Search Results (5,519)

Background/Objectives: Oxidative stress is a major contributor to the pathogenesis of cardiovascular diseases, including hypertension, ischemic cardiomyopathy, and heart failure. MicroRNAs (miRNAs) have been extensively investigated in various contexts, and some of them have been identified to play a role in cardiovascular disease. This narrative review focuses on miR-103 and miR-155, two miRNAs implicated in the modulation of oxidative stress and cardiovascular remodeling. Methods: The following queries were used in PubMed since inception until May 2026: ((“miR-155” OR “microRNA-155” OR miR155) AND (“oxidative stress” OR ROS OR “reactive oxygen species”) AND (“cardiovascular disease” OR cardiovascular OR cardiac OR heart OR vascular)); ((“miR-103” OR “microRNA-103” OR miR103) AND (“oxidative stress” OR ROS OR “reactive oxygen species”) AND (“cardiovascular disease” OR cardiovascular OR cardiac OR heart OR vascular)). Results: A total of seven citations for miR-103 and 79 citations for miR-155 were identified. Reviews and papers about diseases other than those on cardiac/vascular involvement were excluded. miR-155 emerges as a potential regulator of inflammatory-redox signaling, whereas miR-103 appears more closely linked to cell fate and metabolic pathways. In both cases, available evidence supports a context-dependent role that challenges simplistic classification as pro- or antioxidant miRNAs. Conclusions: Available evidence suggests that both miR-103 and miR-155 are important regulators of oxidative stress-related pathways in cardiovascular disease. Nevertheless, the context-dependent effects observed across different cardiovascular disorders raise concerns regarding the safety of systemic miRNA modulation-based therapeutic strategies. Future studies should clarify the determinants of this context-dependent behavior and identify the specific conditions under which these miRNAs exert protective or harmful effects, which might pave the way for the development of miRNA-based therapeutic strategies targeting oxidative stress and cardiovascular remodeling. Full article

Wound healing is a dynamic and highly coordinated process that involves inflammation, cell proliferation, angiogenesis, re-epithelialization, extracellular matrix remodeling, and tissue maturation. The altered expression of important signaling pathways, such as transforming growth factor-β (TGF-β)/Smad, nuclear factor-κB (NF-κB), phosphoinositide 3-kinase/protein kinase B (PI3K/Akt), mitogen-activated protein kinase (MAPK), and Wnt/β-catenin, may be responsible for slower wound healing, chronic inflammation, excessive fibrosis, and impaired tissue regeneration. Multifunctional nanomaterials are a promising strategy for tuning these highly coordinated processes due to their tunable physicochemical properties, high surface area, and the ability to deliver cargo, as well as the integration of antimicrobial, antioxidant, anti-inflammatory, and pro-angiogenic properties. The aim of current review is to summarize the potential of multifunctional nanomaterials to promote wound healing, with a focus on mechanisms of action and modulation of key cellular signaling pathways. A systematic review of the literature was conducted using PubMed, Scopus, Web of Science, and Google Scholar, searching for publications from 1996 to June 2026, and representative experimental, mechanistic, preclinical, and translational studies were critically evaluated. In this review, the authors discuss the role of nanomaterial properties, therapeutic payload, molecular targets, modulation of cellular signaling pathways, and regenerative effects. These platforms have been shown in in vitro and animal studies to influence inflammatory signaling, oxidative stress, angiogenesis, collagen remodeling, re-epithelialization, cellular proliferation, and migration. However, the modulation of these pathways are dose-responsive, time-dependent, and cell- and wound-stage-specific. Despite the promising therapeutic potential of nanomaterial-based wound care strategies, the available evidence remains predominantly preclinical, with relatively limited clinical data supporting their use in humans. Concerns regarding long-term toxicity, biodistribution, batch-to-batch reproducibility, sterilization, scalable manufacturing, regulatory approval, and commercial feasibility further challenge translation into clinical practice. Multifunctional nanomaterials may offer a promising approach for pathway-specific and multimodal wound management; however, comprehensive mechanistic studies, long-term safety and biodistribution assessments, and well-designed clinically relevant investigations are required to establish their efficacy, safety, and true translational potential. Full article

Background: Age-related macular degeneration (AMD) is a leading cause of irreversible vision loss and is strongly driven by oxidative stress and inflammation. This study investigated the protective effects of cynarin against sodium iodate (NaIO₃)-induced retinal pigment epithelium (RPE) injury, focusing on the MAPK and NF-κB signaling pathways. Materials and Methods: Human ARPE-19 cells were exposed to NaIO₃, and cell viability was assessed by the MTT assay. Protein expression of MAPK components (p38, JNK, ERK) and the NF-κB pathway was analyzed by Western blotting, and pro-inflammatory cytokine (IL-1β, IL-6, TNF-α) mRNA expression was measured by RT-qPCR. In vivo, NaIO₃-induced retinal degeneration in C57BL/6 mice was treated with cynarin (3 or 10 mg/kg) for seven days, and retinal changes were evaluated by fundus photography, fluorescein angiography, and OCT. Results: Cynarin preserved ARPE-19 cell viability without cytotoxicity. It significantly attenuated NaIO₃-induced p38 and JNK phosphorylation, IκB degradation, and NF-κB activation while downregulating IL-1β, IL-6, and TNF-α expression. In vivo, cynarin reduced drusen-like lesions, hyperfluorescent abnormalities, and retinal thinning, and dose-dependently suppressed ocular pro-inflammatory cytokines. Conclusions: Cynarin protects against oxidative stress-induced retinal degeneration by suppressing MAPK and NF-κB inflammatory signaling, representing a promising therapeutic candidate for preventing or delaying NaIO₃-induced dry AMD-like retinal injury. Full article

Excessive short-term ethanol intake often causes acute intoxication and multi-organ damage, especially to the liver and brain. Thus, developing safe and effective preparations for hangover relief, liver protection, and brain function regulation is of great practical significance. In this study, we fabricated a thermosensitive chitosan (CS)–sea cucumber peptide (SCP) hydrogel (CS–SCP gel) loaded with SCP using NaHCO₃ as a crosslinker and characterized its properties. Kunming mouse models of anti-intoxication and acute alcohol-induced liver and brain injuries were established. The anti-intoxication and organ-protective effects of the CS–SCP gel were comprehensively evaluated through behavioral observation, liver histopathology, and biochemical assays of serum and liver, kidney, and brain tissues. The CS–SCP gel exhibited a phase transition temperature of 35.7 °C, a water absorption rate of 1015.47%, and a cumulative peptide release of 74.83% within 330 min. In mice, it prolonged the latency to drunkenness; shortened alcohol-induced sleep and sobering time; reduced blood ethanol, transaminase, and lipid levels; upregulated hepatic antioxidant enzymes; downregulated pro-inflammatory cytokines, and alleviated lipid peroxidation. It also enhanced brain antioxidant capacity, suppressed cerebral inflammatory cytokines, and maintained cholinergic neurotransmitter homeostasis. Collectively, with sustained release, CS–SCP gel is expected to prolong the pharmacological action of SCP, enhance therapeutic efficacy, and protect against alcohol-induced liver and brain injury through the regulation of oxidative stress and attenuation of inflammation. Full article

Background/Objectives: Manganese (Mn) is a neurotoxic trace element whose excessive accumulation in the brain can induce hippocampal damage via oxidative stress, mitochondrial dysfunction, neuroinflammation, and apoptosis. This study investigated whether honokiol (HNK) and its liposomal nanoformulation (HNK-LNPs) can ameliorate Mn-induced hippocampal neurotoxicity by modulating key antioxidant and mitochondrial regulatory pathways. Methods: Male Wistar rats were subjected to Mn exposure to induce hippocampal neurotoxicity and were treated with HNK or HNK-LNPs. We assessed oxidative status via NRF2/HO-1 signaling, antioxidant defenses (glutathione, GPx, SOD, CAT), and oxidative indices (ROS, MDA). Neuroinflammatory markers (NF-κB, TNF-α, IL-1β, IL-6, Iba-1), mitochondrial respiratory chain function and ATP levels, SIRT1/PGC-1α signaling, and neurotransmitter homeostasis were evaluated. We analyzed apoptosis using Bax, Bcl-2, caspase-3, and cytochrome c, along with histopathological and ultrastructural examination of the hippocampus. Results: Mn exposure was associated with NRF2/HO-1 downregulation, depleted endogenous antioxidants, increased ROS and MDA levels, and increased NF-κB–driven neuroinflammation and microglial Iba-1 expression. Mn was further associated with reduced ATP synthesis, dysregulation of SIRT1/PGC-1α signaling, and disrupted neurotransmitter balance, with a pro-apoptotic shift (elevated Bax, caspase-3, cytochrome c; reduced Bcl-2) and neuronal degeneration. Co-treatment with HNK, and more prominently with HNK-LNPs, was associated with reversing these alterations, restoring antioxidant and mitochondrial pathways, dampening inflammatory cascades, normalizing neurotransmitters, and favoring neuronal survival, with many indices approaching control values and consistently surpassing free HNK. Conclusions: Liposomal encapsulation significantly enhances honokiol’s neuroprotection against Mn-induced hippocampal neurotoxicity, likely via improved CNS bioavailability and coordinated modulation of NRF2/HO-1 and SIRT1/PGC-1α pathways. These findings support HNK-LNPs as a promising multi-mechanistic therapeutic strategy for metal-induced and related neurotoxic brain disorders. Full article

Cistanche deserticola polysaccharide (CDP) exhibits pleiotropic bioactivities, yet its splenic-protective profile remains incompletely defined. Here, male ICR mice were challenged with cyclophosphamide (CTX) to establish an immunosuppressed model and concurrently treated with CDP. By integrating functional assays, splenic histopathology, and transcriptomic and proteomic analyses, we show that CDP dose-dependently restores splenic mass, rescues white-pulp atrophy, and suppresses megakaryocytic hyperplasia. Functionally, CDP rebalances pro-/anti-inflammatory cytokines, scavenges splenic ROS/MDA, and potentiates GSH-Px/SOD antioxidant capacity versus CTX alone. Multi-omics convergence (3103 DEGs; 1387 DEPs) delineated a CDP-distinctive signature related to innate immune recognition, oxidative stress buffering, and protease/ion-transport modules. Notably, transcriptional enrichment of neutrophil extracellular trap (NET)-associated proxies—synergized with NOD-like receptor/IL-17 signaling—suggests a putative innate-priming mechanism warranting functional validation, rather than confirmed pathway activation. Collectively, CDP mitigates CTX-induced splenic injury primarily through coupled redox restoration and transcriptional-level immune modulation. Full article

β-carotene has excellent antioxidant and anti-inflammatory activities. However, its poor chemical stability and susceptibility to oxidative degradation strongly limit its practical application. Therefore, encapsulation technology serves as a crucial delivery method to achieve the bioavailability of β-carotene. The study aimed to explore effects of microencapsulated and nanoemulsified β-carotene on antioxidant and anti-inflammatory function in weaned piglets. A total of 147 healthy weaned piglets with similar initial body weight (7.75 ± 0.09 kg) were randomly divided into three groups: control group (CON), microencapsulated β-carotene treatment group (B1) and nanoemulsified β-carotene treatment group (B2). Results showed that the two β-carotene preparations remarkably improved growth performance, antioxidant capacity and immunity of weaned piglets compared with the CON group (p < 0.05). In tissues of liver, jejunum and colon, B1 and B2 groups increased antioxidase activity (CAT, SOD, T-AOC) and concentrations of anti-inflammatory cytokines (IL-2, IL-4, IL-10, IFN-γ), with reduced MDA and pro-inflammatory cytokines (IL-1β, IL-6, IL-12, TNF-α) contents. Both B1 and B2 treatments improved intestinal barrier function and optimized jejunal microbial composition compared with the CON group (p < 0.05). The B2 group exerted far superior antioxidant and anti-inflammatory effects compared with the B1 group (p < 0.001). In conclusion, the nanoemulsion delivery system can improve antioxidant and anti-inflammatory function of β-carotene in weaned piglets compared with the traditional microencapsulated form. Our findings provide a theoretical basis for the popularization and application of nanoemulsified β-carotene to improve the bioavailability of β-carotene. Full article

Long-term crop rotation can improve soil function and crop performance, but it remains unclear whether rotation history can simultaneously alleviate drought-induced oxidative injury in spring wheat leaves and roots. To address this gap, we used a long-term field rotation experiment established in 2016 in the western foothills of the Greater Khingan Mountains. Four cropping systems were selected: spring wheat–potato rotation (R1), spring wheat–potato–rape rotation (R2), spring wheat–rape rotation (R3), and continuous spring wheat cropping (C1). In 2022, wheat occurred naturally in all rotation sequences, and all plots were planted with the same spring wheat cultivar (‘Longmai 36’) to enable comparison among different rotation histories. Drought stress was imposed from late jointing, and at anthesis, ROS-related levels, malondialdehyde (MDA), glutathione (GSH), and proline (Pro), as well as the activities of superoxide dismutase (SOD) and peroxidase (POD), were determined in the flag leaves and roots of spring wheat under normal-water (NC) and drought-stress (HC) conditions. Under drought stress, rotation significantly increased yield (R1 and R2 by 73.3% and 77.7% vs. C1, respectively, partly reflecting the low C1 baseline associated with continuous cropping) and reduced drought-induced accumulation of ROS-related levels and MDA, along with excessive antioxidant and osmotic responses. R1 better protected leaves, while R2 optimized root osmotic regulation. Two-way ANOVA revealed significant drought × rotation interactions for most leaf traits (p < 0.01) but not for root ROS-related levels, SOD, or POD, indicating organ-specific regulation. R1 and R2 show strong drought resilience potential, warranting multi-year, multi-site validation. Full article

Metabolic syndrome (MetS) is a clinical condition defined by the coexistence of interconnected cardiometabolic risk factors, including central obesity, dyslipidemia, elevated blood pressure, and impaired glucose regulation, which collectively increase the risk of type 2 diabetes mellitus and cardiovascular disease. Beyond these clinical diagnostic features, MetS is characterized by complex pathophysiological alterations involving systemic dysregulation of metabolic signaling across adipose tissue, skeletal muscle, liver, vascular endothelium, and the immune system. Key molecular alterations include impaired insulin receptor substrate (IRS)–Akt signaling, chronic nuclear factor kappa B (NF-κB) activation, mitochondrial dysfunction, and oxidative stress. Physical exercise is recognized as a pleiotropic biomedical intervention capable of restoring metabolic homeostasis through coordinated modulation of intracellular signaling pathways and inter-organ communication. Exercise activates AMP-activated protein kinase (AMPK), enhances peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α)-mediated mitochondrial biogenesis, and stimulates nuclear factor erythroid 2-related factor 2 (Nrf2)-dependent antioxidant responses. These adaptations improve glucose uptake, enhance fatty acid oxidation, and reduce ectopic lipid accumulation across metabolically active tissues. At the systemic level, skeletal muscle functions as an endocrine organ by releasing myokines such as irisin, interleukin-6 (IL-6), and fibroblast growth factor 21 (FGF21), which contribute to metabolic regulation across the liver, adipose tissue, and vasculature. These exercise-induced signals promote immune modulation, reduce pro-inflammatory cytokine production, and improve endothelial function. Different exercise modalities including aerobic, resistance, and high-intensity interval training (HIIT) activate both common and modality-specific molecular pathways, supporting individualized exercise strategies. Collectively, exercise targets the multi-organ pathophysiology of MetS and provides a mechanistic foundation for precision exercise medicine in cardiometabolic disease management. Full article

The aim of the study was to synthesize nanocomposites based on cerium orthophosphate stabilized with citrate at different ratios for biomedical applications, and to evaluate its safety in different animal species. Nanocomposites were synthesized using four different initial mass ratios of Ce(NO₃)₃ × 6H₂O to citric acid: 1:5 (Ce:5CA), 1:3 (Ce:3CA), 1:1 (Ce:1CA), and 1:0.5 (Ce:0.5CA). The obtained products were characterized by a series of physicochemical methods including X-ray diffraction, transmission electron microscopy, and IR spectroscopy. Biomedical studies of the sols were performed to evaluate redox activity and their effects on the metabolism and proliferation of human fibroblasts. Safety studies were carried out in different animal species, including determination of the acute toxicity of the selected nanocomposite following application to intact skin and intragastric administration, as well as determination of subchronic toxicity using a model of acute experimental full-thickness skin wounds. According to the physicochemical studies, all synthesized nanocomposites contained nanocrystals with bimodal dimensions (width 3–10 nm, length 15–40 nm) and diffraction peaks characteristic of CePO₄. IR spectroscopy demonstrated the formation of new chemical bonds. Antioxidant activity was observed for the Ce:3CA, Ce:1CA, and Ce:0.5CA samples, being most pronounced for Ce:1–0.5CA, whose antioxidant capacity exceeded that of ascorbic acid. In contrast, Ce:5CA exhibited pro-oxidant activity at all tested concentrations. Biocompatibility with human cells was demonstrated. Ce:0.5CA was identified as the most promising candidate for biomedical applications owing to its highest regenerative and antioxidant potential and its demonstrated safety in animals following topical and intragastric administration, as well as in wound models. Histomorphological examination of the internal organs supported the safety and potential of the developed nanocomposites for skin regeneration and wound healing. Full article

Drug-mediated intravesical therapy is a widely used treatment approach for bladder cancer (BCa), which is limited by poor tumor accumulation and the toxicity of drugs. Herein, a facile approach utilizing magnetic hyperthermia therapy (MHT) for BCa treatment is reported through intravesical instillation of tumor-targeting iron oxide nanoparticles (IONPs), which are coated with anti-FGFR3 antibodies for specific binding to FGFR3 overexpressed on BCa cells. The antibody coating significantly enhanced targeting ability and increased cancer cell uptake. Under an alternating magnetic field (AMF), the IONPs magnetothermally activated TRPV1 on the endoplasmic reticulum (ER) of BCa and induced Ca²⁺ overload in RT4 BCa cells. The magnetothermal treatment significantly upregulated the pro-apoptotic gene expression of Bax, Pro-caspase-3, and Cytc in RT4 cells, and downregulated the anti-apoptotic effector gene Bcl-2, ultimately causing augmented apoptosis in cancer cells. The application of intravesical FGFR3-targeting MHT successfully resulted in greater suppression of tumor growth and improved survival rate of mice, compared to the control, IONP, and AMF-treated groups. These results hold significant potential as a transformative modality toward BCa therapeutic application. Full article

This study aimed to explore the protective mechanism of silybin against heat stress-induced liver injury in Peking ducks as a result of oxidative stress, inflammation, and lipid metabolism. One hundred and ninety-five 1-day-old healthy male Peking ducks with similar body weights were randomly divided into a control group, a heat-stress group, and three intervention groups treated with 400, 800, and 1600 mg/kg silybin under heat-stress from 21 d to 35 d for two weeks. The function indices, oxidative stress, inflammatory factor levels, histopathological changes and non-targeted lipidomic profiling in liver as well as growth performance were evaluated. Results showed that silybin supplementation partially alleviated the heat-stress-induced decreases in average daily feed intake and body weight gain (p > 0.05). Silybin supplementation at 400 and 800 mg/kg significantly reduced the heat-stress-induced increases in alanine aminotransferase (ALT), aspartate aminotransferase (AST), and γ-glutamyl transpeptidase (γ-GGT) (p < 0.05), whereas the effect of 1600 mg/kg silybin was not significant. Albumin (ALB) and globulin (GLB) levels were mainly improved in the 800 mg/kg group, and GLB was also increased in the 400 mg/kg group (p < 0.05). Silybin supplementation significantly improved hepatic antioxidant capacity, especially in the 400 and 800 mg/kg groups, as indicated by increased superoxide dismutase (SOD) activity and total antioxidant capacity (T-AOC), and decreased malondialdehyde (MDA) and reactive oxygen species (ROS) levels (p < 0.05). In addition, the 400 and 800 mg/kg groups showed more significant reductions in the pro-inflammatory factors IL-6 and TNF-α, while IL-10 was increased in silybin-supplemented groups (p < 0.05). Lipid metabolism disorders were improved through regulation of the sphingolipid and glycerophospholipid metabolism pathways, while it alleviated heat stress damage by reducing the expression of heat shock proteins. In conclusion, silybin holds promise as an effective feed additive to alleviate heat stress in poultry. This study provides a theoretical basis and practical approach for improving the health and productive performance of Peking ducks under heat-stress conditions. Full article

Skeletal muscle mitochondria possess the ability to autoregulate their health and functioning by the orchestration of mitochondrial quality control (MQC) pathways. This plasticity allows them to adapt to various stimuli, such as exercise. However, under pathological conditions, mitochondria can become dysfunctional, generating damage-associated molecular patterns (DAMPs), such as reactive oxygen species (ROS) and oxidized mitochondrial DNA (mtDNA). These DAMPs can launch an innate immune response, with consequences of widespread inflammation and atrophy. Integral to this is the NLRP3 inflammasome complex. Activation of the NLRP3 inflammasome results in maturation of caspase-1, which processes pro-inflammatory cytokines IL-1β and IL-18, as well as GSDMD. Consequently, the pore-forming GSDMD-N fragment induces pyroptosis, releasing mature IL-1β and IL-18. Exercise training is widely accepted as a potent mechanism to promote skeletal muscle health, particularly by remodeling the mitochondrial network and reducing the production of DAMPs. It has also been shown promote an anti-inflammatory milieu with the release of various myokines. Indeed, the potential of exercise to mitigate NLRP3 inflammasome-mediated inflammation and atrophy is promising. This review will examine the mechanisms underpinning inflammasome priming and activation, as well the effects of exercise, with an emphasis on the skeletal muscle. Full article

Plastic contamination (plastamination) has become a pervasive environmental threat with growing implications for human health. Among plastic-derived contaminants, micro- and nano-plastics (MNPs) are of particular concern due to their persistence, widespread distribution, and capacity to interact with biological systems. Humans are exposed to MNPs through ingestion, inhalation, dermal contact, and maternal transfer, and these particles can cross biological barriers, including the blood–brain barrier, reaching the central nervous system. MNPs disrupt cellular homeostasis by inducing oxidative stress, mitochondrial dysfunction, and inflammation. In the brain, these processes drive glial activation and chronic neuroinflammation, which are closely associated with neuronal damage and neurological disorders, including Parkinson’s disease (PD). MNPs can also affect systemic pathways such as the gut–brain axis (GBA) and neuroendocrine regulation, suggesting broader physiological consequences. This narrative review synthesizes current evidence on the neurotoxic and pro-inflammatory potential of MNPs. Since MNPs may promote the aggregation of proteins implicated in neurodegeneration, such as alpha-synuclein, their possible role in PD is discussed. Despite several knowledge gaps, MNPs may be emerging environmental risk factors for brain health and neurodegenerative diseases such as PD. Nevertheless, there is a need for further studies in the field, standardized methodologies and longitudinal studies to implement effective mitigation strategies. Full article

Obesity-related complications have long been significant risk factors threatening human health. Sanhua tea is an instant tea composed of Rosa rugosa Thunb., Jasminum sambac (L.) Ait., Citrus aurantium L. var. amara Engl., Nelumbo nucifera Gaertn., and Ligusticum chuanxiong Hort. This study aimed to investigate the protective effects and underlying mechanisms of Sanhua tea in obese mice. An obesity model was established by feeding C57BL/6J mice a high-fat diet. Mice received intragastric Sanhua tea at doses (500, 1500, and 2500 mg/kg/day) for three weeks. Biochemical analyses indicated that Sanhua tea significantly reduced total cholesterol, triglyceride, low-density lipoprotein cholesterol, and pro-inflammatory cytokine levels in serum. Sanhua tea also alleviated liver oxidative stress by reducing malondialdehyde levels and regulating the activities of related enzymes. Additionally, Sanhua tea maintained gut microbiota diversity and reshaped microbial composition, reducing the Firmicutes/Bacteroidota ratio, increasing beneficial bacterial communities, and significantly decreasing harmful bacterial communities. Metabolomics analysis revealed that Sanhua tea altered liver metabolites, which were significantly associated with specific gut microbes. These metabolites influenced pathways such as ABC transporters, general metabolic pathways, and central carbon metabolism in cancer, contributing to obesity alleviation. In conclusion, Sanhua tea alleviated obesity symptoms in mice by modulating blood lipid levels, liver metabolism, and gut microbiota. Full article