Search Results (1,304)

The optimization of bioactive compound extraction from medicinal herbs is critical for developing functional food ingredients with substantiated health benefits. This study employed response surface methodology (RSM) and partial least squares (PLS) regression to maximize polyphenol recovery and antioxidant capacity from five medicinal herbs (Helichrysum stoechas, Chelidonium majus, Mentha pulegium, Artemisia absinthium, and Adiantum capillus-veneris). A custom experimental design assessed the effects of herb identity, extraction technique, and solvent-to-solid ratio on total polyphenolic content (TPC), total flavonoid content (TFC), ferric reducing antioxidant power (FRAP), and DPPH radical scavenging activity. The PLS compromise optimum was identified for M. pulegium using 60% ethanol at 55 mL/g, yielding 37.54 ± 2.10 mg GAE/g dw TPC, 21.62 ± 1.15 mg RtE/g dw TFC, 334.38 ± 12.37 µmol AAE/g dw FRAP, and 262.67 ± 9.46 µmol AAE/g dw DPPH. HPLC-DAD profiling revealed 18 polyphenolic compounds (10.22 ± 0.34 mg/g dw), dominated by kaempferol-3-O-β-rutinoside, protocatechuic acid, and luteolin-7-O-glucoside. These compounds contribute complementary mechanisms: protocatechuic acid modulates oxidative and antioxidant pathways, kaempferol-3-O-β-rutinoside exerts cardioprotective and anti-inflammatory effects via VEGF-C binding, and luteolin-7-O-glucoside suppresses NF-κB-mediated inflammatory signaling. Principal component analysis (PCA) explained 84.8% of variance, clearly separating optimized from non-optimized extracts, while PLS confirmed strong correlations between specific phenolics and antioxidant indices. Overall, this integrated chemometric approach demonstrates that data-driven optimization can deliver phenolic-rich herbal extracts with robust and balanced antioxidant potential for functional food applications. Full article

Dynamic environmental changes significantly affect trace element balance and exposure to toxic metals, influencing vascular homeostasis. The endothelium, as a key regulator of vascular tone and inflammation, is highly sensitive to fluctuations in micronutrient and heavy metal concentrations. This review summarizes current evidence on the molecular mechanisms by which essential trace elements, such as zinc, selenium, copper, and magnesium, support endothelial function through antioxidant defense, nitric oxide regulation, and anti-inflammatory signaling. Conversely, exposure to heavy metals including cadmium, lead, mercury, and arsenic induces oxidative stress, disrupts nitric oxide bioavailability, and promotes endothelial dysfunction, accelerating the pathogenesis of many diseases. The paper examines how these alterations contribute to the development of major cardiovascular diseases and outlines preventive measures to reduce associated risks. Understanding these interactions is crucial for society’s health amid growing environmental challenges. Full article

Infertility affects around 10–15% of couples worldwide, out of which male factor contributes to 30–50% of cases of infertility. Oxidative stress, which corresponds to an imbalance between antioxidant capacities and reactive oxygen species, is considered a leading cause of male infertility. Therefore, the ability to monitor antioxidant capacity in seminal fluid is critical as it sustains free radical balance in the sperm. Most currently available methods to assess antioxidant capacity in seminal fluid are time-consuming, require specialized equipment, or are not easily implemented in clinical routine practice. Here, we evaluate the applicability of an electrochemical approach to determine the antioxidant capacity of human seminal fluid. We show that the results of this electrochemical approach are comparable to those of two reference methods for evaluating free radical scavenging activity, namely 2,20-azino-bis-3-ethylbenzothiazoline-6-sulfonic acid (ABTS) and 2,2-diphenyl-1-picrylhydrazyl (DPPH), when measuring the antioxidant capacity of seminal plasma or antioxidant molecules such as 6-hydroxy-2,5,7,8-tetramethylchromane-2-carboxylic acid (Trolox), ascorbic acid and uric acid. Furthermore, we demonstrate the applicability of the method for the assessment of the antioxidant capacity of seminal fluid isolated from 30 normozoospermic patients (528.2 ± 142 nW). Further analysis demonstrates a positive correlation between the antioxidant capacity measured through the electrochemical approach and sperm concentration. Overall, this electrochemical approach provides a fast and accurate assessment of total antioxidant capacity in human seminal fluid. It may be implemented as a complementary tool in the routine evaluation of male infertility. Full article

Background: d-Limonene (LIM) is a food-derived monoterpenoid phytocompound predominantly found in citrus peels, endowed with potent antioxidant and anti-inflammatory properties, and has been reported to inhibit xanthine oxidase (XO) activity in vitro. This study investigated the dose-sparing efficacy of this dietary bioactive compound in combination with low-dose allopurinol (ALP) using a dual rat model combining potassium oxonate (PO)-induced hyperuricemia and monosodium urate (MSU)-triggered gouty arthritis, thereby capturing both metabolic and inflammatory dimensions of gout. Methods: Female Wistar rats were PO-primed and MSU-challenged, then treated with LIM (50 mg/kg), ALP (5 or 10 mg/kg), or LIM + ALP. Outcomes included paw thickness, dysfunction and inflammation indices, serum uric acid, urea, creatinine, AST/ALT, cytokines (IL-1β, TNF-α, IL-6), oxidative stress markers (MDA, SOD, catalase, GSH), and NLRP3 immunoreactivity, supported by radiographic and histopathological analyses. Data were analyzed by one-way ANOVA with Tukey’s post hoc test. Results: LIM improved clinical and biochemical outcomes versus monotherapies. However, LIM + low-dose ALP exhibited the greatest overall efficacy. On Day 30, paw thickness was significantly lower with LIM + ALP than with LIM alone (3.25 ± 0.31 vs. 3.98 ± 0.72 mm; p < 0.001). Serum uric acid and hepatic transaminases declined most with the combination (p < 0.0001 vs. LIM), accompanied by improved renal indices (p < 0.001). Pro-inflammatory cytokines were markedly reduced, NLRP3 immunostaining was minimal, and oxidative balance shifted toward homeostasis (↓ MDA; ↑ SOD, catalase, GSH). Radiographic and histological evaluations corroborated attenuation of joint inflammation and tissue damage. Conclusions: In the PO + MSU gout model, co-administration of the food-derived compound LIM with low-dose ALP achieved additive, dose-sparing benefits across metabolic, inflammatory, and histological endpoints. While in vivo XO activity was not directly assessed, the findings are consistent with XO-pathway modulation, NLRP3–IL-1β suppression, and redox restoration. These results highlight the potential of dietary bioactives such as d-Limonene to complement standard urate-lowering therapy, warranting further pharmacokinetic and safety validation. Full article

Aflatoxin B₁ (AFB₁), a major metabolite of aflatoxin, is a highly toxic carcinogen. It frequently contaminates feed due to improper storage of feed ingredients such as corn and peanut meal, with the contamination risk further escalating alongside the increasing incorporation of plant-based proteins in feed formulations. Upon entering an organism, AFB₁ is metabolized into highly reactive derivatives, which trigger an oxidative stress-inflammation vicious cycle by binding to biological macromolecules, damaging cellular structures, activating apoptotic and inflammatory pathways, and inhibiting antioxidant systems. This cascade leads to stunted growth, impaired immunity, and multisystem dysfunction in animals. Long-term accumulation can also compromise reproductive function, induce carcinogenesis, and pose risks to human health through residues in the food chain. Tannins are natural polyphenolic compounds widely distributed in plants which exhibit significant antioxidant and anti-inflammatory activities and can effectively mitigate the toxicity of AFB₁. They can repair intestinal damage by increasing the activity of antioxidant enzymes and up-regulating the gene expression of intestinal tight junction proteins, regulate the balance of intestinal flora, and improve intestinal structure. Meanwhile, tannins can activate antioxidant signaling pathways, up-regulate the gene expression of antioxidant enzymes to enhance antioxidant capacity, exert anti-inflammatory effects by regulating inflammation-related signaling pathways, further reduce DNA damage, and decrease cell apoptosis and pyroptosis through such means as down-regulating the expression of pro-apoptotic genes. This review summarizes the main harm of AFB₁ to animals and the mitigating mechanisms of tannins, aiming to provide references for the resource development of tannins and healthy animal farming. Full article

Metabolic syndrome (MetS) and its associated conditions, namely, type 2 diabetes mellitus (T2DM), non-alcoholic fatty liver disease (NAFLD), obesity, and polycystic ovary syndrome (PCOS) are characterized by insulin resistance, dyslipidemia, and low-grade inflammation. Curcumin, a polyphenolic compound derived from Curcuma longa Linn., exhibits pleiotropic metabolic and anti-inflammatory properties and has thus been evaluated as a nutraceutical intervention for these conditions, but findings remain inconsistent. This systematic review and meta-analysis evaluated the clinical efficacy of Curcuma longa supplementation on anthropometric, glycemic, lipid, inflammatory, and oxidative stress parameters in adults with MetS or related disorders. A comprehensive search of databases (PubMed, Scopus, AMED, LILACS, and Google Scholar) identified 104 eligible randomized controlled trials (RCTs). The included trials primarily assessed standardized oral turmeric/curcumin supplements and bioavailability-enhanced formulations rather than whole culinary turmeric. Pooled standardized mean differences (SMDs) with 95% confidence intervals (CIs) were computed using random-effects models. Subgroup analyses were conducted by disease category, dose, and formulation. Risk of bias was assessed using the Cochrane RoB 2 tool. Curcumin supplementation significantly reduced fasting blood sugar (SMD = −0.54, 95% CI −0.72 to −0.36) and HbA1c (SMD = −0.41, 95% CI −0.60 to −0.23) in T2DM; decreased triglycerides (SMD = −0.48; 95% CI: −0.70 to −0.25), and LDL cholesterol (SMD = −0.39; 95% CI: −0.59 to −0.18) while elevating HDL cholesterol (SMD = 0.45; 95% CI: 0.25 to 0.65) and total antioxidant capacity (SMD = 0.73; 95% CI: 0.51 to 0.94). Curcuma longa also attenuated systemic inflammation, lowering C-reactive protein (SMD = −0.62; 95% CI: −0.81 to −0.43), TNF-α (SMD = −0.57; 95% CI: −0.80 to −0.34), and IL-6 (SMD = −0.50; 95% CI: −0.70 to −0.29). Heterogeneity was moderate-to-high, reflecting some differences in the formulation, dosage, and duration. Collectively, these findings affirm that Curcuma longa exerts measurable, clinically relevant improvements on glycemic regulation, lipid metabolism, and inflammatory−oxidative balance, supporting its role as a nutraceutical adjunct in metabolic health management, while its bioavailability-enhanced formulations show superior efficacy. Larger, long-term, multicenter RCTs are warranted to confirm durability, optimal dosing, and safety. Full article

Idiopathic nephrotic syndrome (INS) is the most prevalent glomerular illness in children. Even while immunologic processes are well-established, oxidative stress is becoming more widely acknowledged as a significant factor in the etiopathogenesis of illness. Assessing its activity and treatment response may be made easier with the use of trustworthy, non-invasive indicators to track redox balance. We report on the oxidative stress levels of a 10.7-year-old boy with INS with five clinical time points in one year. The FRAS5 analyzer was used to calculate the oxidative stress index (OSI), plasma antioxidant capacity (PAT) and derivatives of reactive oxygen metabolites (d-ROMs) as biomarkers. A 4-tier oxidative state classification scheme based on d-ROM and PAT thresholds was used to interpret the values. The patient had low antioxidant defense, moderate oxidative and increased OSI at relapses, a positive transition to reduced oxidative burden and enhanced defense during remission. The order of events showed a dynamic redox response associated with glucocorticoid (GC) medication and disease activity. The potential value of d-ROM, PAT, and OSI as dynamic biomarkers for tracking disease activity, response to treatment and residual oxidative burden in pediatric INS is supported by this case. To confirm their function in more comprehensive clinical decision-making, more research is required. Full article

Chaenomeles speciosa (Sweet) Nakai (CF), a traditional food in East Asia and a recent addition to clinical dietary recommendations, has demonstrated potential for managing hyperuricemia. However, its bioactive components and therapeutic mechanisms remain largely unexplored. In this study, we used an integrative approach incorporating serum pharmacochemistry, metabolomics, bioinformatics, molecular docking, and in vitro/vivo validation to investigate CF’s effects and mechanisms in hyperuricemia. In hyperuricemic mice, CF significantly reduced serum uric acid, creatinine, and blood urea nitrogen (BUN) levels, improved kidney histopathology, and restored redox balance by increasing antioxidant enzyme activities (SOD and GSH-Px) while lowering malondialdehyde (MDA) levels. Metabolomic analysis revealed that CF modulated pathways associated with oxidative stress, including purine metabolism, arachidonic acid metabolism, and α-linolenic acid metabolism, to reverse hyperuricemia-associated metabolic perturbations. Correlation analysis between differential metabolites and serum-absorbed constituents identified androsin, cynaroside, and salicin as potential bioactive compounds. These compounds showed high predicted binding affinities to COX-1, PGE2, and XOD in molecular docking, and these interactions were validated by in vitro assays, where the compounds effectively suppressed inflammatory cytokine production and inhibited XOD activity. Overall, CF exerts anti-hyperuricemic and renoprotective effects through coordinated regulation of purine metabolism, inflammation, and oxidative stress, supporting its potential as a functional food or complementary therapy for hyperuricemia-related conditions. Full article

In this research, we sought to methodically examine the protective effects of Gastrodia elata extract (GEE) on liver damage induced by D-galactose (D-gal) in mice and clarify the underlying mechanisms. The chemical composition of GEE was characterized using Ultra-Performance Liquid Chromatography–Tandem Mass Spectrometry (UPLC-MS/MS), while network pharmacology analysis was employed to predict potential molecular targets and signaling pathways. A mouse model of liver injury was established through daily intraperitoneal injection of D-gal over a 42-day period, during which the hepatoprotective efficacy of GEE was evaluated. Biochemical, histopathological, and molecular analyses were subsequently performed. UPLC-MS/MS identified ingredients such as amino acids, aromatic compounds, fatty acids, and terpenoids in GEE. A network pharmacology analysis enabled the identification of 272 common targets linked to GEE and liver damage, demonstrating notable enrichment within the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway. In vivo experiments demonstrated that GEE effectively alleviated D-gal-induced body weight loss and elevated liver index values, alleviated hepatic histological damage, and reduced serum levels of Alanine Aminotransferase (ALT), Aspartate Aminotransferase (AST), and Alkaline Phosphatase (ALP). Furthermore, GEE enhanced the activities of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT), decreased malondialdehyde (MDA) levels, and downregulated the mRNA expression of the pro-inflammatory cytokines Interleukin-6 (IL-6), Interleukin-1 beta (IL-1β), and Tumor Necrosis Factor-alpha (TNF-α). Western blot analysis confirmed that GEE activated the PI3K/Akt pathway, as evidenced by increased ratios of phosphorylated Phosphatidylinositol 3-kinase/Phosphatidylinositol 3-kinase (p-PI3K/PI3K) and phosphorylated AKT/Protein Kinase B (p-AKT/AKT); restored the B-cell lymphoma 2-associated X protein/B-cell lymphoma-2 (Bax/Bcl-2) balance; and reduced cyclin-dependent kinase inhibitor 1 (p21) expression. The results suggest that GEE protects against D-gal-induced liver damage by reducing oxidative stress, inhibiting inflammatory responses, and modulating apoptosis through the activation of the PI3K/Akt signaling pathway, providing support for its potential use in hepatoprotection. Full article

Background/Objectives: Capsanthin is a xanthophyll carotenoid from Capsicum species with an extended conjugated polyene chain that underlies both its orange–red color and strong antioxidant potential. In this study, we investigated whether capsanthin protects RA-differentiated SH-SY5Y neuron-like cells against glutamate-induced stress. Methods: Neuronal dysfunction was induced by glutamate exposure, and capsanthin treatment was evaluated using cell viability, reactive oxygen species (ROS) production, antioxidant defense markers, inflammatory cytokines, mitochondrial energy status, and apoptosis-related endpoints. Antioxidant responses were assessed using superoxide dismutase, catalase, glutathione peroxidase activities, and total antioxidant capacity. Cytokine release (TNFα, IL-6, IL-8, IL-4, IL-10) was quantified by ELISA. Mitochondrial function was monitored using ATP content. Apoptosis-associated genes (BAX, BCL-2, CASP3, and CASP9) were analyzed using SYBR Green-based RT-qPCR, complemented by caspase-9 ELISA and caspase-3 Western blotting. Results: Glutamate increased oxidative stress and shifted the cytokine profile toward a pro-inflammatory state, accompanied by reduced ATP levels and a pro-apoptotic transcriptional pattern. Capsanthin significantly attenuated glutamate-induced ROS production, stabilized antioxidant enzyme activities and total antioxidant capacity, reduced pro-inflammatory cytokines while supporting anti-inflammatory signaling, and preserved ATP levels. Conclusions: Overall, capsanthin mitigated excitotoxic stress by maintaining redox balance, limiting inflammatory responses, and protecting mitochondrial energy metabolism in neuron-like cells, supporting its potential as a neuroprotective candidate for glutamate-induced neuronal stress. Full article

Nano-biochar (n-BC) is an emerging eco-friendly material with potential to improve crop performance under salt stress. This study aimed to evaluate the effects of foliar applications of bamboo-derived n-BC on the morphological and biochemical responses of lettuce plants under salt stress (40 mM NaCl). n-BC solutions (1.0, 3.0, and 5.0% w/v) were foliar-applied every five days until harvest. Salt stress markedly increased hydrogen peroxide (H₂O₂) and malondialdehyde (MDA) by 264.54% and 14.02%, disrupted Na⁺/K⁺ homeostasis, and reduced biomass. Foliar n-BC mitigated these effects by reducing Na⁺ accumulation by 22.24–25.11% and enhancing K⁺, Ca²⁺, and Mg²⁺ uptake. The treatments also improved photosynthetic pigments and increased proline, soluble proteins, and soluble sugars. Oxidative damage was alleviated, as reflected by reductions in H₂O₂ and MDA together with enhanced ascorbate peroxidase, catalase, and superoxide dismutase activities. Total phenolics, flavonoids, and ABTS and DPPH scavenging activities also increased under n-BC application. Among all the concentrations, 3.0% (w/v) n-BC consistently produced the greatest improvements in growth, ionic balance, and antioxidant responses. These findings demonstrate that bamboo-derived n-BC is a promising foliar biostimulant for enhancing lettuce performance under saline conditions. Full article

Vitamin E and lutein both belong to food functional factors, which have cytoprotective potential and antioxidant effects. However, mechanism details at cell level remain scarce. In this study, HepG2 cells were utilized to inquire and compare the ameliorative effects of vitamin E and lutein under H₂O₂-induced oxidative stress through a combined transcriptomic and metabolomic profiling, in addition to physiology and biochemistry determination. Cell cytotoxicity caused by H₂O₂ was ameliorated by vitamin E or lutein as evidenced by elevating cell viability and balancing the redox system. Vitamin E had greater efficacy on ameliorating oxidative cytotoxicity than lutein. Transcriptome data revealed that differentially expressed genes were mainly enriched in the transport-related, enzyme-related, and oxidative stress-related GO terms with vitamin E pretreatment. Extracellular organization-related, biological process-related, and apoptosis-related GO terms were meaningfully enriched with lutein pretreatment. Metabolome data showed that with vitamin E ameliorative effects, the disturbed metabolic pathways included thiamine metabolism, vitamin digestion and absorption, and ABC transporters. With lutein ameliorative effects, KEGG pathway analysis showed enrichment of amino sugar and nucleotide sugar metabolism, pyrimidine metabolism, and starch and sucrose metabolism. Collectively, our study provides essential insights into utilization of vitamin E and lutein as a potential supplement for effective therapy of disease associated with oxidative stress. Full article

Objective: This study aimed to apply the Random Forest machine learning model using oxidative stress biomarkers to classify breast cancer status and assess sentinel lymph node (SLN) metastasis, a pathology of high incidence and mortality that represents a major public health challenge. Methods: The breast cancer classification cohort included 188 women with infiltrating ductal carcinoma and 78 healthy volunteers. For SLN metastasis assessment, a subset of 29 women with metastases and 57 controls (n = 86) was used. Data preprocessing and the SMOTE technique were applied to balance the classes in the metastasis set, achieving a perfect balance of 171 examples (57 per class). Random Forest model with a leave-one-out validation strategy was employed and oxidative stress biomarkers (e.g., lipid peroxidation, total antioxidant capacity, superoxide dismutase, catalase, glutathione peroxidase) were used. Results: The model achieved high accuracy (0.996) in classifying breast cancer, representing a substantial improvement over current screening methods such as mammography. In contrast, its performance in detecting SLN metastases was more limited (accuracy = 0.854), likely reflecting the inherent complexity and heterogeneity of the metastatic process. Moreover, these estimates derive from a retrospective case–control cohort and should not be viewed as a substitute for, or a direct comparison with, population-based mammography screening, which would require dedicated prospective validation. Conclusions: The findings underscore the model’s robust performance in distinguishing women with breast cancer from healthy volunteers, but highlight significant gaps in its ability to diagnose metastatic disease. Future research should integrate additional biomarkers, longitudinal data, and explainable artificial intelligence (XAI) methods to improve clinical interpretability and accuracy in metastasis prediction, moving towards precision medicine. Full article

Nuclear factor erythroid 2-related factor 2 (NRF2) orchestrates redox balance, metabolism, and cellular stress responses, acting as both a tumor suppressor and promoter depending on the disease stage. In advanced cancers, persistent NRF2 activation—through KEAP1/NFE2L2 mutations or oxidative adaptation—drives epithelial-to-mesenchymal transition, metabolic reprogramming, and immune evasion, promoting tumor invasion (T) and metastasis (M). Recent pharmacologic efforts seek to exploit this duality. NRF2 inhibitors such as brusatol, halofuginone, and ML385 suppress NRF2 transcriptional activity or disrupt DNA binding, reducing motility, invasion, and metastatic dissemination in preclinical models. In contrast, NRF2 activators, such as bardoxolone methyl (CDDO-Me), sulforaphane, and dimethyl fumarate, exhibit chemopreventive effects by enhancing detoxification and mitigating oxidative DNA damage during early tumorigenesis. Furthermore, metabolic interventions, such as glutaminase or G6PD inhibitors, target NRF2-driven anabolic and antioxidant pathways essential for metastatic fitness. Therefore, understanding the temporal and contextual effects of NRF2 signaling is crucial for therapeutic design. The aim of this review is to examine how pharmacological modulation of NRF2 influences the invasive and metastatic dimensions of tumor progression, in addition to discussing its potential integration into TNM-based prognostic and treatment frameworks. Full article

Inflammatory bowel disease is characterised by chronic mucosal inflammation, oxidative stress, and impaired epithelial barrier function. Current therapies primarily suppress inflammation but do not effectively restore epithelial integrity. In this study, we established in vitro cell cultures of Vitis labrusca var. Isabella to obtain juices that were chemically characterised and assessed for antioxidant and anti-inflammatory activities in human intestinal epithelial cell lines (i.e., Caco-2). Chemical analysis revealed variable levels of stilbenoids, including trans-resveratrol and resveratrol diglucosides depending on culture conditions. The suspension-derived juice grown in darkness (SVMD) significantly reduced lipopolysaccharide-induced IL-1β and TNF-α release and mitigated oxidative stress in Caco-2 cells by lowering levels of intracellular reactive oxygen species. In Caco-2 monolayers infected with Salmonella enterica, SVMD preserved transepithelial electrical resistance, indicating protection of epithelial barrier integrity, without exerting direct antibacterial effects. These findings demonstrate that V. labrusca cell-culture juices exert potent antioxidant and anti-inflammatory actions and promote epithelial protection through modulation of redox balance. Overall, this study highlights the potential of sustainable cell-culture-derived materials as promising natural products for supporting intestinal homeostasis and managing gut inflammatory disorders. Full article