Search Results (319)

The skeletal muscle system is particularly susceptible to degenerative and inflammatory processes that threaten mobility, quality of life, and systemic health. Marine plants, including brown, red, and green algae, are valuable yet understudied sources of bioactive compounds with therapeutic potential against skeletal muscle inflammation and degeneration. This narrative review provides the first overview of polyphenols, polysaccharides, carotenoids, and multiminerals derived from marine plants, with a particular focus on their effects on skeletal muscle, bone, and joint tissues. It highlights both the therapeutic potential and the limitations of marine plant-derived bioactive compounds in the musculoskeletal system. The compounds discussed, such as phlorotannins, ulvan, fucoidan, carotenoids, spirulina derivatives, and Aquamin, modulate key signaling pathways, including NF-κB, JAK/STAT3, and the NLRP3 inflammasome. Among these, MAPK emerges as the most consistently affected axis across all compound classes, leading to a reduction in TNF-α, IL-1β, IL-6, and oxidative stress markers. These bioactive compounds have been shown in both in vitro and in vivo models to reduce muscle catabolism, enhance osteoblast differentiation and mineralization, and reduce cartilage inflammation. Despite favorable safety, biocompatibility, and biodegradability profiles, current evidence shows that systemic applications significantly dominate over local delivery, highlighting the untapped potential of localized delivery strategies. Overall, this narrative review underscores the growing importance of marine plant-derived bioactives as promising natural agents for maintaining musculoskeletal integrity and alleviating degenerative disorders. Full article

Coral reef ecosystems represent one of the most biodiverse and productive marine habitats, yet they are increasingly threatened by a range of anthropogenic stressors. Among these, emerging contaminants including pharmaceutical and personal care products (PPCPs) have started to feature as contaminants of concern due to their persistence, bioaccumulation potential, and complex interactions within reef environments. This review synthesizes current research on the occurrence, transport pathways, and ecological impacts of emerging contaminants, specifically focusing on PPCPs on coral reef systems. Evidence indicates that compounds such as UV filters, antibiotics, and endocrine-disrupting chemicals can impair coral physiology, disrupt symbiotic relationships with zooxanthellae, and contribute to bleaching events. The review further highlights the variability in coral species’ sensitivity to these contaminants, with documented effects ranging from oxidative stress to reduced growth and reproductive capacity. Despite advances in detection and risk assessment, significant knowledge gaps remain regarding long-term exposure, mixture effects, and the influence of local environmental conditions on contaminant toxicity. By consolidating recent findings, this review underscores the urgent need for targeted research and policy action to mitigate the threat of emerging contaminants to coral reef ecosystems. Full article

Atherosclerosis remains a leading cause of cardiovascular mortality despite advances in pharmacological and interventional therapies. Current treatment approaches face limitations including systemic side effects, inadequate local drug delivery, and restenosis following vascular interventions. Gel-based technologies offer unique advantages through tunable mechanical properties, controlled degradation kinetics, high drug-loading capacity, and potential for stimuli-responsive therapeutic release. This review examines gel platforms across multiple scales and applications in atherosclerosis research and intervention. First, gel-based in vitro models are discussed. These include hydrogel matrices simulating plaque microenvironments, three-dimensional cellular culture platforms, and microfluidic organ-on-chip devices. These devices incorporate physiological flow to investigate disease mechanisms under controlled conditions. Second, therapeutic strategies are addressed through macroscopic gels for localized treatment. These encompass natural polymer-based, synthetic polymer-based, and composite formulations. Applications include stent coatings, adventitial injections, and catheter-delivered depots. Natural polymers often possess intrinsic biological activities including anti-inflammatory and immunomodulatory properties that may contribute to therapeutic effects. Third, nano- and microgels for systemic delivery are examined. These include polymer-based nanogels with stimuli-responsive drug release responding to oxidative stress, pH changes, and enzymatic activity characteristic of atherosclerotic lesions. Inorganic–organic composite nanogels incorporating paramagnetic contrast agents enable theranostic applications by combining therapy with imaging-guided treatment monitoring. Current challenges include manufacturing consistency, mechanical stability under physiological flow, long-term safety assessment, and regulatory pathway definition. Future opportunities are discussed in multi-functional integration, artificial intelligence-guided design, personalized formulations, and biomimetic approaches. Gel technologies demonstrate substantial potential to advance atherosclerosis management through improved spatial and temporal control over therapeutic interventions. Full article

Ulcerative colitis (UC) is an inflammatory bowel disease associated with oxidative stress. Pogostemon oil (PO) exhibits potent antioxidant and anti-inflammatory activities but is limited by high volatility and poor gastrointestinal stability. In this study, sporopollenin exine capsules (SECs) were engineered as natural micro-carriers for PO, achieving efficient encapsulation (η > 69%) and a high adsorption capacity (27.64 g/g). A pH-sensitive calcium alginate shell was subsequently applied to construct colon-targeted microspheres (Ca-Alg@PO-SECs). The resulting system improved the thermal and photostability of PO. In vitro dissolution assays confirmed the system’s pH-responsiveness, maintaining integrity under simulated gastric conditions while enabling localized release at intestinal pH. In a DSS-induced acute UC mouse model, Ca-Alg@PO-SECs effectively alleviated clinical symptoms, as evidenced by improved body weight, colon length, and disease activity index. At the inflammatory level, the formulation modulated key cytokines (IL-1β, IL-6, and IL-10). Overall, Ca-Alg@PO-SECs provides a biocompatible, colon-targeted delivery strategy that preserves the bioactivity of essential oils and offers a promising preclinical approach for localized UC therapy. Full article

Trypanosoma cruzi is the protozoan parasite responsible for Chagas disease, a neglected tropical disease caused by trypanosomatids. Its success as pathogen relies on remarkable metabolic adaptability, stress tolerance, and complex interactions with mammalian hosts. Among the proteins contributing to these processes, nucleoside diphosphate kinases (NDPKs) and arginine kinase (AK) have emerged as central enzymes for parasite metabolism. NDPKs, beyond their canonical role in nucleotide homeostasis, are implicated in DNA repair and oxidative stress responses and are also secreted enzymes. AK, on the other hand, serves as a unique energy-buffering system absent in mammals, supporting parasite growth and adaptation to oxidative and metabolic stresses, including modulation of host immunity. Both enzymes display distinct subcellular localizations all along the parasite and through the life cycle, linking them to multiple roles important for parasite biology and survival. Recent studies have highlighted the impact of interfering these enzymes with several compounds on the viability of the organisms, suggesting new avenues to explore them as drug targets. This review provides a general overview of NDPKs and AK in T. cruzi, aiming to underline their relevance to a broader context of trypanosomatids. Their study not only broadens our understanding of parasite biology but also opens perspectives for applied research, including therapeutic alternatives for Chagas and related diseases. Full article

The enteric nervous system (ENS) constitutes a highly organized and intricate neuronal network comprising two principal plexuses: myenteric and submucosal. These plexuses consist of neurons and enteric glial cells (EGCs). Neurons ensure innervation throughout the intestinal wall, whereas EGCs, distributed within the mucosa, contribute to epithelial barrier integrity and modulation of local inflammatory responses. The ENS orchestrates essential gastrointestinal functions, including motility, secretion, absorption, vascular regulation, and immune interactions with gut microbiota. Under physiological conditions, intestinal homeostasis involves moderate generation of reactive oxygen species (ROS) through endogenous processes such as mitochondrial oxidative phosphorylation. Cellular antioxidant systems maintain redox equilibrium; however, excessive ROS production induces oxidative stress, promoting EGCs activation toward a reactive phenotype characterized by pro-inflammatory cytokine release. This disrupts neuron–glia communication, predisposing to enteric neuroinflammation and neurodegeneration. Obesity, associated with hyperglycemia, hyperlipidemia, and micronutrient deficiencies, enhances ROS generation and inflammatory cascades, thereby impairing ENS integrity. Nevertheless, non-pharmacological strategies—including synthetic and natural antioxidants, bioactive dietary compounds, probiotics, and prebiotics—attenuate oxidative and inflammatory damage. This review summarizes preclinical and clinical evidence elucidating the interplay among the ENS, obesity-induced oxidative stress, inflammation, and the modulatory effects of antioxidant interventions. Full article

Background: Oncological treatment remains a major clinical challenge. Despite therapeutic advances and the diversity of available approaches, many tumors continue to exhibit limited responsiveness to chemotherapy. In this context, nutrition has emerged as a promising complementary strategy to support cancer therapy. In particular, interventions based on nutritional deprivation have gained prominence due to their ability to modulate tumor metabolism, inducing alterations that may increase the sensitivity of cancer cells to conventional treatments. Accordingly, the present study aimed to evaluate the safety and efficacy of caloric restriction combined with chemotherapy in a Sarcoma-180 model, investigating its effects on immunological and hematological parameters, antioxidant activity, oxidative stress, and tumor and liver morphology, as well as DNA damage. Methods: Mice bearing Sarcoma-180 were randomly assigned to four groups: Ad Libitum (AL), Ad Libitum + Doxorubicin (ALDOX), Caloric Restriction (CR), and Caloric Restriction + Doxorubicin (CRDOX). Assessment included tumor weight and volume, food and caloric intake, hematotoxicity, lipid metabolism, oxidative stress and antioxidant markers, genotoxicity, morphological alterations in the tumor and liver, and overall survival. Results: The data obtained demonstrate that caloric restriction combined with doxorubicin is both safe and feasible, as it preserves body weight and does not induce metabolic disturbances. Importantly, this combined strategy produced a marked reduction in tumor volume and mass while also mitigating the hematotoxicity typically associated with doxorubicin. In peripheral blood, the regimen decreased chemotherapy-induced DNA damage, supporting a systemic protective effect. Consistently, the combination reduced oxidative stress markers (NOx and MDA) and enhanced antioxidant activity within the tumor. Histological analyses further confirmed these outcomes, showing tumor cell death with features compatible with apoptosis and reduced local invasion. Together, these data indicate that caloric restriction enhances the antitumor efficacy of doxorubicin while simultaneously improving treatment tolerance. Conclusions: This study demonstrates that caloric restriction, combined with doxorubicin, is safe, well-tolerated, and enhances the antitumor response in the Sarcoma-180 model. Full article

Ischemic heart disease (IHD), the leading causes of cardiovascular morbidity and mortality worldwide, is currently treated though revascularization strategies such as pharmacological thrombolysis, coronary artery bypass grafting (CABG), and percutaneous coronary intervention (PCI). However, the restoration of blood flow often induces cardiac dysfunction, known as myocardial ischemia–reperfusion injury (MIRI). The pathogenesis of MIRI involves a complex, multifactorial process characterized by the interplay of diverse pathophysiological mechanisms, including oxidative stress, intracellular calcium overload, inflammatory cascade activation, apoptosis, autophagy, and microvascular endothelial dysfunction. In recent years, modified RNA (modRNA) technology has emerged as a novel therapeutic strategy for MIRI due to its enhanced molecular stability, reduced immunogenicity, and controllable transient protein expression. Studies have demonstrated that optimized modRNA delivery systems enable efficient, localized expression of therapeutic genes (e.g., antioxidant, anti-apoptotic, and pro-angiogenic factors) at injury sites, significantly mitigating MIRI-associated pathological damage. Nevertheless, significant challenges remain in clinical translation, such as delivery system targeting, transfection efficiency and cytotoxicity. This review focuses on recent advances in the development and application of modRNA-based delivery systems for MIRI treatment. Understanding the molecular mechanisms of MIRI and the structural characteristics and application of modRNA may encourage researchers to explore promising therapeutic modalities for addressing reperfusion-related cardiac injury. Full article

Background: Atherosclerosis is the pathological basis for lethal cardio-cerebral vascular diseases, such as coronary artery disease and stroke. Fructus Choerospondiatis (FC) has demonstrated cardiac protective effects in multiple ethnomedicine. Whether these protective effects are attributed to the prevention of vascular atherosclerosis, however, remains unknown. We aim to examine the anti-atherosclerotic effect of FC aqueous extract and elucidate the underlying mechanism. Methods: FC was separated into peel and pulp, and the aqueous extract was obtained separately by boiling in water to mimic decocting. Atherosclerosis model was established in ApoE^−/− mice fed with a high-fat diet, and histological analysis were utilized to evaluate the development of atherosclerosis. Various inflammatory models were constructed in mice to evaluate the anti-inflammatory effect of FC extract systemically, including acute local inflammation induced by traumatic injury (ear/foot swelling), acute systemic inflammation triggered by pathogenic infection (LPS- and POLY (I:C)-induced), as well as chronic inflammatory conditions associated with oxidative stress (D-galactose-induced), metabolic disorder (db/db mice), and aging. LC-MS and network pharmacology identified bioactive components and targets. Western blotting, ELISA, qPCR, and immunofluorescence were utilized to analyze the key genes involved in the mechanisms. Results: FC peel extract reduced serum IL-6 level, atherosclerotic plaque area, and macrophage content in the plaque, while pulp extract showed no protective effects. Peel extract exhibits anti-inflammatory effects in all models. The integrative application of LC-MS and network pharmacology identified ellagic acid as the major bioactive component and AKT as its target protein. Mechanistically, FC peel extract inhibits AKT phosphorylation, suppresses c-FOS expression and nuclear translocation, reduces IL-6 transcription and inflammation, and thus alleviates atherosclerosis. Conclusions: FC peel aqueous extract exerts anti-atherosclerotic effect by inhibiting inflammation through AKT/c-FOS/IL-6 axis. This study provides novel insights into the protective effects against atherosclerosis of FC peel and highlights its potential application in the prevention and treatment of coronary artery diseases. Full article

Background/Objectives: We evaluated Goreisan, a traditional Chinese medicine, for its effects on nephrotic syndrome in a rat model. Methods: Male Sprague–Dawley rats underwent right nephrectomy at 5 weeks of age, followed by adriamycin administration (5 mg/kg) at 6 and 8 weeks of age to induce nephrotic syndrome. At 10 weeks, rats were divided into three groups: vehicle (control), Goreisan 0.5 g/kg (GL), and Goreisan 1.0 g/kg (GH). Goreisan was administered daily for 4 weeks. At 14 weeks, blood, urine, mRNA expressions, and kidney histopathology were analyzed. Data were analyzed using one-way ANOVA followed by Tukey–Kramer post hoc testing. Results: Goreisan prevented worsening kidney function, with reduced glomerular and tubulointerstitial damage, lower systemic and intrarenal 8-hydroxy-2′-deoxyguanosine levels, and lower plasma aldosterone levels and expression of intrarenal renin–angiotensin–aldosterone system (RAAS)-related factors. Urine volume significantly increased in GL and GH groups compared with the control group. In the GH group, urine volume increased markedly (Δ urine volume: 10.0 ± 2.6 mL/day), whereas it tended to decrease in the Vehicle group (Δ urine volume: −1.3 ± 2.5 mL/day). Urine osmolality was lower in the GH group, with a larger decrease in Δ urine osmolality (−616.3 ± 132.8 mOsm/L). These changes occurred without an increase in urinary sodium excretion, suggesting an aquaretic effect independent of natriuresis. Creatinine clearance (CCr/kg) declined markedly in the Vehicle group but was significantly preserved in the GH group (Δ CCr/kg: −2.2 ± 0.19 vs. −0.7 ± 0.28), indicating renoprotective effects. No differences were found in serum arginine–vasopressin levels. Real-time PCR and immunohistochemical staining showed no significant differences in aquaporin (AQP) mRNA expression (AQP1, AQP2, AQP3, and AQP4), but AQP2 localization to the apical membrane in the collecting ducts was reduced with Goreisan treatment. Conclusions: Goreisan demonstrates kidney-protective and diuretic effects in nephrotic syndrome, potentially through reducing systemic oxidative stress, modulating RAAS activation, and altering AQP2 trafficking. Full article

Thanks to both endogenous and exogenous antioxidants (AOs), the antioxidant defense system ensures redox homeostasis, which is crucial for protecting the body from oxidative stress and maintaining overall health. The food industry also exploits the antioxidant properties to prevent or delay the oxidation of other molecules during processing and storage. There are many classical methods for assessing antioxidant capacity/activity, which are based on mechanisms such as hydrogen atom transfer (HAT), single electron transfer (SET), electron transfer with proton conjugation (HAT/SET mixed mode assays) or the chelation of selected transition metal ions (e.g., Fe²⁺ or Cu¹⁺). The antioxidant capacity (AOxC) index value can be expressed in terms of standard AOs (e.g., Trolox or ascorbic acid) equivalents, enabling different products to be compared. However, there is currently no standardized method for measuring AOxC. Nanoparticle sensors offer a new approach to assessing antioxidant status and can be used to analyze environmental samples, plant extracts, foodstuffs, dietary supplements and clinical samples. This review summarizes the available information on nanoparticle sensors as tools for assessing antioxidant status. Particular attention has been paid to nanoparticles (with a size of less than 100 nm), including silver (AgNPs), gold (AuNPs), cerium oxide (CeONPs) and other metal oxide nanoparticles, as well as nanozymes. Nanozymes belong to an advanced class of nanomaterials that mimic natural enzymes due to their catalytic properties and constitute a novel signal transduction strategy in colorimetric and absorption sensors based on the localized surface plasmon resonance (LSPR) band. Other potential AOxC sensors include quantum dots (QDs, <10 nm), which are particularly useful for the sensitive detection of specific antioxidants (e.g., GSH, AA and baicalein) and can achieve very good limits of detection (LOD). QDs and metallic nanoparticles (MNPs) operate on different principles to evaluate AOxC. MNPs rely on optical changes resulting from LSPR, which are monitored as changes in color or absorbance during synthesis, growth or aggregation. QDs, on the other hand, primarily utilize changes in fluorescence. This review aims to demonstrate that, thanks to its simplicity, speed, small sample volumes and relatively inexpensive instrumentation, nanoparticle-based AOxC assessment is a useful alternative to classical approaches and can be tailored to the desired aim and analytes. Full article

This review examines scientific and engineering strategies for adapting bituminous and asphalt concrete materials to the highly diverse climates of Central Asia. The region’s sharp gradients—from arid lowlands to cold mountainous zones—expose pavements to thermal fatigue, photo-oxidative aging, freeze–thaw cycles, and wind abrasion. Existing climatic classifications and principles for designing thermally and radiatively resilient pavements are summarized. Special emphasis is placed on linking binder morphology, rheology, and climate-induced transformations in composite bituminous systems. Advanced characterization methods—including dynamic shear rheometry (DSR), multiple stress creep recovery (MSCR), bending beam rheometry (BBR), and linear amplitude sweep (LAS), supported by FTIR, SEM, and AFM—enable quantitative correlations between phase composition, oxidative chemistry, and mechanical performance. The influence of polymeric, nanostructured, and biopolymeric modifiers on stability and durability is critically assessed. The review promotes region-specific material design and the use of integrated accelerated aging protocols (RTFOT, PAV, UV, freeze–thaw) that replicate local climatic stresses. A climatic rheological profile is proposed as a unified framework combining climate mapping with microstructural and rheological data to guide the development of sustainable and durable pavements for Central Asia. Key rheological indicators—complex modulus (G*), non-recoverable creep compliance (Jnr), and the BBR m-value—are incorporated into this profile. Full article

Background: Prostacyclin (PGI₂), an abundantly produced bioactive lipid by oviductal epithelial cells, supports preimplantation embryo development by buffering oxidative stress. However, the mechanism linking PGI₂ signaling to embryonic redox control remains unclear. We investigated whether Iloprost (Ilo), a stable PGI₂ analogue, enhances preimplantation embryo development by alleviating oxidative stress via activation of the Nrf2/Keap1 pathway, and whether these effects depend on Nrf2 activity using the inhibitor brusatol. Methods: Porcine embryos were treated with Ilo to model oviductal PGI₂ signaling during in vitro culture. Developmental competence was evaluated by cleavage and blastocyst formation rates, and blastocyst quality by total cell number and TUNEL assays. Oxidative status was quantified by fluorescence detection of reactive oxygen species (ROS), and Nrf2 activation was assessed by nuclear localization and antioxidant-related gene expression. Results: Embryos treated with Ilo showed significantly increased blastocyst formation, reduced ROS, and upregulated antioxidant genes. Immunofluorescence confirmed increased nuclear translocation of Nrf2, indicating activation of the Nrf2/Keap1 signaling pathway. In contrast, embryos treated with brusatol showed reduced blastocyst formation, increased ROS, and downregulated antioxidant-related gene expression, whereas co-treatment with Ilo reversed these effects. Conclusions: This study demonstrates that PGI₂ protects embryos by activating Nrf2/Keap1 signaling, establishing this axis as a key antioxidant defense during embryonic development and highlighting its potential to improve embryo culture systems. Full article

Gingival crevicular fluid (GCF) reflects both local periodontal inflammation and systemic conditions. This review highlights the role of oxidative stress, oxidised low-density lipoprotein (oxLDL), and apolipoprotein B (apoB) as molecular links between periodontitis and metabolic disorders. Elevated GCF levels of oxLDL and apoB indicate enhanced vascular permeability and local oxidative modification, particularly in diabetes. Furthermore, oxLDL promotes the formation of neutrophil extracellular trap (NET) via connecting oxidative stress with immune-mediated tissue injury. These insights establish GCF as a valuable, non-invasive biomarker for understanding the interplay between periodontal and systemic diseases. Full article

Coccomyxa parasitica-like algae pose a growing threat to bivalve aquaculture. In this work, for the first time under controlled conditions, the effect of the green parasitic microalgae of genus Coccomyxa sp. in the Sea of Japan on the immune and antioxidant protection of Mytilus galloprovincialis was studied in two ways of infection—through filtration (with feed) and injection (into an adductor). By day 7, mortality in both experimental groups reached 68%. The phagocytic activity of hemocytes significantly decreased in the feed group, which may be due to the masking of the parasite as a food particle. Despite transcriptional activation of catalase and superoxide dismutase genes in hemocytes upon injection, a decrease in enzyme activity and an increase in lipid peroxidation were observed in the gills, indicating local oxidative stress. Catalase activity in the gills was increased when mussels receive cells as food. DNA damage in hemocytes did not reach statistical significance. After injection, there was a significant decrease in the galectin gene expression. The data obtained confirm that Coccomyxa sp. is an active parasite capable of infecting the Mediterranean mussel and modulating the host’s defense systems. Full article