovery, reduced follicular loss, improved serum hormone levels, enhanced antioxidant capacity in serum and ovarian tissue, and decreased levels of inflammatory cytokines. Furthermore, melatonin exerted its antioxidant and anti-inflammatory effects through activation of the Nrf2/ARE signaling pathway via the MT1 receptor. These protective effects were abolished by the inhibition of either Nrf2 or MT1 receptor. In conclusion, these findings demonstrate that melatonin mitigates oxidative stress and inflammatory damage in intact transplanted ovaries through the MT1/Nrf2/ARE signaling axis, thereby preserving ovarian function post-transplantation. Full article

Background: In this study, hydroponic experiments were conducted to examine the roles of sulphur (S), calcium (Ca), and nitric oxide (NO) in alleviating salt stress (20 mM NaCl) in tomato (Solanum lycopersicum L.) seedlings. Methods: Analyses included Na⁺/K⁺ contents, inorganic nitrogen (nitrate, nitrite, ammonium), nitrogen- and ammonium-assimilating enzymes (NR, NiR, GS, GOGAT), sulphur-assimilating enzymes (ATPS, OASTL), protein content, ROS (O₂^∙−, H₂O₂), and in vivo NO visualization were conducted. Results: We observed that salt stress increased Na⁺, reduced K⁺, disrupted nitrogen and sulphur metabolism, elevated ROS, and decreased NO, causing oxidative stress and reduced enzymatic activity. Supplementation with potassium sulphate (40 µM), calcium chloride (30 µM), and sodium nitroprusside (SNP; 40 µM) mitigated these effects, enhancing enzymatic activities, restoring Na⁺/K⁺ balance, improving protein content, and lowering ROS. The protective role of NO was confirmed using inhibitors L-NAME (500 µM) and cPTIO (100 µM), which reversed SNP’s benefits and aggravated stress damage. Conclusion: Overall, S, Ca, and NO were found to synergistically improve salt stress tolerance by modulating ion homeostasis, nitrogen and sulphur metabolism, and oxidative balance, offering nutrient- and signal-based strategies to enhance tomato resilience under salinity. Full article

Cannabidiol (CBD) is a non-psychotropic compound found in plants of the Cannabis genus, extensively studied for its therapeutic potential. Research has shown that CBD possesses anti-inflammatory, antioxidant, and regenerative properties, and may contribute to the recovery of neural and bone tissues. In light of the aging population and the resulting rise in neurodegenerative and osteodegenerative conditions, exploring novel therapeutic strategies that promote cellular regeneration is increasingly important. This review aims to compile and critically analyze key studies published in recent decades regarding the effects of CBD on the regeneration of the central and peripheral nervous systems, as well as bone tissue. Findings from in vivo studies indicate that CBD can attenuate inflammatory responses, inhibit oxidative stress, and modulate cellular pathways involved in tissue repair, thereby supporting neuronal and bone regeneration. Moreover, evidence suggests that CBD may protect cells from structural damage, enhancing the functional recovery of affected tissues. Despite scientific advances highlighting cannabidiol as a promising agent for bone and nerve regeneration, its therapeutic application still faces significant limitations. The primary challenge lies in the lack of robust clinical trials in humans, as most existing evidence is derived from in vitro and in vivo studies, making it difficult to confirm its efficacy and safety in clinical contexts. Additionally, CBD’s low bioavailability—due to first-pass hepatic metabolism—hinders dose standardization and reduces the predictability of therapeutic outcomes. Compounding these issues are regulatory constraints and the persistent social stigma surrounding cannabis-derived compounds, which further impede their integration and acceptance in regenerative medicine. Therefore, future research is essential to validate the therapeutic benefits of CBD and to establish its clinical applicability in treating neurological and bone disorders. Full article

Acute kidney injury (AKI) is a frequent clinical and pathological condition, often resulting from factors like ischemia, toxins, or infections, which cause a sudden and severe decline in renal function. This, in turn, significantly affects patients’ overall health and quality of life. The Sirtuin family (SIRTs), a group of Nicotinamide Adenine Dinucleotide (NAD+)-dependent deacetylases, is critically involved in key biological processes such as cellular metabolism, stress responses, aging, and DNA repair. Recent research has highlighted the vital role of SIRTs, such as SIRT1, SIRT3, and SIRT6, in the development and progression of AKI. These proteins help mitigate renal injury and facilitate kidney repair through mechanisms like antioxidant activity, anti-inflammatory responses, cellular repair, and energy metabolism. Additionally, the deacetylase activity of the SIRTs confers protection against AKI by modulating mitochondrial function, decreasing oxidative stress, and regulating autophagy. Although the precise mechanisms underlying the role of Sirtuins in AKI are still being explored, their potential as therapeutic targets is increasingly being recognized. This paper will discuss the mechanisms by which the SIRTs influence AKI and examine their potential in a future therapeutic strategy. Full article

Methacrylate photopolymer resin (MPR) is widely used in various fields, including the biomedical field. There are several problems associated with their use: the potential toxicity of monomer residues during incomplete polymerization and the possibility of bacterial expansion. Doping polymers with nanoparticles is one of the ways to increase the degree of polymerization (protection from toxicity), improve the performance characteristics of the polymer, and add antibacterial properties. We used an in situ polymerization method to obtain the composites of MPR with tellurium nanoparticles (TeNPs) with a dopant concentration of 0.001, 0.01, or 0.1% (v/v). The composite of MPR+TeNPs had a higher degree of polymerization compared to MPR without NPs, improved mechanical properties, and pronounced antibacterial activity. The effects depended on the concentration of TeNPs. All of the studied composites had no cytotoxic effect on human cells. MPR+TeNPs 0.1% had the maximum antibacterial effect, which is probably realized through Te-dependent induction of oxidative stress (increase in the generation of 9-oxoguanine and long-lived reactive forms of proteins). The results obtained deepen the knowledge about the influence of NPs of leading metals on photopolymerization and the final properties of the methacrylate matrix, and the synthesized MPR+TeNP composites may find potential biomedical applications in the future. Full article

MicroRNA-22 (miR-22) is a negative regulator of mitochondrial biogenesis, as well as lipid and glucose metabolism, in metabolically active tissues. Silencing miR-22 holds promise as a potential treatment of obesity and metabolic syndrome, as it restores metabolic capacity—enhancing oxidative metabolism—and reduces ectopic fat accumulation in chronic obesity, a driver of impaired metabolic flexibility and muscle mass loss. Intramuscular adipose accumulation and defective mitochondrial function are features associated with obese-mediated muscle atrophy and hallmarks of neuromuscular disorders such as Duchenne muscular dystrophy. Therefore, miR-22 could represent a compelling molecular target to improve muscle health across various muscle-wasting conditions. This study describes a pharmacological strategy for the inhibition of miR-22 in skeletal muscle by employing a mixmer antisense oligonucleotide (ASO, anti-miR-22). Administration of the ASO in a mouse model of obesity positively modulated myogenesis while protecting dystrophic mice from muscle function decline, enhancing fatigue resistance, and limiting pathological fibrotic remodeling. Mechanistically, we show that anti-miR-22 treatment promotes derepression of genes involved in mitochondrial homeostasis, favoring oxidative fiber content regardless of the disease model, thus promoting a more resilient phenotype. Furthermore, we suggest that miR-22 inhibition increases autophagy by transcriptional activation of multiple negative regulators of mammalian target of rapamycin (mTOR) signaling to decrease immune infiltration and fibrosis. These findings position miR-22 as a promising therapeutic target for muscle atrophy and support its potential to restore muscle health. Full article

Sleep bruxism (SB) is a masticatory muscle activity during sleep which can be categorized as primary, when it remains unclear whether the phenomenon is directly linked to a specific disorder, or if it only coexists, and secondary, when it is proven to be associated with a particular disorder, treatment or lifestyle and bruxism that is part of the signs of a disorder. In this way, SB is associated with various factors, including obstructive sleep apnea and gastroesophageal reflux (GER), where evidence suggests SB has a protective role in airway patency, potentially triggered by microarousals and autonomic instability, especially under hypoxia conditions. Since hypobaric hypoxia exposition—generated by high-altitude exposure—produces a decrease in the partial pressure of oxygen, it triggers alterations in cardiac rhythm and gastric function, which could be associated with physiological alterations mentioned in SB. Therefore, the aim of this review is to determine the effect of hypobaric hypoxia exposure on the physiological and molecular alterations during sleep bruxism. Method: The SANRA-guided narrative review synthesized recent human and animal studies on hypoxia’s physiological and molecular effects in sleep bruxism. In conclusion, SB is associated with GER and autonomic dysregulation, which are present in hypobaric hypoxia conditions, where respiratory disturbances, microarousals, and increased muscle activity are associated with SB. High-altitude exposure triggers oxidative stress, genetics, and sleep alteration, which exacerbate its severity. Moreover, neurophysiological and molecular mechanisms, including TRPV1 and HIF-1α activation, are implicated. Finally, polysomnography remains the gold standard for diagnosis; however, studies at high altitude are needed to confirm this association. Full article

The Atlantic blue crab (Callinectes sapidus) is an opportunistic invasive species in the Mediterranean that is negatively affecting biodiversity, fisheries, and tourism. In Italy, it is appreciated for its good meat quality, but the processing yield is low (21.87 ± 2.38%), generating a significant amount of by-products (72.45 ± 4.08%), which are underutilized. Valorizing this biomass is in line with circular economy principles and can improve both environmental and economic sustainability. This study aimed to valorize Atlantic blue crab by-products (BCBP), producing protein hydrolysates and assessing their in vitro bioactivities, in order to plan applications in animal food and related sectors. BCBP hydrolysates were obtained by enzymatic hydrolysis using Alcalase and Protamex enzymes. The treatment with Alcalase resulted in a higher degree of hydrolysis (DH = 23% in 205 min) compared to Protamex (DH = 14% in 175 min). Antioxidant activity of the hydrolisates was evaluated through DPPH, ABTS, reducing power and FRAP assays, as well as in vitro test in fibroblasts (HS-68). At 10 mg/mL, hydrolysates from both enzymes exhibited the maximum radical scavenging activity in DPPH and ABTS assays. In HS-68 cells, 0.5 mg/mL hydrolysates protected against H₂O₂-induced oxidative stress, showing a cell viability comparable to cells treated with 0.5 mM N-acetyl cysteine (NAC), as an antioxidant. Statistical analyses were performed using one-way ANOVA followed by Student–Newman–Keuls (SNK) or Games–Howell post hoc tests, with significance set at p < 0.05. Overall, both enzymes efficiently hydrolyzed BCBP proteins, generating hydrolysates with significant antioxidant activity and cytoprotective effects. These results demonstrate the potential to produce high-quality bioactive compounds from BCBPs, suitable for food, nutraceutical, and health applications. Scaling up this valorization process represents a viable strategy to improve sustainability and add economic value to the management of this invasive species, turning a problem in a resource. Full article

Microbiologically Influenced Corrosion (MIC) significantly endangers steel infrastructure, particularly in marine and buried environments, causing considerable economic and environmental damage. Sulphate-reducing bacteria (SRB) are primary supporters of MIC, accelerating iron corrosion through hydrogen sulfide production. Conventional mitigation strategies, including protective coatings and cathodic protection, often face challenges such as limited effectiveness against SRB and the aggressiveness of saltwater corrosion. This study explores a novel approach by directly introducing zinc oxide (ZnO) nanoparticles into the microbial medium to inhibit SRB activity and reduce MIC. Iron metal coupons were immersed in seawater under three conditions: control (seawater only), seawater with SRB, and SRB with ZnO nanoparticles. These coupons were used as electrodes in microbial fuel cells to obtain real-time voltage readings. At the same time, corrosion was evaluated using cyclic voltammetry (CV), scanning electron microscopy (SEM), energy-dispersive X-ray spectroscopy (EDX), mass loss, and pH measurements. Results demonstrate that ZnO nanoparticles significantly inhibited SRB growth, as confirmed by the antibiotic susceptibility test (ABST). It was revealed that the corrosion rate increased by 21.3% in the presence of SRB compared to the control, whereas the ZnO-added electrode showed a 21.7% reduction in corrosion rate relative to the control. SEM showed prominent corrosive products on SRB-exposed coupons. ZnO-added coupons exhibited a protective layer with grass-like whisker structures, and EDX results confirmed reduced sulfur and iron sulfide deposits, indicating suppressed SRB metabolic activity. ABST confirmed ZnO’s antimicrobial properties by producing clear inhibition zones. ZnO nanoparticles offer the dual benefits of antimicrobial activity and corrosion resistance by forming protective self-coatings and inhibiting microbial growth, making them a scalable and eco-friendly alternative to traditional corrosion inhibitors. This application can significantly extend the lifespan of iron structures, particularly in environments prone to microbial corrosion, demonstrating the potential of nanomaterials in combating microbiologically influenced corrosion (MIC). Full article

Dermatan sulfate (DS) is an animal glycosaminoglycan with significant structural heterogeneity and a high, but variable density of negative electric charge. Owing to these characteristics DS displays a high degree of biological reactivity that is subject to regulation. We previously demonstrated that structural variants of DS rapidly induce moderate necroptosis in luminal breast cancer cells. In the present study, we investigated the intracellular molecular mechanism(s) that may underlie this effect, focusing on the expression of key regulators of intrinsic (BCL-2A1) and extrinsic (cFLIP) apoptosis, autophagy (Beclin-1), and oxidative stress protection (heme oxygenase-1 (HO-1)). Using RT-qPCR, Western blotting, immunofluorescence, and pharmacological inhibition, we have shown for the first time that DS, depending on its structure and the cancer cell line, can rapidly, albeit transiently, upregulate either the long or short cFLIP splicing variant and also reduce the level of HO-1. These effects are mediated via DS-triggered PI3K and/or NFκB signaling. Moreover, DS can also influence the intracellular distribution of these proteins. In contrast, this glycan did not affect the expression of BCL-2A1 and BECN1. These findings indicate that DS induces coordinated molecular remodeling in luminal breast cancer cells that creates an intracellular environment favorable for necroptosis induction. Full article

Linezolid, a synthetic antimicrobial agent, may induce oxidative damage in ocular tissues, particularly in the optic nerve. Adenosine triphosphate (ATP) is involved in the production of antioxidants that scavenge and neutralize reactive oxygen species. This study aims to evaluate the potential protective effect of exogenous ATP against linezolid-induced ocular damage in rats, in comparison with methylprednisolone. Wistar-type rats were divided into five groups as follows: healthy (HG), ATP-only (ATPG), linezolid-only (LZDG), ATP + linezolid (ATLDG), and methylprednisolone + linezolid groups (MPLDG). Oxidative stress markers, antioxidant biomarkers, and proinflammatory cytokines were analyzed in isolated ocular tissues. Optic nerve tissue was also evaluated histopathologically. Linezolid administration increased the oxidative stress marker MDA and the proinflammatory cytokine TNF-α, while decreasing antioxidant parameters such as tGSH, SOD and CAT in rat ocular tissues, compared to the healthy group. However, it did not significantly alter serum troponin I levels. Histopathological analysis revealed that linezolid induced oxidative damage and inflammation in optic nerve tissue, with marked glial alterations. ATP administration reduced linezolid-induced oxidative stress in ocular tissue, as indicated by decreased MDA levels. It also enhanced antioxidant defenses by increasing tGSH, SOD, and CAT levels. In addition, ATP lowered proinflammatory cytokine levels, thereby alleviating inflammation. These effects collectively contributed to the restoration of biochemical parameters toward normal levels. In addition, ATP mitigated linezolid-induced optic nerve damage and glial alterations. The critical role of ATP in reducing oxidative stress, restoring antioxidant balance, and suppressing inflammation may represent a promising therapeutic approach for linezolid-induced ocular toxicity. Full article

In the production of stainless steel, chromium losses, particularly in the electric arc furnace (EAF) phase, pose a challenge. This study addresses these issues by reviewing and analyzing the thermodynamics of the Fe-Cr-C-O-(Si) system, highlighting discrepancies in existing literature regarding Gibbs free energies, interaction parameters, and other thermodynamic data. We developed a simple to use thermodynamic model to simulate the oxidation process using established data from scientific literature. The model calculates the equilibrium solubilities of chromium and carbon, showing how process variables like temperature, partial pressure of carbon monoxide, and silicon concentration influence chromium oxidation. The findings confirm that higher temperatures and the presence of silicon significantly reduce chromium loss by favoring carbon oxidation over chromium. The research concludes by providing practical guidelines for minimizing chromium losses in EAFs, such as protecting scrap with carbon, silicon, and aluminum; controlling oxygen intake; and ensuring a high melt temperature during decarburization. These guidelines aim to improve the economic efficiency and sustainability of stainless steel production. The paper is an expanded version of a prior conference paper. Full article

TRIC-A is an intracellular cation channel enriched in excitable tissues that is recently identified as a key modulator of sarcoplasmic reticulum (SR) Ca²⁺ homeostasis through direct interaction with type 2 ryanodine receptors (RyR₂). Given the intimate anatomical and functional coupling between the SR and mitochondria, we investigated whether TRIC-A contributes to SR–mitochondrial crosstalk under cardiac stress conditions. Using a transverse aortic constriction (TAC) model, we found that TRIC-A^−/− mice developed more severe cardiac hypertrophy, underwent maladaptive remodeling, and activated apoptotic pathways compared with wild-type littermates. At the cellular level, TRIC-A-deficient cardiomyocytes were more susceptible to H₂O₂-induced mitochondrial injury and displayed abnormal mitochondrial morphology. Live-cell imaging revealed exaggerated mitochondrial Ca²⁺ uptake during caffeine stimulation and increased propensity for store-overload-induced Ca²⁺ release (SOICR). Complementary studies in HEK293 cells expressing RyR₂ demonstrated that exogenous TRIC-A expression attenuates RyR₂-mediated mitochondrial Ca²⁺ overload, preserves respiratory function, and suppresses superoxide generation. Together, these findings identify TRIC-A as a critical regulator of SR–mitochondrial Ca²⁺ signaling. By constraining mitochondrial Ca²⁺ influx and limiting oxidative stress, TRIC-A safeguards cardiomyocytes against SOICR-driven injury and confers protection against pressure overload-induced cardiac dysfunction. Full article