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Antioxidants
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Novel Strategies for Oxidative Stress Management: Dietary Interventions for Liver...
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Novel Strategies for Oxidative Stress Management: Dietary Interventions for Liver and Gut Health

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 30 August 2026 | Viewed by 10581

Special Issue Editors

Dr. Antonio Cilla

E-Mail Website
Guest Editor
Bionutest Research Group—Nutrition and Food Science Area, Faculty of Pharmacy and Food Sciences, University of Valencia, Av. Vicente Andrés Estellés s/n, 46100 Burjassot, Valencia, Spain
Interests: functional foods; bioactive compounds; antioxidant capacity; sterols; phytochemicals; bioaccessibility; bioavailability; bioactivity; cell cultures; chemoprevention; oxidative stress; eryptosis; food by-products
Special Issues, Collections and Topics in MDPI journals
Dr. Mussa Makran

E-Mail Website
Guest Editor Assistant
Nutrition Department, Faculty of Health Sciences, Fernando Pessoa Canarias University, Calle la Juventud s/n, 35450 Las Palmas, Spain
Interests: functional foods; bioactive compounds

Special Issue Information

Dear Colleagues,

Oxidative stress is a critical driver in the pathogenesis and progression of liver and gastrointestinal diseases, including nonalcoholic fatty liver disease, hepatocellular carcinoma, and inflammatory bowel diseases. Growing evidence highlights the potential of dietary interventions to modulate oxidative stress pathways, restore redox homeostasis, and slow or prevent disease progression. Bioactive dietary compounds with antioxidant properties act on multiple biological levels, influencing inflammatory signaling, mitochondrial function, endogenous antioxidant systems, and gut–liver axis communication.

This Special Issue aims to showcase innovative research on dietary strategies to mitigate oxidative stress and improve liver and gut health. We welcome original research articles and comprehensive reviews that investigate the molecular mechanisms by which dietary components attenuate oxidative damage. Topics of interest include the regulation of antioxidant defense networks, activation of redox-sensitive transcription factors, modulation of inflammatory pathways, and role of gut microbiota in maintaining redox balance across hepatic and intestinal systems.

Submissions may include preclinical models (cellular and animal) and human intervention studies. By bringing together mechanistic insights and translational findings, this Special Issue seeks to support the development of evidence-based dietary recommendations for the prevention and management of oxidative stress-related liver and gastrointestinal disorders.

Dr. Antonio Cilla
Guest Editor

Dr. Mussa Makran
Guest Editor Assistant

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • antioxidant compounds
  • phytochemicals
  • dietary interventions
  • hepatic disease
  • intestinal disease
  • redox homeostasis

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Published Papers (3 papers)

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Research

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21 pages, 1764 KB  
Article
Anti-Inflammatory Activity of In Vitro Digested Manna in a Caco-2 and RAW264.7 Cells Co-Culture Model of Inflammatory Bowel Disease
by Ilenia Concetta Giardina, Mussa Makran, Ignazio Restivo, Francesco Pappalardo, Guadalupe Garcia-Llatas, Maria Cristina Barbalace, Luisa Tesoriere, Antonio Cilla and Alessandro Attanzio
Antioxidants 2026, 15(5), 601; https://doi.org/10.3390/antiox15050601 - 9 May 2026
Viewed by 437
Abstract
Inflammatory bowel disease (IBD) involves intestinal barrier dysfunction and chronic inflammation. Manna, derived from the solidified phloem sap of Fraxinus species, is rich in mannitol and polyphenols and valued for its laxative, antioxidant, and anti-inflammatory properties. In this study, manna was digested in [...] Read more.
Inflammatory bowel disease (IBD) involves intestinal barrier dysfunction and chronic inflammation. Manna, derived from the solidified phloem sap of Fraxinus species, is rich in mannitol and polyphenols and valued for its laxative, antioxidant, and anti-inflammatory properties. In this study, manna was digested in vitro to obtain its bioaccessible fraction (BFM), whose anti-inflammatory activity was tested in a Caco-2/RAW264.7 co-culture model. Caco-2 cells were pretreated with BFM (1/20 v/v, 6 mg/mL) 90 min before LPS stimulation (1 µg/mL, 24 h) of macrophages, using budesonide (1 μM) as reference. BFM pretreatment significantly reduced IL-8 secretion (70.8%) in Caco-2 cells, and IL-6 (43.1%) and TNF-α (83.1%) in RAW264.7 macrophages. It also improved redox balance in Caco-2 cells by decreasing iNOS (48.2%), NOx (33.2%), and ROS (26.4%), while stabilizing tight junctions through occludin upregulation (18.3%). Mechanistically, BFM downregulated NF-κB-COX-2-PGE2 signaling in macrophages, reducing NF-κB p65 nuclear translocation (65.6%), COX-2 levels (79.3%), and PGE2 production (50.8%). Co-treatment with budesonide showed antagonism for most markers (Combination Index (CI), 0.41–0.76), but additive/synergistic effects on ROS (CI, 1.06 ± 0.06) and NOx (CI, 1.10 ± 0.04). These findings highlight manna’s strong anti-inflammatory activity at a low, non-laxative dose (3.8 g/day), supporting its nutraceutical potential in IBD management. Full article
(This article belongs to the Special Issue Novel Strategies for Oxidative Stress Management: Dietary Interventions for Liver and Gut Health)
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25 pages, 6588 KB  
Article
Spirulina Preconditioning Attenuates Ischemia–Reperfusion Injury in a Steatotic Rat Liver Model
by Eya Baily, Kamel Mhalhel, Soumaya Ben Ahmed, Mohamed Amine Zaouali, Giuseppe Montalbano, Ines Naouar, Antonino Germanà and Hassen Ben Abdennebi
Antioxidants 2026, 15(3), 390; https://doi.org/10.3390/antiox15030390 - 19 Mar 2026
Viewed by 941
Abstract
Ischemia and reperfusion (IR) injuries may produce deleterious effects on hepatic tissue after liver surgery and transplantation. The consequences of IR are more evident in pathological steatotic livers. Spirulina (Arthrospira platensis) is known for its potential to modulate inflammatory responses and [...] Read more.
Ischemia and reperfusion (IR) injuries may produce deleterious effects on hepatic tissue after liver surgery and transplantation. The consequences of IR are more evident in pathological steatotic livers. Spirulina (Arthrospira platensis) is known for its potential to modulate inflammatory responses and enhance antioxidant defenses. The current investigation assessed whether spirulina pretreatment mitigates hepatic IR injury exacerbated by steatosis in rats. Thirty male Wistar rats were divided into five groups: sham, IR, HFD, HFD + IR, and SP1000 (HFD + IR + spirulina 1000 mg/kg/day; oral gavage). Liver injury, oxidative stress, inflammatory signaling, and inflammasome/pyroptosis-related markers were assessed using serum transaminases, hematoxylin–eosin staining, immunofluorescence, and qRT-PCR. High-fat diet-fed rats developed steatosis, which significantly worsened IR-induced liver damage, as shown by the respective steatosis histological score, the elevated alanine aminotransferase (ALT) and aspartate aminotransferase (AST), and higher expression of inflammatory markers, including Toll-like receptor (TLR4), nuclear factor kappa B (NF-κB), tumor necrosis factor alpha (TNF-α), and interleukin-1 beta (IL-1β) and inflammasome/pyroptosis-related transcripts, namely NOD-like receptor family pyrin domain-containing 3 (NLRP3), interleukin-18 (IL18), and gasdermin D (GSDMD). Oxidative stress was exacerbated, as reflected by higher levels of malondialdehyde (MDA) and reduced antioxidant defenses (superoxide dismutase (SOD) activity, reduced glutathione (GSH) content, glutathione peroxidase (GPx) expression, and heme oxygenase-1 (HO-1) expression). Furthermore, HFD + IR upregulated sterol regulatory element-binding protein-1c (SREBP-1c) expression and downregulated AMP-activated protein kinase (AMPK) expression. Spirulina supplementation significantly attenuated liver injury and transaminase release, reduced MDA, restored antioxidant parameters, downregulated inflammatory and inflammasome-related gene expression, and shifted both SREBP-1c and AMPK expressions toward control levels. Full article
(This article belongs to the Special Issue Novel Strategies for Oxidative Stress Management: Dietary Interventions for Liver and Gut Health)
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Review

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22 pages, 4394 KB  
Review
Bilirubin Hepatic and Intestinal Transport and Catabolism: Physiology, Pathophysiology, and Benefits
by Zachary A. Kipp, Sally N. Pauss, Genesee J. Martinez, Terry D. Hinds, Jr. and Wang-Hsin Lee
Antioxidants 2025, 14(11), 1326; https://doi.org/10.3390/antiox14111326 - 3 Nov 2025
Cited by 7 | Viewed by 8636
Abstract
Bilirubin, a metabolite derived from heme degradation, has traditionally been regarded as a waste product and a marker of liver injury. However, increasing evidence suggests that bilirubin also functions as a hormone, and reduced levels are associated with metabolic dysfunction. Studies have shown [...] Read more.
Bilirubin, a metabolite derived from heme degradation, has traditionally been regarded as a waste product and a marker of liver injury. However, increasing evidence suggests that bilirubin also functions as a hormone, and reduced levels are associated with metabolic dysfunction. Studies have shown a strong association between low circulating bilirubin levels and an increased risk of metabolic disorders and cardiovascular disease. To advance bilirubin-based treatment strategies, it is essential to elucidate the mechanisms underlying bilirubin transport and metabolism. Therefore, we provide an in-depth discussion of bilirubin production and its subsequent fates, with a particular focus on the transport between the liver and the intestine. We describe the molecular players involved in heme degradation and biliverdin formation, leading to bilirubin production, followed by its transport from the bloodstream to hepatocytes and from the liver to the intestine. We discuss intestinal bilirubin catabolism, including the microbiome generation of urobilinogen, urobilin, and other metabolites. Finally, we discuss how bilirubin clearance and catabolism intersect with its metabolic effects, highlighting potential therapeutic targets. By integrating these aspects, this review provides a comprehensive understanding of bilirubin’s physiological importance, intestinal transport, and breakdown, as well as insights into novel strategies for treating hypobilirubinemia-associated disorders. Full article
(This article belongs to the Special Issue Novel Strategies for Oxidative Stress Management: Dietary Interventions for Liver and Gut Health)
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