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Glutathione-Mediated Redox Regulation of Immune Dysfunction in COVID-19 and Tuberculosis -
Essential Oils as Antioxidants: Mechanistic Insights from Radical Scavenging to Redox Signaling -
Traffic-Related Emissions Induce Angiotensin II-Dependent Oxidative Stress in the Hippocampus of ApoE-Null Male Mice
Journal Description
Antioxidants
Antioxidants
is an international, peer-reviewed, open access journal related to the science and technology of antioxidants, published monthly online by MDPI. The International Coenzyme Q10 Association (ICQ10A), Israel Society for Oxygen and Free Radical Research (ISOFRR) and European Academy for Molecular Hydrogen Research (EAMHR) are affiliated with Antioxidants and their members receive discounts on the article processing charge.
- Open Access— free for readers, with article processing charges (APC) paid by authors or their institutions.
- High Visibility: indexed within Scopus, SCIE (Web of Science), PubMed, PMC, FSTA, PubAg, CAPlus / SciFinder, and other databases.
- Journal Rank: JCR - Q1 (Chemistry, Medicinal) / CiteScore - Q1 (Food Science)
- Rapid Publication: manuscripts are peer-reviewed and a first decision is provided to authors approximately 18.7 days after submission; acceptance to publication is undertaken in 2.6 days (median values for papers published in this journal in the second half of 2025).
- Recognition of Reviewers: reviewers who provide timely, thorough peer-review reports receive vouchers entitling them to a discount on the APC of their next publication in any MDPI journal, in appreciation of the work done.
- Testimonials: See what our editors and authors say about Antioxidants.
- Companion journal: Oxygen.
Impact Factor:
6.6 (2024);
5-Year Impact Factor:
7.3 (2024)
Latest Articles
Oxidative Stress and Antioxidant Defense Mechanisms in Sepia esculenta Larvae Induced by Co-Exposure to Environmental Cadmium and Copper
Antioxidants 2026, 15(6), 695; https://doi.org/10.3390/antiox15060695 (registering DOI) - 30 May 2026
Abstract
Cu and Cd, as common heavy metals occurring in the oceans, can induce oxidative stress and toxic responses in marine organisms. Important economic cephalopods inhabit the eastern coastal areas of China, and exposure to Cu and Cd poses a threat to their normal
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Cu and Cd, as common heavy metals occurring in the oceans, can induce oxidative stress and toxic responses in marine organisms. Important economic cephalopods inhabit the eastern coastal areas of China, and exposure to Cu and Cd poses a threat to their normal physiological activities, resulting in serious inhibition of their growth. However, the underlying toxicological mechanisms affecting these cephalopods’ larval stages remain to be elucidated. Here, indicators of oxidative stress and transcriptomics were employed to analyze the toxicological mechanisms of S. esculenta larvae exposed to Cd and Cu. GO and KEGG analysis results indicated that material transport, cellular processes, DNA replication, and other processes were inhibited. A comprehensive analysis of a protein–protein interaction network and KEGG pathways was used to explore the mechanism underlying the toxicity of co-exposure to Cu and Cd toward S. esculenta larvae. We found that Cu and Cd induce significant damage and oxidative stress. The results showed that among 20 identified key genes, ITGA4, LAMA1, and LAMC1, which are involved in the adhesion and connection between cells and the extracellular matrix; COL6A1, COL6A3, COL6A4, and COL6A6, which maintain the integrity of the extracellular matrix; and ABCA1, ABCC5, and ABCC7, which regulate the transmembrane transport of Cu and Cd were involved in the mechanism of toxicity. We suggest that co-exposure to the metals primarily inhibits the connection and adhesion between the cells of the larvae and disrupts the structure and function of the extracellular matrix. The results provide a foundation for understanding the toxicological mechanism of S. esculenta and should be of benefit to artificial breeding programs.
Full article
(This article belongs to the Special Issue Oxidative Stress and Antioxidant Defenses in Aquatic Animals)
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Open AccessReview
Cluster of Differentiation 36-Mediated Inflammation and Lipid Metabolism in Cardiovascular Diseases: From Mechanisms to Novel Therapies
by
Jiayin Song, Xiangnuo Han, Yu Zhang and Meixiu Jiang
Antioxidants 2026, 15(6), 694; https://doi.org/10.3390/antiox15060694 (registering DOI) - 30 May 2026
Abstract
Cardiovascular diseases (CVDs) continue to pose a key challenge to public health because of their high prevalence, mortality, and disability rates, together with a trend toward younger age at onset. Chronic inflammation and disordered lipid metabolism are key pathological mechanisms underlying the development
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Cardiovascular diseases (CVDs) continue to pose a key challenge to public health because of their high prevalence, mortality, and disability rates, together with a trend toward younger age at onset. Chronic inflammation and disordered lipid metabolism are key pathological mechanisms underlying the development and progression of CVDs. Although numerous pharmacological agents have been developed to intervene in CVDs, current therapies are still limited by adverse effects, suboptimal efficacy, and insufficient anti-inflammatory properties. Consequently, effective drug-based strategies for the prevention and treatment of certain CVDs are still insufficient. Cluster of differentiation 36 (CD36), a class B scavenger receptor, mediates the recognition and uptake of long-chain fatty acids, oxidized low-density lipoprotein, and other ligands, and is present in diverse tissues and cell types. Accumulating evidence indicates that CD36 plays a critical role in lipid metabolism and inflammatory signalling pathways implicated in CVDs, suggesting that it represents a promising focus for treatment-oriented interventions. This review synthesizes current evidence on the multifaceted roles of CD36 in lipid metabolism dysregulation and inflammation-associated pathways in CVDs and evaluates its potential as a tractable target for disease prevention and management.
Full article
(This article belongs to the Section Health Outcomes of Antioxidants and Oxidative Stress)
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Open AccessSystematic Review
Polyphenol-Mediated Modulation of Oxidative Stress Pathways in Type 1 Diabetes: A Systematic Review
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Alan Ho, Harini Adivikolanu, Dilan Patel, Xinyue Wang, Rahul Mittal and Khemraj Hirani
Antioxidants 2026, 15(6), 693; https://doi.org/10.3390/antiox15060693 (registering DOI) - 30 May 2026
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Oxidative stress is a central component of type 1 diabetes (T1D) pathophysiology, contributing to pancreatic β-cell vulnerability and the development of chronic complications. Current therapeutic strategies are primarily focused on glycemic control and do not directly address underlying redox imbalance. Dietary polyphenols, a
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Oxidative stress is a central component of type 1 diabetes (T1D) pathophysiology, contributing to pancreatic β-cell vulnerability and the development of chronic complications. Current therapeutic strategies are primarily focused on glycemic control and do not directly address underlying redox imbalance. Dietary polyphenols, a structurally diverse class of plant-derived compounds, have been investigated for their antioxidant and cytoprotective properties, yet their role in T1D has not been systematically defined. This systematic review evaluates the effects of polyphenols on oxidative stress and glycemic parameters in preclinical models of T1D. Across studies, polyphenols were consistently associated with attenuation of oxidative stress, as evidenced by reductions in lipid peroxidation and reactive oxygen and nitrogen species, along with restoration of endogenous antioxidant defenses, including superoxide dismutase, catalase, and glutathione. These effects were frequently linked to modulation of redox-sensitive signaling pathways, particularly Nrf2-dependent mechanisms. In contrast, glycemic outcomes were heterogeneous and influenced by compound-specific and experimental factors. Modulation of oxidative stress markers was often observed independently of changes in glycemic parameters, suggesting a primary redox-mediated mode of action. These findings provide a mechanistic rationale for prioritizing oxidative-stress-focused endpoints in future translational studies and support the evaluation of polyphenols as adjunctive strategies targeting redox imbalance in T1D.
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Open AccessArticle
Bioactive Silages from Agro-Industrial By-Products Based on Grape Pomace or Olive Mill Wastewater for Ruminants: Evolution of Phenolic Profiles, Antioxidant Activity, and Fatty Acid Composition
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Roberta Savina Dibenedetto, Mónica Sánchez-Parra, José Luis Ordóñez-Díaz, Alessio Di Luca, Giovanni Martemucci, José Manuel Moreno-Rojas and Angela Gabriella D’Alessandro
Antioxidants 2026, 15(6), 692; https://doi.org/10.3390/antiox15060692 (registering DOI) - 30 May 2026
Abstract
This study investigated the chemical composition, fermentation dynamics, fatty-acid profile, and polyphenolic evolution of two mixed silages designed to valorize agro-industrial by-products for ruminant feeding. Silages were produced by co-ensiling wheat straw, cheese-whey, and molasses with grape pomace (SIL-1) or olive mill wastewater
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This study investigated the chemical composition, fermentation dynamics, fatty-acid profile, and polyphenolic evolution of two mixed silages designed to valorize agro-industrial by-products for ruminant feeding. Silages were produced by co-ensiling wheat straw, cheese-whey, and molasses with grape pomace (SIL-1) or olive mill wastewater (SIL-2), and were monitored over a 150-day ensiling period. The two formulations exhibited distinct compositional characteristics and fermentation kinetics. SIL-1 showed higher crude protein content and a more favorable fatty-acid profile, with greater levels of selected long-chain fatty acids, whereas SIL-2 had higher dry matter and structural fiber fractions. Both silages achieved effective fermentation, reaching stable acidic conditions (pH < 4.0), although SIL-1 consistently maintained lower pH and higher buffering capacity. Fermentation end-products differed between silages, with higher concentrations of short-chain fatty acids in SIL-1 and greater lactic acid accumulation in SIL-2, under significant treatment × time interactions. Bioactive compound analysis revealed higher total phenolic content and antioxidant capacity in SIL-1, whereas SIL-2 showed marked degradation of phenolic compounds, including the loss of characteristic secoiridoids. Polyphenolic profiles displayed compound-specific temporal dynamics during ensiling. Overall, both silages were well preserved; however, SIL-1 demonstrated superior nutritional quality and bioactive stability, supporting its potential as a functional feed ingredient for ruminant nutrition.
Full article
(This article belongs to the Section Natural and Synthetic Antioxidants)
Open AccessArticle
Green-Extracted Ficus carica L. Fruit Polysaccharides Promote Longevity in Caenorhabditis elegans via Modulation of SKN-1 and IIS Pathway
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Lianyu Li, Feng Ding, Yong Sheng and Yan Zhao
Antioxidants 2026, 15(6), 691; https://doi.org/10.3390/antiox15060691 (registering DOI) - 30 May 2026
Abstract
In this study, polysaccharides from Ficus carica L. fruits (FCPs) were extracted using a deep eutectic solvent (DES)-based ultrasound-assisted extraction (UAE) method. The physicochemical properties of the FCPs were then characterized, and the anti-aging effects of FCPs were evaluated in Caenorhabditis elegans (
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In this study, polysaccharides from Ficus carica L. fruits (FCPs) were extracted using a deep eutectic solvent (DES)-based ultrasound-assisted extraction (UAE) method. The physicochemical properties of the FCPs were then characterized, and the anti-aging effects of FCPs were evaluated in Caenorhabditis elegans (C. elegans). It was demonstrated that FCPs significantly extended the lifespan of the nematodes, while improving locomotor activity without affecting the body size or reproductive capacity. Meanwhile, FCPs reduced lipofuscin accumulation, decreased intracellular reactive oxygen species (ROS) levels, and increased the survival of C. elegans under oxidative stress. Moreover, FCPs upregulated the expression of antioxidant genes sod-1, sod-3, ctl-2, ctl-3 and gst-4. The expression of skinhead-1 (skn-1), a homologue gene of mammalian nuclear factor erythroid 2-related factor (Nrf) in C. elegans, was also elevated upon FCPs treatment. Knockdown of skn-1 expression by RNA interference abolished the lifespan extension and ROS reduction in FCPs-treated C. elegans, indicating that the SKN-1-mediated signaling was essential for the anti-aging effects of FCPs. Additionally, FCPs caused downregulation of the key components of the insulin/IGF-1 signaling (IIS) pathway, age-1, akt-1, and akt-2. Overall, these results suggested that FCPs promoted longevity in C. elegans via modulation of SKN-1 and IIS pathway.
Full article
(This article belongs to the Special Issue Green Extraction Technologies for Bioactive Compounds from Foods and Natural Products: Antioxidant Potential and Health Applications)
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Open AccessArticle
Metabolic Responses of Melanocytes and Melanoma Cells to UVA Radiation and Phytocannabinoids Exposure
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Michał Biernacki, Ernest Gieniusz, Agnieszka Gęgotek, Morana Jaganjac and Elżbieta Skrzydlewska
Antioxidants 2026, 15(6), 690; https://doi.org/10.3390/antiox15060690 (registering DOI) - 30 May 2026
Abstract
Ultraviolet A (UVA) radiation disrupts the redox balance of melanocytes and may lead to the development of melanoma, highlighting the need for new skin protection strategies. This study assessed the effect of phytocannabinoids [cannabigerol (CBG), cannabidiol (CBD), and CBG + CBD] on redox
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Ultraviolet A (UVA) radiation disrupts the redox balance of melanocytes and may lead to the development of melanoma, highlighting the need for new skin protection strategies. This study assessed the effect of phytocannabinoids [cannabigerol (CBG), cannabidiol (CBD), and CBG + CBD] on redox homeostasis in control and UVA-exposed melanocytes and in melanoma cells (SK-Mel-5). UVA radiation increased the activity of prooxidant enzymes in both melanocytes and SK-Mel-5 cells and, consequently, the level of reactive oxygen species (ROS) (approx. 2-fold). It also activated nuclear factor erythroid 2 (Nrf2), as reflected by increased expression of heme oxygenase 1 (HO-1) (melanocytes approx. 2-fold; SK-Mel-5 approx. 7-fold). Concomitantly, antioxidant mechanisms were impaired, as demonstrated by reduced superoxide dismutase (SOD1/SOD2) activity and impaired glutathione and thioredoxin function. These changes were accompanied by increased levels of oxidative damage markers (isoprostanes, 4-hydroxynonenal-4-HNE, and 4-HNE-protein adducts) (43–100%) and increased inflammatory signaling, including increased expression of nuclear factor kappa B (NF-κB) subunits (melanocytes: p52 ~2-fold, p65 ~75%; SK-Mel-5: ~4–4.5-fold) and tumor necrosis factor alpha (TNF-α; ~30%). Phytocannabinoid treatment modulated these UVA-induced changes. In SK-Mel-5 cells, phytocannabinoids normalized the activity of prooxidant enzymes and consequently reduced ROS levels (~30%). They also reduced Nrf2 activation and HO-1 expression; however, CBG increased HO-1 level in melanocytes (~25–40%). Furthermore, phytocannabinoids enhanced antioxidant defense by increasing SOD activity, particularly in melanocytes (~10–40%), and restoring the glutathione and thioredoxin systems. Markers of oxidative damage were reduced by approximately 23–37% after treatment. Furthermore, phytocannabinoids attenuated NF-κB activation (p52 ~18–28%, p65 ~25–29% in melanocytes; ~20% in SK-Mel-5), while TNF-α levels remained unchanged. The effects in non-irradiated cells were modest (<15%). These results suggest that phytocannabinoid-mediated modulation of redox balance may stabilize melanocytes exposed to UVA radiation and potentially reduce the risk of neoplastic transformation. However, the observed protective effects in SK-Mel-5 cells require further investigation and detailed molecular analysis.
Full article
(This article belongs to the Special Issue Natural Antioxidants: Multiple Mechanisms for Skin Protection and Skin Disease)
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Open AccessArticle
Ginkgo Biloba Extract Ameliorates Age-Related Mitochondrial Deficits in Human iPSCs and Their Derived Neurons and Astrocytes
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Imane Lejri, Amandine Grimm and Anne Eckert
Antioxidants 2026, 15(6), 689; https://doi.org/10.3390/antiox15060689 (registering DOI) - 29 May 2026
Abstract
Mitochondrial dysfunction is a central feature of aging, driving bioenergetic decline, increased oxidative stress, and increased vulnerability to neurodegenerative diseases. Human induced pluripotent stem cells (iPSCs) and iPSC-derived neurons provide powerful models to study these processes. Ginkgo biloba extract GBE LI1370 (GBE) has
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Mitochondrial dysfunction is a central feature of aging, driving bioenergetic decline, increased oxidative stress, and increased vulnerability to neurodegenerative diseases. Human induced pluripotent stem cells (iPSCs) and iPSC-derived neurons provide powerful models to study these processes. Ginkgo biloba extract GBE LI1370 (GBE) has demonstrated antioxidant and mitochondria-protective properties in preclinical models, including improvements in mitochondrial membrane potential, reduction in reactive oxygen species, and enhanced neuronal survival. However, its effects on mitochondrial function in human iPSCs and their differentiated derivatives in the context of aging have not yet been investigated. This study evaluated the mitochondrial protective effects of GBE (100 µg/mL) in an established iPSC-based model of aging and in neurons and astrocytes derived from aged iPSCs. Mitochondrial parameters, including ATP production, mitochondrial membrane potential (MMP), mitochondrial reactive oxygen species (mtROS), superoxide levels, and mitochondrial respiration, were assessed. Aged iPSCs exhibited reduced ATP production and MMP, together with increased mtROS and superoxide levels compared to young controls. Astrocytes derived from aged iPSCs also displayed mitochondrial dysfunction. Treatment with GBE for 24 h increased ATP production and MMP, reduced oxidative stress, and improved mitochondrial respiration in both young and aged iPSCs, as well as in aged iPSC-derived neurons and astrocytes. These preliminary donor-based findings support further investigation of GBE-associated mitochondrial responses in human donor-derived cellular models of aging and warrant validation in larger donor cohorts.
Full article
(This article belongs to the Special Issue Oxidative Stress and Its Mitigation in Neurodegenerative Disorders)
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Open AccessArticle
Bioactive Extracts and Constituents from Taraxacum mongolicum: Antioxidant, Anti-Inflammatory, Enzyme-Inhibitory, and Molecular Docking Studies
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Kuan-Ying Huang, Sin-Min Li and Jih-Jung Chen
Antioxidants 2026, 15(6), 688; https://doi.org/10.3390/antiox15060688 (registering DOI) - 29 May 2026
Abstract
Taraxacum mongolicum, a medicinal and edible plant of the Asteraceae family, is widely consumed in East Asia and contains diverse bioactive compounds. This study systematically evaluated the bioactivities of whole-plant extracts and their components and elucidated the underlying anti-inflammatory mechanisms. Among the
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Taraxacum mongolicum, a medicinal and edible plant of the Asteraceae family, is widely consumed in East Asia and contains diverse bioactive compounds. This study systematically evaluated the bioactivities of whole-plant extracts and their components and elucidated the underlying anti-inflammatory mechanisms. Among the extracts, the methanol fraction exhibited the strongest antioxidant activity, effective inhibition of nitric oxide (NO) production, and modulation of inflammation-related proteins. In addition, the extracts demonstrated α-glucosidase and acetylcholinesterase (AChE) inhibitory activities, indicating multifunctional bioactive potential. Activity-guided analysis identified luteolin (2) and apigenin (4) as key active compounds with strong NO inhibitory effects. Western blot analysis revealed that both compounds significantly downregulated NO-related protein expression. Mechanistically, luteolin attenuated inflammatory responses by inhibiting NF-κB signaling and modulating the MAPK pathway, whereas apigenin primarily exerted its effects through NF-κB suppression. Both compounds also promoted M2 macrophage marker expression, suggesting a role in immune regulation. Molecular docking analysis further confirmed stable binding interactions of luteolin and apigenin with iNOS and COX-2. Overall, these findings demonstrate that T. mongolicum possesses antioxidant, enzyme-inhibitory, and anti-inflammatory activities and supports its further investigation as a multifunctional bioactive resource.
Full article
(This article belongs to the Special Issue Phytochemical Analysis and Evaluation of Antioxidant Properties in Medicinal Plants)
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Open AccessArticle
Selenium Status Is Associated with Inflammation in Epicardial Adipose Tissue in Elderly Patients with Coronary Artery Disease
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Trine Baur Opstad, Fredrik Lossius Opdahl, Steen Larsen, Sissel Åkra, Sheryl Palmero, Theis Tønnessen, Svein Solheim, Jan Alexander, Urban Alehagen and Ida Gjervold Lunde
Antioxidants 2026, 15(6), 687; https://doi.org/10.3390/antiox15060687 (registering DOI) - 29 May 2026
Abstract
Background: Inflammation in epicardial adipose tissue (EAT) contributes to cardiovascular disease through the local production of pro-inflammatory cytokines affecting the adjacent myocardium. Selenium (Se) is essential for selenoprotein-mediated antioxidant and anti-inflammatory functions. We investigated associations between Se status and inflammatory markers in EAT
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Background: Inflammation in epicardial adipose tissue (EAT) contributes to cardiovascular disease through the local production of pro-inflammatory cytokines affecting the adjacent myocardium. Selenium (Se) is essential for selenoprotein-mediated antioxidant and anti-inflammatory functions. We investigated associations between Se status and inflammatory markers in EAT and in the circulation in patients with coronary artery disease (CAD). Methods: Patients with CAD undergoing coronary artery bypass grafting (n = 52) and valve disease patients receiving valve replacement serving as controls (n = 22) were included from the ATICH study. EAT biopsies were obtained during open-chest chest surgery. Serum Se was measured by inductively coupled plasma mass spectrometry. Associations between Se and EAT mRNA expression of Nod-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome components and cytokines, as well as circulating inflammatory markers, were assessed using Spearman’s rho and group comparisons based on median Se levels. Results: Se concentrations were lower in CAD patients than controls (0.9 vs. 1.1 µmol/L, p = 0.025). In CAD patients, Se levels correlated with EAT expression of CASP1 and IL18, and with circulating IL-6. Se levels above the median were associated with lower EAT expression of CASP1 and NLRP3 and reduced IL-6 levels (p < 0.05, all). Our analysis of publicly available RNA seq data demonstrated selenoprotein’s presence in EAT. Conclusion: Lower Se status in CAD was associated with increased systemic and EAT inflammation, suggesting a role for selenoprotein-dependent antioxidant mechanisms in regulating cardiac adipose tissue inflammation.
Full article
(This article belongs to the Special Issue Biological Activities of Antioxidant Selenoproteins)
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Open AccessArticle
Characterization of Phenolic Profiles Using UPLC-Q-TOF-MS/MS and NMR in the Biofunctional Fraction of Korean Winter Spinach (Spinacia oleracea L.) Leaves: Evaluation of Major Phenolics and Their Bioactivities Under Optimized Extraction Conditions
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Eun Young Seo, Eun Jeong Ko, Du Yong Cho, Ye Ri Jeong, Se Hyeon Jeon, Dong Hyun Park, Mu Yeun Jang, Jeong Yoon Kim, Kye Man Cho and Jin Hwan Lee
Antioxidants 2026, 15(6), 686; https://doi.org/10.3390/antiox15060686 (registering DOI) - 29 May 2026
Abstract
This study is the first to demonstrate fluctuations in major phenolics and biofunctional properties under various extraction conditions of Korean winter spinach (Allseason cultivar) leaves. In contrast to earlier reports on summer- or greenhouse-cultivated spinach, which mainly relied on HPLC-DAD or
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This study is the first to demonstrate fluctuations in major phenolics and biofunctional properties under various extraction conditions of Korean winter spinach (Allseason cultivar) leaves. In contrast to earlier reports on summer- or greenhouse-cultivated spinach, which mainly relied on HPLC-DAD or LC-MS profiling and one or two bioactivity assays, the present work combines UPLC-Q-TOF-MS/MS with NMR-based structural confirmation of three major flavone glucuronides (11–13) and integrates five complementary bioactivity assays (DPPH, ABTS, FRAP, DNA protection, and tyrosinase inhibition) within a single optimization framework. A 50% methanol extract yielded twelve phenolics (patuletin, spinacetin, spinatoside, jaceidin, and methylenedioxyflavone-glucuronide derivatives) elucidated by UPLC-Q-TOF-MS/MS, with the isolated major phenolics 11–13 further verified by NMR. Total phenols and total flavonoids of biofunctional characteristics varied significantly depending on the solvent system. The optimal extraction conditions (50% methanol, 72 h, 35 °C) resulted in the highest phenolic levels of phenolics 11–13 (total: ~6.5 mg/g) and bioactivities (DNA protection > ABTS > tyrosinase inhibition > FRAP > DPPH, at 500 μg/mL). PCA and hierarchical clustering distinguished extraction profiles, with 50–70% methanol extracts forming clear clusters. Among the isolated phenolics, phenolic 12 showed the strongest antioxidant activity (DPPH IC50 = 57.6 μM; ABTS IC50 = 21.9 μM). These findings suggest that spinach leaves are a valuable source of bioactive phenolics for nutraceutical applications under optimized extraction conditions.
Full article
(This article belongs to the Special Issue Innovative Processing Technologies and Their Effects on Antioxidant Activity in Plant-Derived Natural Products)
Open AccessArticle
Natural Extracts of Alnus japonica Induce BAK-Dependent Autophagy to Inhibit Liver Cancer Stem Cell Tumorigenesis
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Kenly Wuputra, Yoshimasa Matsuura, Satoshi Gushiken, Hirosuke Fukuda, Ya-Han Yang, Chia-Chen Ku, Chun-Chieh Wu, Ying-Chu Lin, Yi-Chun Tsai, Deng-Chyang Wu, Toshihiko Nozaki, Kohsuke Kato, Atsushi Kawaguchi, Kyosuke Nagata, Yoshiharu Tanaka and Kazunari K. Yokoyama
Antioxidants 2026, 15(6), 685; https://doi.org/10.3390/antiox15060685 (registering DOI) - 29 May 2026
Abstract
Background: Cancer stem cells (CSCs) contribute to hepatocellular carcinoma (HCC) progression and therapeutic resistance. Natural products with antioxidant and bioactive properties may offer novel strategies to suppress CSC-driven tumorigenesis. Methods: We investigated the effects of unfermented and fermented Alnus japonica bark extracts on
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Background: Cancer stem cells (CSCs) contribute to hepatocellular carcinoma (HCC) progression and therapeutic resistance. Natural products with antioxidant and bioactive properties may offer novel strategies to suppress CSC-driven tumorigenesis. Methods: We investigated the effects of unfermented and fermented Alnus japonica bark extracts on CSC-like rG2-DC-1C cells. Cell proliferation, invasion, and xenograft tumor formation were assessed, and autophagy/apoptosis markers were analyzed. Results: Bark extracts reduced OCT4 expression, suppressed CSC proliferation and invasion, and inhibited xenograft tumor formation. Mechanistically, extracts activated BAK-dependent autophagy, evidenced by LC3B accumulation and p62 modulation, whereas diarylheptanoids Hirsutenone (Hir) and Oregonin (Ore) primarily induced apoptosis via Caspase-3 cleavage. Blocking autophagy with chloroquine or BAK knockdown reversed the anti-invasive effects of bark extracts, confirming BAK’s role in CSC suppression. Component analysis suggests quercetin contributes to autophagy induction, though synergistic effects of other constituents remain possible. Conclusions: Together, these findings indicate that Alnus japonica bark extracts suppress CSC-driven liver tumorigenesis through autophagy, while Hir and Ore act via apoptosis, highlighting complementary mechanisms that broaden the therapeutic potential of this traditional medicinal plant and support further preclinical validation.
Full article
(This article belongs to the Special Issue Oxidative Stress in Hepatic Diseases)
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Open AccessSystematic Review
Inflammatory Adipokines and Potential Oxidative Stress-Related Mechanisms Linking MASLD with Subclinical Atherosclerosis Within CKM Syndrome: A Systematic Review and Meta-Analysis
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Cezara-Andreea Gerdanovics, Șoimița-Mihaela Suciu, Olga-Hilda Orășan, Ioana Para, Vladiana-Romina Turi, Adela-Sitar Tăut, Mircea-Vasile Milaciu, Mirela-Georgiana Perne, Teodora-Gabriela Alexescu, Lorena Ciumărnean, Alexandru Gerdanovics, Vlad-Dumitru Brata and Angela Cozma
Antioxidants 2026, 15(6), 684; https://doi.org/10.3390/antiox15060684 (registering DOI) - 29 May 2026
Abstract
Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as a systemic disorder linked to cardio-kidney–metabolic (CKM) syndrome, early vascular injury and redox imbalance. Inflammatory adipokines such as retinol-binding protein 4 (RBP4) and lipocalin-2 (LCN2) may contribute to this hepatic–vascular interplay
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Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as a systemic disorder linked to cardio-kidney–metabolic (CKM) syndrome, early vascular injury and redox imbalance. Inflammatory adipokines such as retinol-binding protein 4 (RBP4) and lipocalin-2 (LCN2) may contribute to this hepatic–vascular interplay by integrating metabolic inflammation, oxidative stress and endothelial dysfunction. Therefore, the present study aimed to investigate the contribution of the inflammatory adipokines retinol-binding protein 4 (RBP4) and lipocalin-2 (LCN2) to the hepatic–vascular interplay in MASLD within the cardio-kidney–metabolic (CKM) syndrome. Materials and Methods: We performed a systematic review and meta-analysis of studies evaluating circulating RBP4 and LCN2 levels in MASLD. PubMed, Scopus, and Web of Science were searched. Twenty studies were included in the qualitative synthesis, and ten in the quantitative meta-analysis. Standardized mean differences (SMDs) with 95% confidence intervals (CIs) were calculated. Vascular findings were synthesized narratively because of heterogeneity in outcomes. Results: Circulating RBP4 levels were significantly higher in MASLD patients than in controls (SMD = 0.64, 95% CI: 0.08 to 1.20, p = 0.026; I2 = 91.2%). LCN2 levels were also significantly elevated (SMD = 1.92, 95% CI: 0.83 to 3.00, p < 0.001; I2 = 98.0%). Compared with RBP4, LCN2 showed a larger pooled effect size, although heterogeneity remained very high. In the qualitative synthesis, adipokines, particularly LCN2, were associated with markers of vascular injury, including carotid intima–media thickness, plaque burden, arterial stiffness, endothelial dysfunction, coronary severity, and cardiovascular events. Conclusions: Both RBP4 and LCN2 were elevated in MASLD, supporting a link between adipokine dysregulation and hepatic metabolic dysfunction within the broader cardio-kidney–metabolic (CKM) syndrome. LCN2 appeared to better reflect the inflammatory, metabolic, and vascular burden of disease. These findings support the view of MASLD as a systemic disorder within the CKM syndrome and highlight the potential of inflammatory adipokines as non-invasive biomarkers of integrated hepatic, metabolic, and vascular dysfunction.
Full article
(This article belongs to the Special Issue Oxidative Stress in Hepatic Diseases)
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Open AccessArticle
Ulmus pumila Linné (Ulmi) Extract Attenuates Inflammatory Responses in Atopic Dermatitis by Modulating Lipid Peroxidation and Oxidative Stress
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Min Jung Kim, Mi Jin Jang, Young Zoo You, Ye Jin Yang, Ji Woong Heo, Hee Ho Kim, Hun Hwan Kim, Se Hyo Jeong, Gon Sup Kim, Young Woo Kim, Ju-Hye Yang, Ryounghoon Jeon, Sang-Hyun An and Kwang Il Park
Antioxidants 2026, 15(6), 683; https://doi.org/10.3390/antiox15060683 (registering DOI) - 29 May 2026
Abstract
Background: Atopic dermatitis (AD) is a chronic inflammatory skin disorder characterized by oxidative stress and impaired skin barrier function. These pathological features contribute to persistent inflammation and symptom exacerbation, highlighting the need for therapies that can both reduce oxidative stress and modulate inflammatory
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Background: Atopic dermatitis (AD) is a chronic inflammatory skin disorder characterized by oxidative stress and impaired skin barrier function. These pathological features contribute to persistent inflammation and symptom exacerbation, highlighting the need for therapies that can both reduce oxidative stress and modulate inflammatory pathways. Methods: Ulmus pumila Linné (Ulmi) was prepared via hot water extraction and tested for cytotoxicity, antioxidant activity, and anti-inflammatory effects in HaCaT keratinocytes stimulated with tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ). in vivo efficacy was assessed using a 2,4-dinitrochlorobenzene (DNCB)-induced AD model in SKH-1 hairless mice. Bioactive compounds were identified using liquid chromatography–quadrupole time-of-flight tandem mass spectrometry (LC-QTOF-MS/MS), and molecular docking analysis was performed to evaluate the binding affinity of these compounds to aldehyde dehydrogenase 2 (ALDH2). Results: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays confirmed that Ulmi was safe at concentrations up to 400 μg/mL. In TNF-α/IFN-γ-stimulated HaCaT cells, Ulmi significantly upregulated ALDH2 expression in a dose-dependent manner and reduced reactive oxygen species (ROS) production. The extract also suppressed pro-inflammatory mediators such as inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), while inhibiting the activation of nuclear factor kappa B (NF-κB) and Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathways. In the AD mouse model, Ulmi treatment improved clinical skin scores, reduced epidermal thickness, and decreased inflammatory markers compared to untreated controls. LC-QTOF-MS/MS analysis identified eight bioactive compounds, with procyanidin B2, catechin, and epicatechin as major constituents. Molecular docking revealed that procyanidin B2 had the strongest binding affinity to ALDH2 (−9.5 kcal/mol). Conclusions: These findings demonstrate that Ulmi effectively ameliorates AD-like symptoms through ALDH2-mediated antioxidant mechanisms and anti-inflammatory effects. The results suggest that Ulmi may serve as a promising natural therapeutic agent for the management of atopic dermatitis.
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(This article belongs to the Special Issue Antioxidants for Skin Health—2nd Edition)
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Open AccessArticle
Antioxidant Recovery from Massachusetts Cranberry Pomace: The Role of Solvent
by
Maureen Otieno, Elena De Pra, Ryley Thatcher and Catherine Neto
Antioxidants 2026, 15(6), 682; https://doi.org/10.3390/antiox15060682 (registering DOI) - 29 May 2026
Abstract
Cranberry pomace is a rich, but underutilized source of polyphenols and other bioactive compounds. This study assessed the efficacy of six solvent mixtures comprising combinations of ethanol, methanol, acetone, formic acid, and water for extraction of antioxidants from pomace. The antioxidant activity and
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Cranberry pomace is a rich, but underutilized source of polyphenols and other bioactive compounds. This study assessed the efficacy of six solvent mixtures comprising combinations of ethanol, methanol, acetone, formic acid, and water for extraction of antioxidants from pomace. The antioxidant activity and total phenolic content of the cranberry pomace extracts were evaluated using DPPH (2,2-diphenyl-1-picrylhydrazyl), ABTS•+(2,2′-azinobis(3-ethylbenzthiazolin-6-sulfonic acid), FRAP (ferric reducing power), and Folin–Ciocâlteu assays, the total proanthocyanidin content was estimated using the dimethylaminocinnamaldehyde (DMAC) method, and individual polyphenolics and triterpenoids were determined using HPLC-DAD and UPLC-MS. Extracts exhibited a broad range of total phenolic content at 21–166 mg gallic acid equivalents (GAE)/g extract), total PACs (proanthocyanidins) at 6–240 mg PAC equivalents/g extract, anthocyanins at 0.42–1.77 mg/g extract, flavonols at 4.09–11.7 mg/g extract, and triterpenoids at 85.6–287 mg/g extract. Antioxidant activities varied widely and correlated positively with all polyphenol categories, but negatively with triterpenoids. An extract produced using an acetone, methanol, water and formic acid mixture demonstrated optimal antioxidant properties, total phenolic content, and total proanthocyanidin content and was further characterized. Our findings emphasize the importance of solvent selection for targeted bioactive constituents and highlight cranberry pomace as a promising source of antioxidants.
Full article
(This article belongs to the Special Issue Agri-Food Wastes as Natural Source of Bioactive Antioxidants: Fourth Edition)
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Open AccessArticle
Cold Plasma Treatment Enhances Drought Tolerance of Alfalfa (Medicago sativa L.) Seeds by Modulating Physiological Responses and Transcriptomic Profiles
by
Weicheng Gong, Chunxu Qin, Zhiqing Song, Xiliang Hao, Aozhe Li, Yaxin Liu and Chengzhi Ma
Antioxidants 2026, 15(6), 681; https://doi.org/10.3390/antiox15060681 (registering DOI) - 28 May 2026
Abstract
Drought stress is a major limiting factor for alfalfa (Medicago sativa L.) production in arid and semi-arid regions. Cold plasma treatment has emerged as a promising physical technology for improving seed germination and stress tolerance, but its underlying mechanisms remain poorly understood.
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Drought stress is a major limiting factor for alfalfa (Medicago sativa L.) production in arid and semi-arid regions. Cold plasma treatment has emerged as a promising physical technology for improving seed germination and stress tolerance, but its underlying mechanisms remain poorly understood. In this study, alfalfa seeds were treated with cold plasma (plasma discharge voltage: 0, 5, 10, 15 kV) for 5 min and exposed to PEG 6000 stress at 0, 5, 10, and 15%. Results showed that cold plasma treatment significantly alleviated the inhibitory effects of drought stress on seed germination, with the Plasma-15 kV treatment exhibiting the highest germination potential and germination rate compared to the control (p < 0.05). Plasma treatment enhanced the activities of superoxide dismutase (SOD), peroxidase (POD), and catalase (CAT), while reducing malondialdehyde (MDA) content (p < 0.05), indicating mitigated oxidative damage under drought conditions. Transcriptomic analysis revealed that cold plasma regulated the expression of genes involved in the MAPK signaling pathway and other drought-responsive pathways, leading to metabolic reallocation (Q < 0.05) and enhanced drought tolerance. In conclusion, 5 min of Plasma-15 kV treatment effectively enhances drought tolerance via physiological and transcriptional regulation, providing an eco-friendly strategy for alfalfa cultivation in dry regions.
Full article
Open AccessArticle
Two New Alkaloids and a Triterpenoid Glycoside from Rosa roxburghii with Antioxidant and Enzyme Inhibitory Activities
by
Lang Zhou, Yin-Ju Zhang, Wen-Xia Dai, Fa-Ju Chen, Xiong Pan, Yu Wang, Li-Shou Yang, Qi-Ji Li and Xiao-Sheng Yang
Antioxidants 2026, 15(6), 680; https://doi.org/10.3390/antiox15060680 - 28 May 2026
Abstract
Rosa roxburghii is a distinctive medicinal and edible plant resource. In an effort to uncover structurally novel secondary metabolites from this plant and explore their pharmacological potential, a phytochemical investigation of the fresh fruits of R. roxburghii led to the isolation of two
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Rosa roxburghii is a distinctive medicinal and edible plant resource. In an effort to uncover structurally novel secondary metabolites from this plant and explore their pharmacological potential, a phytochemical investigation of the fresh fruits of R. roxburghii led to the isolation of two new dihydroavicine alkaloids, roxburghcids D (1) and E (2), and a new triterpenoid glycoside, roxburghcid C (6), together with five known compounds (3–5, 7–8). The structures of the new compounds were unambiguously elucidated through extensive spectroscopic analyses (including 1D and 2D NMR and HRESIMS), quantum chemical calculations, and single-crystal X-ray diffraction. In bioassay evaluations, compounds 2 and 3 exhibited significant ABTS radical scavenging activities, with IC50 values of 39.59 and 17.38 μM, respectively. Additionally, compounds 2, 6, and 8 exhibited modest α-glucosidase inhibitory activities, with inhibition rates of 33.13%, 38.61%, and 36.85%, respectively, at a concentration of 100 μM. Furthermore, compounds 2 and 4 showed significant cytotoxicity against the A549 human cancer cell lines, with IC50 values of 7.23 and 8.36 μM, respectively. This study represents the first report of alkaloids isolated from R. roxburghii, enriching its phytochemical profile and providing valuable chemotaxonomic insights for this species.
Full article
(This article belongs to the Section Natural and Synthetic Antioxidants)
Open AccessReview
Silent Inflammation: A Critical Narrative Review of the Relationship Between Periodontal Disease and Psychosis—The Role of Oxidative Stress and Iatrogenic Comorbidities
by
Brindusa E. Focseneanu, Roxana M. Ciobanu, Anna M. Pangica, Petru T. Ionescu, Teodora M. Pangica, Gabriela Marian and Florentina C. Biclesanu
Antioxidants 2026, 15(6), 679; https://doi.org/10.3390/antiox15060679 - 28 May 2026
Abstract
Extensive epidemiological evidence links psychosis (PZ)—particularly schizophrenia (SCZ)—with disproportionate periodontal destruction, suggesting shared biological vulnerability. Beyond local tissue damage, periodontitis provides a clinically accessible translational paradigm for systemic redox dysregulation, where sustained inflammatory activation coincides with measurable oxidative injury and exhaustion of antioxidant
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Extensive epidemiological evidence links psychosis (PZ)—particularly schizophrenia (SCZ)—with disproportionate periodontal destruction, suggesting shared biological vulnerability. Beyond local tissue damage, periodontitis provides a clinically accessible translational paradigm for systemic redox dysregulation, where sustained inflammatory activation coincides with measurable oxidative injury and exhaustion of antioxidant (AO) defenses across cardiometabolic and neuropsychiatric domains. In this critical narrative review, we argue that the excess periodontal burden in PZ reflects a “pathological confluence” shaped by antipsychotic-associated iatrogenic factors, rapid metabolic deterioration, and chronic oxidative distress. We appraise the thioredoxin-interacting protein (TXNIP)–NOD-like receptor (NLR) family pyrin domain-containing 3 (NLRP3) axis as a metabolic–redox sensor linking dysglycemia to periodontal inflammasome activation and downstream cytokine signaling, and address the advanced glycation end-products (AGEs)–receptor for advanced glycation end-products (RAGE) axis as a key immunometabolic redox pathway. We further discuss mitochondrial dysfunction, impaired mitophagy, and mitochondrial deoxyribonucleic acid (mtDNA) leakage as damage-associated molecular patterns (DAMPs) that can amplify systemic “silent inflammation”. Integrating evidence on periodontal pathogen–host interactions and redox-sensitive neuroimmune pathways (including NADPH oxidase 4 (NOX4)-linked microglial activation), we propose periodontitis as a plausible upstream amplifier that may exacerbate vascular dysfunction and compromise blood–brain barrier (BBB) integrity. Finally, we outline clinically measurable biomarker readouts to operationalize redox-informed integrated care and highlight the need for pragmatic trials targeting clinically meaningful endpoints to improve somatic longevity in PZ-spectrum populations. We acknowledge that current human evidence is largely associative and that the proposed mechanistic links remain hypothesis generating.
Full article
(This article belongs to the Special Issue Roles of Oxidative Stress in Human Pathophysiology)
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Open AccessReview
Skeletal Muscle Redox Signaling in Health and Disease: From Molecular Mechanisms to Therapeutic Exercise Strategies
by
Hyeong Rok Yun, Manish Kumar Singh, Sunhee Han, Jyotsna S. Ranbhise, Hanjoon Seo, Sung Soo Kim and Insug Kang
Antioxidants 2026, 15(6), 678; https://doi.org/10.3390/antiox15060678 - 28 May 2026
Abstract
Skeletal muscle plasticity is modulated by a delicate equilibrium between reactive oxygen species (ROS)-mediated signaling and oxidative distress. Although excessive oxidant accumulation impairs excitation–contraction coupling, accelerates fatigue, and contributes to muscle dysfunction, transient and compartmentalized ROS signals are now recognized as important modulators
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Skeletal muscle plasticity is modulated by a delicate equilibrium between reactive oxygen species (ROS)-mediated signaling and oxidative distress. Although excessive oxidant accumulation impairs excitation–contraction coupling, accelerates fatigue, and contributes to muscle dysfunction, transient and compartmentalized ROS signals are now recognized as important modulators of mitochondrial biogenesis, metabolic remodeling, proteostasis, and tissue repair processes after contractile stress. This review synthesizes the biphasic nature of redox biology in exercise physiology, interpreting this duality through the paradigm of hormesis. We discuss modality-specific redox responses associated with endurance, resistance and high-intensity interval training, emphasizing that adaptive outcomes depend not on global redox shifts, but on spatiotemporally confined signaling cascades within specific nanodomains. Furthermore, we evaluate the controversial role of antioxidant supplementation, highlighting evidence that high-dose or poorly timed antioxidant intake attenuates specific exercise-induced adaptive responses. We further discuss how aging and chronic disease narrow the adaptive redox window by impairing mitochondrial quality control, inflammatory resolution, and recovery capacity. This paradigm supports a precision exercise strategy in which training modality, intensity, recovery, and nutritional interventions are aligned to preserve adaptive redox signaling while avoiding cumulative oxidative injury.
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(This article belongs to the Topic Skeletal Muscle Adaptations to Oxidative Stress)
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Potential of Native Brazilian Fruits in Modulating Oxidative Stress and Inflammation: A Focused Review
by
Maria Carolina Zsigovics Alfino, Geni Rodrigues Sampaio, Adriano Costa de Camargo and Elizabeth Aparecida Ferraz da Silva Torres
Antioxidants 2026, 15(6), 677; https://doi.org/10.3390/antiox15060677 - 28 May 2026
Abstract
Chronic non-communicable diseases are closely linked to low-grade inflammation and oxidative stress. Native Brazilian fruits, rich in bioactive compounds such as polyphenols and carotenoids, have recognized antioxidant, anti-inflammatory, and neuroprotective properties. Mechanisms of action included inhibition of NF-κB signaling, downregulation of pro-inflammatory cytokines,
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Chronic non-communicable diseases are closely linked to low-grade inflammation and oxidative stress. Native Brazilian fruits, rich in bioactive compounds such as polyphenols and carotenoids, have recognized antioxidant, anti-inflammatory, and neuroprotective properties. Mechanisms of action included inhibition of NF-κB signaling, downregulation of pro-inflammatory cytokines, modulation of oxidative biomarkers, and improvement of metabolic parameters. Several studies demonstrate protective effects against insulin resistance, hepatic steatosis, cardiovascular alterations, and neuroinflammation, alongside modulation of gut microbiota. Most evidence is from animal or cell models, with scarce clinical trials, limiting translational applicability. Overall, native Brazilian fruits represent promising dietary sources of bioactive compounds that may contribute to the modulation of oxidative stress and chronic inflammation. Challenges include variability in phytochemical content due to species, maturity, processing, a lack of standardized extraction and dosage protocols, and limited bioavailability data. Although preclinical findings are robust, further controlled human trials are necessary to confirm their efficacy and clarify their role in the clinical management of inflammatory and neurodegenerative diseases.
Full article
(This article belongs to the Special Issue Bioactive Compounds: Antioxidant, Antibacterial, and Anti-Inflammatory Modulation—2nd Edition)
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Open AccessArticle
Phenyllactic Acid Restores Intestinal Epithelial Barrier to Alleviate Hypertriglyceridemic Acute Pancreatitis via a PPARγ-Dependent Mechanism
by
Ze-Yun Cao, Xun Zou, Hong-Li Li, Xuan Kong, Li-Long Pan, Jun Yang and Xiao-Liang Dong
Antioxidants 2026, 15(6), 676; https://doi.org/10.3390/antiox15060676 - 28 May 2026
Abstract
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Hypertriglyceridemic acute pancreatitis (HTG-AP) progresses rapidly with poor prognosis. Intestinal barrier dysfunction and excessive oxidative stress contribute to its pathogenesis, but specific mediators linking gut injury, oxidative stress and pancreatic damage remain unclear. Here, we identify endogenous phenyllactic acid (PLA) as a critical
[...] Read more.
Hypertriglyceridemic acute pancreatitis (HTG-AP) progresses rapidly with poor prognosis. Intestinal barrier dysfunction and excessive oxidative stress contribute to its pathogenesis, but specific mediators linking gut injury, oxidative stress and pancreatic damage remain unclear. Here, we identify endogenous phenyllactic acid (PLA) as a critical metabolite regulating intestinal barrier integrity and oxidative homeostasis in HTG-AP. We noted serum PLA, a disease-associated metabolite whose reduction correlates with gut dysbiosis and pancreatic inflammation in HTG-AP. PLA supplementation in HTG-AP mice attenuated intestinal barrier dysfunction and mitigated intestinal oxidative stress, as evidenced by improved gut dysbiosis, reduced reactive oxygen species accumulation, restored superoxide dismutase activity, restored barrier integrity, reduced bacterial translocation to the pancreas, and decreased serum lipopolysaccharide levels, ultimately mitigating pancreatic injury. RNA sequencing of colonic tissue revealed peroxisome proliferator-activated receptor (PPAR) signaling as one of the most significantly altered pathways in HTG-AP. PPARγ expression was markedly reduced in colonic epithelial cells and upregulated upon PLA treatment. Knockdown of colonic epithelial PPARγ via adeno-associated virus abrogated the beneficial effects of PLA on intestinal barrier integrity, oxidative stress and pancreatic injury in HTG-AP mice. The protective effects of PLA were phenocopied by the PPARγ agonist rosiglitazone. Collectively, these findings identified gut microbiota-derived PLA as an endogenously derived metabolite modulating intestinal oxidative stress and barrier function. Using male C57BL/6J mice to establish an HTG-AP model, we further revealed that PLA exerts protective effects against HTG-AP by targeting colonic PPARγ to modulate the gut–pancreas axis, highlighting PLA as a promising candidate for targeted intervention in HTG-AP.
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Nutrients 2026—Clinical Nutrition: From Research to Practice—Submissions Approaching & Plenary Speaker Announcement, 22–24 October 2026, Barcelona, Spain
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