AntioxidantsPub Date : 2025-06-17DOI: 10.3390/antiox14060745
Ahyeong Yun, Hwa Yong Oh, Tae Hoon Lee, Da Ye Kang, Ki-Tae Kim, Hyun-Soo Kim, Hee Sung Kim
{"title":"Blood Orange (<i>Citrus sinensis</i> L. Osbeck) Juice By-Product Extract as a Functional Feed Additive: Effects on Growth Performance, Digestive Enzyme Activity, Antioxidant Status, Immune Parameters, and Disease Resistance Against <i>Vibrio harveyi</i> in Juvenile Black Rockfish (<i>Sebastes schlegelii</i>).","authors":"Ahyeong Yun, Hwa Yong Oh, Tae Hoon Lee, Da Ye Kang, Ki-Tae Kim, Hyun-Soo Kim, Hee Sung Kim","doi":"10.3390/antiox14060745","DOIUrl":"10.3390/antiox14060745","url":null,"abstract":"<p><p>This study evaluated the antibacterial activity and residual functional compounds of blood orange (<i>Citrus sinensis</i> L. Osbeck) juice by-product extract (BJBE). The effects of dietary BJBE on growth performance, digestive enzyme activity, antioxidant status, immune parameters, and disease resistance against <i>Vibrio harveyi</i> were examined in juvenile black rockfish (<i>Sebastes schlegelii</i>). In total, 630 juvenile rockfish were randomly assigned to 21 rectangular tanks (50 L) for a feeding trial, with 30 fish per tank in triplicate. Seven isonitrogenous and isolipidic experimental diets were formulated with BJBE at 0 (control, BJBE0), 0.1 (BJBE0.1), 0.2 (BJBE0.2), 0.3 (BJBE0.3), 0.5 (BJBE0.5), 0.7 (BJBE0.7), and 1.0 (BJBE1) g kg<sup>-1</sup>. A disk diffusion assay confirmed BJBE's strong antibacterial efficacy against <i>V</i>. <i>harveyi</i>. After an 8-week feeding trial, fish fed BJBE0.7 and BJBE1 exhibited significantly a greater final weight, weight gain, and specific growth rate compared with those fed BJBE0. Feed efficiency was significantly higher in fish fed BJBE0.7 than in those fed BJBE0. The protein efficiency ratio was significantly higher in fish fed BJBE0.3, BJBE0.5, BJBE0.7, and BJBE1 relative to those fed BJBE0. Intestinal amylase activity was significantly higher in fish fed BJBE0.7 and BJBE1 compared with those fed BJBE0, and trypsin activity was significantly higher in BJBE0.7-fed fish than in BJBE0-fed fish. In comparison to the BJBE0 diet, the plasma superoxide dismutase, catalase, and glutathione levels of fish fed BJBE0.7 and BJBE1 diets were significantly higher. Lysozyme activity and immunoglobulin M level in fish fed BJBE0.7 and BJBE1 were significantly higher than that in fish fed BJBE0. After a challenge with <i>V</i>. <i>harveyi</i>, disease resistance was significantly higher in fish fed BJBE0.5, BJBE0.7, and BJBE1 compared with those fed BJBE0. Overall, 0.7-1.0 g kg<sup>-1</sup> is proposed as the optimal dietary BJBE inclusion level for enhancing growth performance, digestive enzyme activity, antioxidant status, immune parameters, and disease resistance against <i>V</i>. <i>harveyi</i> infection in juvenile black rockfish.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 6","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189218/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Transcriptomic Redox Dysregulation in a Rat Model of Metabolic Syndrome-Associated Kidney Injury.","authors":"Chien-Lin Lu, Yi-Yun Wang, Yih-Jeng Tsai, Hsuan-Ting Chen, Ming-Chieh Ma, Wen-Bin Wu","doi":"10.3390/antiox14060746","DOIUrl":"10.3390/antiox14060746","url":null,"abstract":"<p><p>Metabolic syndrome (MetS), characterized by obesity, insulin resistance, and dyslipidemia, is a major risk factor for renal injury. Oxidative stress (OxS) plays a pivotal role in its progression; however, the underlying molecular mechanisms are not fully understood. In this study, we established a rat model of MetS using a high-fat diet combined with a single-dose streptozotocin injection in male Wistar rats. MetS rats exhibited systemic OxS, evidenced by elevated circulating levels of free oxygen radicals and decreased antioxidant defense capacity, as well as hypertension, renal lipid peroxidation, glomerular hyperfiltration, and renal tubular injury. Transcriptomic profiling of renal tissue revealed significant downregulation of six OxS-related genes: C-C motif chemokine ligand 5 (CCL5), glutamate-cysteine ligase catalytic subunit, glutathione peroxidase 6, recombination activating gene 2, NAD(P)H: quinone oxidoreductase 1, and selenoprotein P-1. Among these downregulated genes, CCL5 was further confirmed to be repressed at both mRNA and protein levels across intrarenal and systemic compartments. Given its documented functions in immune signaling and redox homeostasis, CCL5 downregulation may contribute to enhanced oxidative damage in MetS-associated renal injury. These findings highlight the role of redox gene dysregulation in the pathogenesis of MetS-related kidney disease and support the potential of CCL5 as a biomarker for oxidative renal injury.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 6","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189155/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
AntioxidantsPub Date : 2025-06-17DOI: 10.3390/antiox14060747
Yaroslav R Nartsissov, Irena P Seraya
{"title":"A Theoretical Analysis of the Effects That the Glycocalyx and the Internal Elastic Lamina Have on Nitric Oxide Concentration Gradients in the Arterial Wall.","authors":"Yaroslav R Nartsissov, Irena P Seraya","doi":"10.3390/antiox14060747","DOIUrl":"10.3390/antiox14060747","url":null,"abstract":"<p><p>Nitric oxide (NO) is a well-known member of the reactive oxygen species (ROS) family. The extent of its concentration influences whether it produces beneficial physiological effects or harmful toxic reactions. In a blood system, NO is generally produced by nitric oxide synthase (NOS) in the endothelium. Then, it diffuses into the smooth muscle wall causing a vasodilatation, and it can also be diluted in a lumen blood stream. In the present study, we analyzed a convectional reaction-diffusion of NO in a 3D digital phantom of a short segment of small arteries. NO concentrations were analyzed by applying numerical solutions to the boundary problems, which included the Navier-Stokes equation, Darcy's law, varying consumption of NO, and the dependence of NOS activity on shear stress. All the boundary problems were evaluated using COMSOL Multiphysics software ver. 5.5. The role of two diffusive barriers surrounding the endothelium producing NO was theoretically proven. When the eNOS rate remains unchanged, an increase in the fenestration of the internal elastic lamina (IEL) and a decrease in the diffusive permeability of a thin layer of endothelial surface glycocalyx (ESG) lead to a notable rise in the NO concentration in the vascular wall. The alterations in pore count in IEL and the viscosity of ESG are considered to be involved in the physiological and pathological regulation of NO concentrations.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 6","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189559/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Aerobic Exercise Alleviates Cardiac Dysfunction Correlated with Lipidomics and Mitochondrial Quality Control.","authors":"Kunzhe Li, Sujuan Li, Hao Jia, Yinping Song, Zhixin Chen, Youhua Wang","doi":"10.3390/antiox14060748","DOIUrl":"10.3390/antiox14060748","url":null,"abstract":"<p><p>Cardiac adaptations induced by aerobic exercise have been shown to reduce the risk of cardiovascular disease, and the autonomic nervous system is closely associated with the development of cardiovascular disease. Aerobic exercise intervention has been shown to enhance cardiac function and mitigate myocardial fibrosis and hypertrophy in heart failure mice. Further insights reveal that cardiomyocytes experiencing chronic heart failure undergo modifications in their lipidomic profile, including remodeling of multiple myocardial membrane phospholipids. Notably, there is a decrease in the total content of cardiolipin, as well as in the levels of total lysolipid CL and the CL (22:6). These alterations disrupt mitochondrial quality control processes, leading to abnormal expressions of proteins such as Drp1, MFN2, OPA1, and BNIP3, thereby resulting in a disrupted mitochondrial dynamic network. Whereas aerobic exercise ameliorated mitochondrial damage to a large extent by activating parasympathetic nerves, this beneficial effect was accomplished by modulating myocardial membrane phospholipid remodeling and restoring the mitochondrial dynamic network. In conclusion, aerobic exercise activated the parasympathetic state in mice and attenuated lipid peroxidation and oxidative stress injury, thereby maintaining mitochondrial dynamic homeostasis and improving cardiac function.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 6","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189445/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
AntioxidantsPub Date : 2025-06-16DOI: 10.3390/antiox14060740
Violeta Cepeda, Marina Ródenas-Munar, Silvia García, Cristina Bouzas, Josep A Tur
{"title":"Unlocking the Power of Magnesium: A Systematic Review and Meta-Analysis Regarding Its Role in Oxidative Stress and Inflammation.","authors":"Violeta Cepeda, Marina Ródenas-Munar, Silvia García, Cristina Bouzas, Josep A Tur","doi":"10.3390/antiox14060740","DOIUrl":"10.3390/antiox14060740","url":null,"abstract":"<p><p>Magnesium plays a crucial role in over 300 enzymatic reactions related to energy production, muscle contraction, and nerve function. Given its essential biological functions and increasing prevalence of suboptimal intake, magnesium supplementation has gained attention for its potential health benefits, particularly in mitigating oxidative stress and inflammation. This systematic review and meta-analysis aimed to evaluate the antioxidant effects of dietary and supplemental magnesium on several biomarkers related to oxidative stress and inflammation. A systematic search of studies published from 2000 to 2025 identified 28 relevant articles, including both animal and human studies. The meta-analysis assessed the effects of magnesium supplementation on oxidative stress biomarkers such as nitric oxide (NO), total antioxidant capacity (TAC), malondialdehyde (MDA), glutathione (GSH), and C-reactive protein (CRP). While results showed a statistically significant reduction in CRP levels, suggesting an anti-inflammatory effect, no conclusive impact on oxidative stress biomarkers was observed. The findings highlight magnesium's potential role in inflammation regulation, though its direct antioxidant effects remain uncertain. Further high-quality clinical trials are needed to clarify the impact of magnesium supplementation on oxidative stress and to explore its broader health implications.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 6","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189353/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
AntioxidantsPub Date : 2025-06-16DOI: 10.3390/antiox14060741
José Manuel Romero-Domínguez, Paula Cilleros-Holgado, David Gómez-Fernández, Rocío Piñero-Pérez, Diana Reche-López, Ana Romero-González, Mónica Álvarez-Córdoba, Alejandra López-Cabrera, Marta Castro De Oliveira, Andrés Rodríguez-Sacristán, Susana González-Granero, José Manuel García-Verdugo, Angeles Aroca, José A Sánchez-Alcázar
{"title":"Mitochondrial Unfolded Protein Response (mtUPR) Activation Improves Pathological Alterations in Cellular Models of Ethylmalonic Encephalopathy.","authors":"José Manuel Romero-Domínguez, Paula Cilleros-Holgado, David Gómez-Fernández, Rocío Piñero-Pérez, Diana Reche-López, Ana Romero-González, Mónica Álvarez-Córdoba, Alejandra López-Cabrera, Marta Castro De Oliveira, Andrés Rodríguez-Sacristán, Susana González-Granero, José Manuel García-Verdugo, Angeles Aroca, José A Sánchez-Alcázar","doi":"10.3390/antiox14060741","DOIUrl":"10.3390/antiox14060741","url":null,"abstract":"<p><p>Ethylmalonic encephalopathy (EE) is a serious metabolic disorder that usually appears in early childhood development and the effects are seen primarily in the brain, gastrointestinal tract, and peripheral vessels. EE is caused by pathogenic variants in the gene that encodes the ETHE1 protein, and its main features are high levels of acidic compounds in body fluids and decreased activity of the mitochondrial complex IV, which limits energy production in tissues that require a large supply of energy. ETHE1 is a mitochondrial sulfur dioxygenase that plays the role of hydrogen sulfide (H<sub>2</sub>S) detoxification, and, when altered, it leads to the accumulation of this gaseous molecule due to its deficient elimination. In this article, we characterised the pathophysiology of ETHE1 deficiency in cellular models, fibroblasts, and induced neurons, derived from a patient with a homozygous pathogenic variant in <i>ETHE1</i>. Furthermore, we evaluated the effect of the activation of the mitochondrial unfolded protein response (mtUPR) on the mutant phenotype. Our results suggest that mutant fibroblasts have alterations in ETHE1 protein expression levels, associated with elevated levels of H<sub>2</sub>S and protein persulfidation, mitochondrial dysfunction, iron/lipofuscin accumulation, and oxidative stress. We also identified a cocktail of compounds consisting of pterostilbene, nicotinamide, riboflavin, thiamine, biotin, lipoic acid, and L-carnitine that improved the cellular and metabolic alterations. The positive effect of the cocktail was dependent on sirtuin 3 activation (SIRT3) and was also confirmed in induced neurons obtained by direct reprogramming. In conclusion, personalised precision medicine in EE using patient-derived cellular models can be an interesting approach for the screening and evaluation of potential therapies. In addition, the activation of the SIRT3 axe of mtUPR is a promising therapeutic strategy for rescuing <i>ETHE1</i> pathogenic variants.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 6","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189359/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
AntioxidantsPub Date : 2025-06-16DOI: 10.3390/antiox14060743
Olena Popazova, Igor Belenichev, Nina Bukhtiyarova, Victor Ryzhenko, Nadia Gorchakova, Valentyn Oksenych, Oleksandr Kamyshnyi
{"title":"Molecular and Biochemical Mechanisms of Cardiomyopathy Development Following Prenatal Hypoxia-Focus on the NO System.","authors":"Olena Popazova, Igor Belenichev, Nina Bukhtiyarova, Victor Ryzhenko, Nadia Gorchakova, Valentyn Oksenych, Oleksandr Kamyshnyi","doi":"10.3390/antiox14060743","DOIUrl":"10.3390/antiox14060743","url":null,"abstract":"<p><p>Prenatal hypoxia (PH) adversely affects the development of the fetal heart, contributing to persistent cardiovascular impairments in postnatal life. A key component in regulating cardiac physiology is the nitric oxide (NO) system, which influences vascular tone, myocardial contractility, and endothelial integrity during development. Exposure to PH disrupts NO-related signaling pathways, leading to endothelial dysfunction, mitochondrial damage, and an escalation of oxidative stress-all of which exacerbate cardiac injury and trigger cardiomyocyte apoptosis. The excessive generation of reactive nitrogen species drives nitrosative stress, thereby intensifying inflammatory processes and cellular injury. In addition, the interplay between NO and hypoxia-inducible factor (HIF) shapes adaptive responses to PH. NO also modulates the synthesis of heat shock protein 70 (HSP70), a critical factor in cellular defense against stress. This review emphasizes the involvement of NO in cardiovascular injury caused by PH and examines the cardioprotective potential of NO modulators-Angiolin, Thiotriazoline, Mildronate, and L-arginine-as prospective therapeutic agents. These agents reduce oxidative stress, enhance endothelial performance, and alleviate the detrimental effects of PH on the heart, offering potential new strategies to prevent cardiovascular disorders in offspring subjected to prenatal hypoxia.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 6","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189570/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
AntioxidantsPub Date : 2025-06-16DOI: 10.3390/antiox14060738
Hualiang Liang, Haifeng Mi, Kai Wang, Mingchun Ren, Lu Zhang, Dongyu Huang, Jiaze Gu
{"title":"Enhancement of Hypoxia Tolerance of Gibel Carp (<i>Carassius auratus gibelio</i>) via a Ferroporphyrin-Rich Diet.","authors":"Hualiang Liang, Haifeng Mi, Kai Wang, Mingchun Ren, Lu Zhang, Dongyu Huang, Jiaze Gu","doi":"10.3390/antiox14060738","DOIUrl":"10.3390/antiox14060738","url":null,"abstract":"<p><p>Gibel carp (<i>Carassius auratus gibelio</i>) were hypoxia stressed for 12 h after an 8-week FPR nutrient-enriched feeding experiment, which was to evaluate the role of FPR in hypoxic stress in gibel carp (<i>Carassius auratus gibelio</i>). The dissolved oxygen was reduced to a range of 0.6 ± 0.2 mg/L. Results showed that FPR supplementation could maintain the osmotic pressure equilibrium by improving the ion concentrations of plasma including Na<sup>+</sup>, Ca<sup>+</sup> and K<sup>+</sup>, and Na<sup>+</sup>/K<sup>+</sup>-ATPase activity of liver. FPR supplementation could effectively enhance the antioxidant capacity by improving the levels of GPX, SOD, CAT, and GSH, and reduce the level of MDA. FPR supplementation could improve the core gene expressions of Nrf2 signalling pathway including <i>nrf2</i>, <i>sod</i>, <i>ho-1</i>, <i>gpx,</i> and <i>cat</i>. The high levels of FPR supplementation (0.04%) might had a negative effect on immunity. FPR supplementation could improve the expression levels of HIF-1 signalling pathway-related genes to adapt to hypoxia condition including <i>hif-1α</i>, <i>epo</i>, <i>angpt1</i>, <i>vegf</i>, <i>et1</i>, and <i>tfr-1</i>. These results also were supported by higher SR and number of gill mitochondria in FPR supplementation. In general, the appropriate FPR supplementation was 0.01% based on the results of this study and economic cost, which could heighten hypoxic adaptation and SR.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 6","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189492/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493669","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Food Grade Synthesis of Hetero-Coupled Biflavones and 3D-Quantitative Structure-Activity Relationship (QSAR) Modeling of Antioxidant Activity.","authors":"Hongling Zheng, Xin Yang, Qiuyu Zhang, Joanne Yi Hui Toy, Dejian Huang","doi":"10.3390/antiox14060742","DOIUrl":"10.3390/antiox14060742","url":null,"abstract":"<p><p>Biflavonoids are a unique subclass of dietary polyphenolic compounds known for their diverse bioactivities. Despite these benefits, these biflavonoids remain largely underexplored due to their limited natural availability and harsh conditions required for their synthesis, which restricts broader research and application in functional foods and nutraceuticals. To address this gap, we synthesized a library of rare biflavonoids using a radical-nucleophile coupling reaction previously reported by our group. The food grade coupling reaction under weakly alkaline water at room temperature led to isolation of 28 heterocoupled biflavones from 11 monomers, namely 3',4'-dihydroxyflavone, 5,3',4'-trihydroxyflavone, 6,3',4'-trihydroxyflavone, 7,3',4'-trihydroxyflavone, diosmetin, chrysin, acacetin, genistein, biochanin A, and wogonin. The structures of the dimers are characterized by nuclear magnetic resonance spectroscopy (NMR) and high-resolution mass spectroscopy (HRMS). In addition, we evaluated the antioxidant potential of these biflavones using a DPPH (2,2-diphenyl-1-picrylhydrazyl) radical scavenging assay and the DPPH value ranges between 0.75 to 1.82 mM of Trolox/mM of sample across the 28 synthesized dimers. Additionally, a three-dimensional quantitative structure-activity relationship (3D-QSAR) analysis was conducted to identify structural features associated with enhanced antioxidant activity. The partial least squares (PLS) regression QSAR model showed acceptable r<sup>2</sup> = 0.936 and q<sup>2</sup> = 0.869. Additionally, the average local ionization energy (ALIE), electrostatic potential (ESP), Fukui index (F-), and electron density (ED) were determined to identify the key structural moiety that was capable of donating electrons to neutralize reactive oxygen species.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 6","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189461/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
AntioxidantsPub Date : 2025-06-16DOI: 10.3390/antiox14060737
Yuxin Jin, Zehui Niu, Menglin Feng, Huilian Che, Zhihong Liang
{"title":"Inactivated Cells and Metabolites of <i>Saccharomyces boulardii</i> Alleviate Inflammation Damage in Caco-2 Monolayer Cells and Mice with Ulcerative Colitis.","authors":"Yuxin Jin, Zehui Niu, Menglin Feng, Huilian Che, Zhihong Liang","doi":"10.3390/antiox14060737","DOIUrl":"10.3390/antiox14060737","url":null,"abstract":"<p><p><i>Saccharomyces boulardii</i> (<i>S. boulardii</i>) has attracted widespread attention due to its antimicrobial and anti-inflammatory properties. In this study, we prepared postbiotics from the heat-inactivated cells (HIC) and cell-free supernatant (CFS) of <i>S. boulardii</i>, with the important component L-arginine (Arg) from the metabolic products included as one of the experimental groups. The results showed that in LPS-stimulated Caco-2 cells, HIC, CFS, and Arg protect intestinal epithelial barrier integrity by inhibiting the expression of TNF-α, IL-1β, and IL-6 while enhancing the expression of occludin and ZO-1 proteins. In dextran sulfate sodium (DSS)-induced colitis mice, HIC, CFS, and Arg alleviate symptoms such as weight loss and colonic damage while suppressing the upregulation of pro-inflammatory factors and the downregulation of tight junction proteins. Moreover, these postbiotics help restore the gut microbiota composition and functionality in colitis mice, with potentially superior regulatory effects compared to sulfasalazine (SASP). Overall, HIC and CFS protect the intestinal barrier function and improve DSS-induced colitis, supporting the development of functional food supplements.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 6","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189787/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}