Search Results (13,692)

Ulcerative colitis (UC) is a highly prevalent chronic non-specific intestinal inflammatory disorder for which effective therapeutic options are urgently needed. The active component cimigenoside (CIM) possesses promising anti-inflammatory bioactivity; however, its therapeutic efficacy and underlying molecular mechanism against UC remain to be fully elucidated. The present study aimed to investigate the effects and possible mechanisms of CIM on dextran sodium sulfate (DSS)-induced UC. Mice received drinking water containing 2.5% DSS to induce a UC model, and were then treated with different dosages of CIM for 10 consecutive days. The results found that CIM restored the colonic length, alleviated pathological damage to the colon, preserved intestinal mucosal barrier integrity, and inhibited colonic oxidative stress and inflammatory responses in DSS-induced mice. Additionally, DSS induction reduced the expression of sirtuin 3 (SIRT3) protein in the colonic tissues of mice; however, this was improved by treatment with CIM. Notably, the above protective roles of CIM on DSS-induced UC were unavailable in SIRT3-knockout (SIRT3-KO) mice. Notably, the docking score of CIM binding to SIRT3 is −11.3 kcal/mol, suggesting that CIM could directly bind to SIRT3. Collectively, CIM directly binds to SIRT3 and upregulates its protein expression, which in turn inhibits colonic inflammation and oxidative stress, thereby exerting anti-UC effects. Full article

Oxidative stress is no longer viewed as a random imbalance between reactive oxygen species and antioxidants, but as a failure of an integrated redox network that connects metabolism, immunity, and metal homeostasis. Classical markers such as malondialdehyde and 4-hydroxynonenal define oxidative damage, yet they cannot explain how redox adaptation occurs or fails. Over the past decade, the discovery of regulated cell-death pathways (ferroptosis, cuproptosis) and emerging metabolic signals has revealed a new generation of adaptive redox mediators—including itaconate, nitro-fatty acids, reactive sulfur species and succinate—that act as electrophilic or persulfidating regulators rather than passive by-products of oxidation. This review integrates mechanistic, biochemical and clinical evidence to define how these mediators remodel the nuclear factor erythroid 2-related factor 2/Kelch-like ECH-associated protein 1, nuclear factor kappa-light-chain-enhancer of activated B cells, and hypoxia-inducible factor 1-alpha axes, coordinate lipid–metal–sulfur cross-talk, and shape vulnerability or resistance to ferroptosis and cuproptosis. By combining deep molecular research with translational perspectives, we propose a unifying framework for predictive redox medicine based on composite biomarker panels and AI-assisted phenotyping. Understanding and quantifying these next-generation mediators will open new avenues for precision nutrition, drug development, and disease prevention—transforming oxidative-stress biology from a descriptive field into an actionable platform for human health. Full article

Background: Apigenin, as a flavonoid, can be protective against oxidative damage in hypoxic events due to its antioxidant properties. Here, we have investigated the neuroprotective effects of apigenin in an ex vivo model of ischemic damage, using cerebellar slices from postnatal day (P)8–12 reporter mice to identify oligodendrocytes (SOX10-EGFP) and astrocytes (GFAP-EGFP). Methods: Apigenin (10 and 20 μM) was administered preventively at 60 min prior to and during inducing ischemic damage by oxygen and glucose deprivation (OGD); controls were maintained with glucose and normoxia (OGN). Results: OGD induced a marked retraction of oligodendroglial processes without reducing the oligodendrocyte number. This structural disruption was prevented by apigenin; notably, 10 μM apigenin blocked process retraction, whereas 20 μM did not, indicating a dose-dependent effect on the oligodendroglial morphology. Consistent with this, MBP and NF70 immunofluorescence analyses of axonal myelination demonstrated that OGD caused a significant loss of myelin sheaths, and this was prevented by pre-treatment with apigenin. In addition, apigenin prevented astrocyte reactivity induced by OGD, as assessed by increased GFAP-EGFP expression and decreased expression of glutamine synthetase. Moreover, immunofluorescence for calbindin indicated that apigenin protected Purkinje neurons from ischemic damage. Conclusions: These results demonstrate that apigenin is neuroprotective in ischemia and this is associated with modulation of astrocyte reactivity and maintenance of oligodendrocyte and myelin integrity. Full article

Ulcerative colitis (UC) is a multifactorial disease characterized by chronic intestinal inflammation and disrupted oxidative balance, significantly impairing patients’ quality of life. Tannins, a class of polyphenolic compounds widely distributed in plants, have demonstrated notable therapeutic potential against UC due to their inherent antioxidant and anti-inflammatory properties. This study employs a systematic literature review of databases, including PubMed and Web of Science, to investigate the molecular mechanisms by which tannins restore intestinal inflammatory and oxidative homeostasis. The findings indicate that tannins directly scavenge reactive oxygen species (ROS) via their polyphenolic structure, mitigate oxidative damage, upregulate antioxidant enzyme expression, suppress pro-inflammatory cytokine secretion, and preserve intestinal barrier integrity. Despite their significant therapeutic promise, challenges such as low bioavailability and structural complexity remain. Future research should prioritize bioavailability enhancement, clarification of structure-activity relationships, and translational studies to facilitate the clinical application of tannin-based therapies for UC. Full article

Zinc-based coatings are insufficient as surface coatings; they corrode rapidly and can cause long-term damage to subsea pipelines and other instruments. Therefore, this research was undertaken by manufacturing a sacrificial nano-reinforced Zn coating combined with additives via electrodeposition onto a mild steel S235 substrate, which provides excellent corrosion resistance under severe marine conditions. The electrodeposited coatings were characterized using SEM/EDS and XRD, revealing the effective incorporation of cerium oxide nanoparticles and high-quality graphene (Gr) in the zinc matrix. Vickers microhardness measurements, mechanical resilience, and surface roughness of the Zn-CeO₂-Gr coating showed an inverse correlation between improved microhardness (+65.85%) and mechanical resilience (+31.49%), while surface roughness decreased (−81.48%) compared to pure zinc electrodeposited coatings. These characteristics indicate grain refinement and greater reliability under mechanical stress. Electrochemical impedance spectroscopy (EIS) and DC polarization measurements indicate a significant improvement in corrosion resistance compared to pure zinc, due to the synergistic effect between graphene and cerium oxide nanoparticles, which reduces the cathodic activity of the surface. These findings offer promising applications for cutting-edge materials in saline environments. Full article

Glaucoma, characterized by progressive retinal ganglion cell degeneration and optic nerve damage, is the leading cause of irreversible blindness worldwide. Multiple risk factors influence the pathogenesis and progression of glaucoma. Food-derived bioactive components have emerged as a new area of interest to overcome the limitations of current standard treatments due to their antioxidant and anti-inflammatory activities and multi-target mechanisms. In this context, various plant-derived foods, such as Lycium barbarum, Ganoderma lucidum, Cryptotanshinone, Scutellaria baicalensis, Silybum marianum, Astragalus membranaceus, Ginkgo biloba, Panax ginseng, Crocus sativus, and resveratrol, have shown potential mechanisms for treating glaucoma. These bioactive components may address oxidative damage, neuroinflammation, and elevated intraocular pressure, which may be due to the modulation of multiple signaling pathways, including JAK2/STAT3, PI3K/AKT, MEK/ERK/CREB, cAMP/PKA/CREB, and others. However, further clinical trials are needed to validate dosage, bioavailability, and long-term safety. This review highlights the potential of bioactive components from plant-derived foods, offering a reference for further investigation into their effects on glaucoma. Full article

Diabetic retinopathy (DR) is a leading cause of vision loss worldwide and represents a complex neurovascular complication of diabetes mellitus driven by chronic hyperglycemia. Increasing evidence identifies oxidative stress—defined as an imbalance between reactive oxygen species (ROS) production and antioxidant defenses—as a central pathogenic mechanism linking metabolic dysregulation to retinal injury. The retina is particularly vulnerable to oxidative damage due to its high metabolic demand, elevated oxygen consumption, and abundance of polyunsaturated fatty acids. Hyperglycemia activates multiple interconnected biochemical pathways, including the polyol and hexosamine pathways, protein kinase C signaling, advanced glycation end-product formation, and lipid peroxidation, all of which converge on excessive ROS production and mitochondrial dysfunction. Growing attention has focused on oxidative stress biomarkers as tools to characterize DR severity and progression. Elevated systemic markers of lipid, protein, and DNA oxidation, together with impaired antioxidant capacity, correlate with disease stage, while oxidative biomarkers detected in aqueous and vitreous humor reflect localized retinal injury. Importantly, oxidative stress biomarkers are also associated with functional outcomes, including best-corrected visual acuity and diabetic macular edema. Integration of systemic and ocular oxidative biomarkers with clinical staging may improve risk stratification and support personalized therapeutic strategies in DR. Full article

Background: Caffeic acid (CA), with antioxidant and immunomodulatory properties, was formulated in liposomes to increase its efficacy. The study targets triple-negative breast cancer (TNBC), characterized by the absence of ER, PR, and HER2 receptors. Methods: For CA-loaded liposomes, the pharmacological effects on TNBC cell lines, parental Hs578T (HS) and Doxorubicin-resistant Hs578T (HSD) cells were evaluated by determining the cell growth inhibition ratio measured by the (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide) assay, oxidative stress, apoptosis rate, membrane damage and transcription factor expressions, and DNA damage, with or without exposure to Doxorubicin (Dox). The Results: demonstrated that CA-loaded liposomes were stable and had high entrapment capacity. They exerted apoptotic effects on both cells, comparable to Doxorubicin, and increased cell membrane damage. The liposomes increased STAT3 expression in HS cells, while they reduced NRF2 and STAT3 in HSD cells, suggesting beneficial effects on Dox-resistant breast tumor cells. In HS cells exposed to Dox, CA treatment improved the number of viable tumor cells and decreased the rate of apoptosis, while in HSD cells it enhanced apoptosis as a mechanism of cell death and decreased pro-survival molecules, STAT3 expression in parallel with reduced NRF2 activation. Conclusions: The results indicated that CA encapsulated in liposomes was able to interfere with some survival mechanisms of triple-negative cells and could inhibit their proliferation. Full article

(1) Background: The search for new polymodal antioxidants to correct oxidative stress of various origins and its consequences remains one of the most pressing and rapidly developing areas of biomedical research. (2) Methods: Hydrogen peroxide and hydroxyl radical detection, induced luminescence assay, ELISA for 8-oxoguanine detection, animal survival, blood cell count, micronucleus test, and PCR were used. (3) Results: 2R,3R-trans-dihydroquercetin (DHQ) was shown to reduce the amount of hydrogen peroxide and hydroxyl radicals formed during water radiolysis, leading to reduced damage to biomolecules. DHQ is a radioprotector, most effective at a dose of 300 mg/kg administered 15 min before radiation exposure. The dose reduction factor is 1.22. DHQ administration reduces the severity of radiation-induced leukopenia and thrombopenia by protecting red bone marrow cells. The mechanism of DHQ’s radioprotective action is fundamentally different from that of classical stress response inducers and is based on the normalization of the target cell transcriptional profile, rather than its hyperstimulation. (4) Conclusions: DHQ’s ability to restore the expression of antioxidant defense, DNA repair, and apoptotic genes to physiological levels under radiation exposure allows it to be considered a promising pharmacological agent for the correction of radiation-induced damage to normal tissues. Full article

Inhibition of inflammation and oxidative stress is increasingly recognized as a promising therapeutic strategy for neurodegenerative diseases. In this study, we isolated two new dimeric naphtho-γ-pyrone (aS)-fonsecinones B and D (1 and 2) and 14 known compounds (3–16) from the deep-sea-derived fungus Aspergillus niger 3A00562. Their structures were unambiguously determined through integrated physicochemical and spectroscopic analyses. Screening for neuroinflammatory inhibitors using a BV2 microglial cell model identified TMC 256 A1 (10) as the most potent candidate. Compound 10 significantly suppressed LPS-induced inflammation in BV2 cells without cytotoxicity. It concurrently inhibited LPS-triggered ROS overproduction and neutrophilic infiltration in zebrafish. Subsequent proteomics revealed that 10 targets NOS2 to modulate Alzheimer’s disease (AD)-associated pathways and the KEAP1-NRF2 axis. Molecular docking and dynamics simulations demonstrated that 10 occupies the NOS2 heme-binding pocket, thereby preventing dimerization and inhibiting enzymatic activity. Finally, 10 ameliorated locomotor deficits in an AD zebrafish model. Collectively, these findings highlight compound 10 as a candidate compound for preventing inflammatory and oxidative stress damage during treatment of neurodegenerative diseases, particularly AD. Full article

Many advances in enhanced oil recovery (EOR) take advantage of the unique properties of nanomaterials to improve characterization of formation properties, achieve conformance control during flood operations, and extend the controlled release time of polymers. Magnetite nanoparticles (nMag) have been employed in these processes due to their low cost, low toxicity, and ability to be engineered to meet desired needs, especially with the application of a magnetic field. Similarly, silica dioxide (SiO₂) and aluminum oxide (Al₂O₃) nanoparticles have been evaluated for the delivery of scale and asphaltene inhibitors. However, the injection of nanoparticles into porous media comes with the risk of formation damage due to particle deposition, which can lead to increased injection pressures and reductions in permeability. The goal of this study was to develop a method to evaluate and assess nanoparticle formulations for their potential to cause formation damage. A screening apparatus was constructed to hold small sandstone discs (~2 mm) or cores (~2.5 cm) for rapid testing with minimal material use and the capability to be used with either aqueous brine solutions or non-polar solvents as the mobile phase. Image analysis of the disc and pressure measurements demonstrated increasing deposition of nMag and face-caking when the salinity was increased from 500 mg/L NaCl (8.56 mM) to API brine (2.0 M). Similarly, when the injected concentration of silica nanoparticles in 500 mg/L NaCl was increased from 1 to 10 wt%, the back pressure increased by 55 psi, and face-caking was observed. The screening test results were consistent with traditional core-flood tests and was able to be modified to accommodate organic liquid mobile phases. The screening test results closely matched nanoparticle transport and retention measured in sandstone cores, confirming the ability of the system to rapidly screen nanoparticle formulations for potential formation damage. Full article

Neurodegenerative diseases of the central nervous system, such as Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis, represent a growing health challenge in ageing populations. Among the mechanisms underlying these disorders, increasing attention has been directed toward the role of cellular senescence. This process, triggered by chronic cellular and oxidative stress as well as DNA damage, leads to irreversible cell-cycle arrest and the development of the senescence-associated secretory phenotype (SASP). Within the central nervous system, the accumulation of senescent cells induces chronic inflammation, blood–brain barrier disruption, and progression of neurodegenerative processes. In this review, we present current evidence regarding the mechanisms of cellular senescence in the central nervous system, with particular emphasis on the role of SASP in neuroinflammation, vascular dysfunction, and neural tissue damage. Experimental and clinical data supporting the involvement of cellular senescence in the pathogenesis of Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis are discussed. The review also covers methods for identifying senescent cells in the brain, including molecular marker-based approaches and machine learning-based tools. Importantly, we discuss the methodological limitations of commonly used senescence markers, such as their limited specificity and the risk of false-positive detection, particularly in the heterogeneous cellular environment of the central nervous system. Strategies to improve detection reliability discussed in this review include the use of multimarker signatures, analysis of SASP components using qRT-PCR and ELISA, as well as transcriptomic approaches such as RNA sequencing and single-cell RNA sequencing. Furthermore, we analyze therapeutic strategies targeting senescent cells—senolytics, senomorphics, and SASP modulation—together with their limitations and associated clinical challenges. The collected evidence indicates that precise characterization of senescent cell populations in the brain is essential for the development of disease-modifying therapies for neurodegenerative disorders. Full article

Species of the Opuntia genus are widely recognized for their richness in bioactive metabolites and antioxidant potential, particularly in their cladodes. However, despite increasing interest in cochineal-resistant cultivars, their genotoxic safety remains poorly explored. In this study, the phytochemical composition, antioxidant activity, and genotoxic effects of cladode extracts from three Dactylopius opuntiae-resistant Opuntia species (O. ficus-indica, O. robusta, and O. stricta) collected in eastern Morocco were comparatively evaluated. Hydroethanolic extracts were characterized for their biochemical composition and screened for antioxidant activity using DPPH, β-carotene bleaching, FRAP, and total antioxidant capacity assays. An untargeted UHPLC-Orbitrap MS/MS approach was applied to profile secondary metabolites, while genotoxicity was assessed using the comet assay on rat leukocyte DNA. The three species exhibited distinct phytochemical and antioxidant profiles. O. ficus-indica showed the highest total phenolic and flavonoid contents and the strongest radical scavenging and reducing capacities, whereas O. stricta was particularly rich in ascorbic acid and exhibited the highest total antioxidant capacity. Metabolomic analysis revealed a predominance of phenolic acids and flavonoids, with piscidic acid as a major constituent, along with isorhamnetin derivatives and organic acids. Importantly, none of the extracts induced genotoxic effects compared to the negative control, while all differed significantly from the oxidative damage induced by hydrogen peroxide. Overall, these findings demonstrate the phytochemical richness, antioxidant potential, and genotoxic safety of cochineal-resistant Opuntia cladodes, supporting their sustainable valorization in food, nutraceutical, cosmetic, and agricultural applications. Full article

Winter rapeseed (Brassica rapa L.) is an important crop for vegetable oil production in China. However, its productivity is frequently threatened by severe cold waves during winter. To investigate the role of the microtubule cytoskeleton in cold adaptation of winter rapeseed, a microtubule stabilizer paclitaxel (Tax) and a microtubule depolymerizer colchicine (Col) were sprayed on winter rapeseed and transgenic proBrAFP1 Arabidopsis, respectively. The mRNA levels of cold-induced genes, along with cell membrane stability, antioxidant enzyme activities, and hormone levels were assessed under cold stresses of 4 °C and −4 °C. The results showed that low temperature significantly activated the proBrAFP1 promoter activity and increased the mRNA levels of core cold signaling pathway genes, such as C-REPEAT BINDING FACTORS (CBFs), Cyclic Nucleotide-Gated Channel (CNGC), OPEN STOMATA 1 (OST1) and Inducer of CBF EXPRESSION 1 (ICE1). Notably, under low-temperature stress, exogenous application of the microtubule stabilizer Tax markedly suppressed proBrAFP1-driven reporter activity in transgenic Arabidopsis, with consistent inhibition observed across both stem and leaf tissues; meanwhile, the Tax application alleviated reactive oxygen species (ROS) accumulation and mitigated membrane damage. In contrast, under the same low-temperature stress, the Col treatment exacerbated oxidative stress, enhanced lipid peroxidation, and elevated membrane damage. Collectively, these findings establish that microtubule regulators play indispensable roles in the cold stress response of winter rapeseed. It provides new insights into the mechanism by which plant microtubule cytoskeleton regulators mediate the cold response. Full article

Nateglinide (Nat) is an oral antidiabetic agent of the meglitinide class that has been reported to exert protective effects beyond glycemic control, particularly against oxidative stress and inflammation. Since oxidative stress and inflammation play a key role in the pathogenesis of acute kidney injury (AKI), especially following ischemia/reperfusion (I/R), this study aimed to evaluate the potential renoprotective effects of Nat in a rat model of I/R-induced AKI. Forty male Sprague Dawley rats were randomly divided into four groups (n = 10): Control, I/R, I/R + Nat (50 mg/kg), and I/R + Nat (100 mg/kg). Bilateral renal ischemia was induced by clamping renal arteries for 45 min, followed by 24 h of reperfusion. Nat was administered orally 1 h before ischemia. Renal levels of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and thiobarbituric acid reactive substances (TBARSs) were assessed. Serum blood urea nitrogen (BUN), creatinine, tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) were also measured, and histopathological analyses were performed. Nat significantly increased renal antioxidant parameters and reduced TBARS levels. Moreover, Nat markedly decreased serum BUN, creatinine, TNF-α, and IL-1β levels compared with the I/R group (p < 0.05). Histopathology confirmed attenuated renal damage in Nat-treated groups (p < 0.0001). These results indicate that Nat confers significant renoprotection against renal I/R injury via suppression of oxidative stress and inflammation. Full article