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Antioxidants
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Oxidative Stress and Inflammation as Targets for Novel Preventive and...
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Oxidative Stress and Inflammation as Targets for Novel Preventive and Therapeutic Approaches in Non-Communicable Diseases: 4th Edition

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: 30 April 2025 | Viewed by 4315

Special Issue Editors

Dr. Jessica Ruzzolini

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Guest Editor
Department of Experimental and Clinical Biomedical Sciences “Mario Serio”, University of Florence, 50134 Florence, Italy
Interests: cancer; drug resistance; nutraceutics; complementary therapy; tumor microenvironment
Special Issues, Collections and Topics in MDPI journals
Dr. Silvia Peppicelli

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Guest Editor
Department of Experimental and Clinical Biomedical Sciences “Mario Serio”, University of Florence, 50134 Florence, Italy
Interests: tumor microenvironment; melanoma progression; cancer stem cells; tumor acidosis; tumor metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Considering the great success of the Special Issue “Oxidative Stress and Inflammation as Targets for Novel Preventive and Therapeutic Approaches in Non-Communicable Diseases III” we are pleased to announce the fourth edition of this fascinating topic. Non-communicable diseases (NCDs) are chronic diseases characterized by a long duration and very slow progression, a profile that includes most aging-related diseases. NCDs account for approximately 70% of the deaths from cardiovascular diseases, cancer, diabetes mellitus, chronic kidney disease, and Alzheimer’s disease. This group of diseases is characterized by an altered inflammatory status, a redox imbalance, and compromised autophagy, which are critical to consider in the development of novel therapeutic strategies. We welcome contributions to this Special Issue that are either reviews of the literature or original research articles describing the role of oxidative stress and inflammation, their interplay with autophagy, and their modulation by novel preventative and therapeutic strategies targeting signaling pathways and gender responses. These can include drug combinations with natural active compounds, in-cell culture systems, preclinical animal models, and human clinical studies. Human clinical studies aiming to analyze the effects (and eventually the gender response) of diets, functional foods, or natural bioactive compounds in the prevention or therapy of NCDs are also welcome.

Dr. Jessica Ruzzolini
Dr. Silvia Peppicelli
Guest Editors

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 100 words) can be sent to the Editorial Office for announcement on this website.

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

  • oxidative stress
  • inflammation
  • redox signaling
  • bioactive compounds
  • cancer
  • cardiovascular disease
  • metabolic disease
  • chronic kidney disease
  • aging
  • Alzheimer's disease
  • gender difference
  • dietary intervention
  • meta-analysis

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Published Papers (3 papers)

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Research

20 pages, 8537 KiB  
Article
Protective Effects of Tormentic Acid on Unilateral Ureteral Obstruction-Induced Renal Injury, Inflammation, and Fibrosis: A Comprehensive Approach to Reducing Oxidative Stress, Apoptosis, and Ferroptosis
by Ah Young Yang, Jung-Yeon Kim, Mi-Gyeong Gwon, Hyun Hee Kwon, Jaechan Leem and Eon-Ju Jeon
Antioxidants 2025, 14(1), 13; https://doi.org/10.3390/antiox14010013 - 25 Dec 2024
Viewed by 746
Abstract
Chronic kidney disease (CKD) progresses through mechanisms involving inflammation, fibrosis, and oxidative stress, leading to the gradual structural and functional deterioration of the kidneys. Tormentic acid (TA), a triterpenoid compound with known anti-inflammatory and antioxidant properties, shows significant potential in counteracting these pathological [...] Read more.
Chronic kidney disease (CKD) progresses through mechanisms involving inflammation, fibrosis, and oxidative stress, leading to the gradual structural and functional deterioration of the kidneys. Tormentic acid (TA), a triterpenoid compound with known anti-inflammatory and antioxidant properties, shows significant potential in counteracting these pathological processes. This study explored the protective role of TA in a unilateral ureteral obstruction (UUO)-induced CKD model. Mice received TA through intraperitoneal injections at a dosage of 5 mg/kg per day for 8 consecutive days, commencing a day before the UUO procedure. The TA treatment significantly improved both structural and functional kidney injury. It suppressed cytokine expression and reduced immune cell infiltration, inhibited the activation of the mitogen-activated protein kinase cascade, and alleviated endoplasmic reticulum stress. Moreover, TA displayed potent anti-fibrotic effects by reversing epithelial-to-mesenchymal transition and inhibiting Smad2/3 activation, reducing extracellular matrix deposition. TA also mitigated oxidative stress by attenuating lipid peroxidation and boosting antioxidant defenses. Additionally, it inhibited apoptosis and ferroptosis by reducing oxidative stress and modulating key cell death markers. Collectively, these findings indicate that TA provides comprehensive renoprotection in the UUO model by effectively targeting inflammation, fibrosis, oxidative stress, and tubular cell death in CKD progression. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation as Targets for Novel Preventive and Therapeutic Approaches in Non-Communicable Diseases: 4th Edition)
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19 pages, 3294 KiB  
Article
Gut Microbiota-Derived Trimethylamine Promotes Inflammation with a Potential Impact on Epigenetic and Mitochondrial Homeostasis in Caco-2 Cells
by Laura Bordoni, Irene Petracci, Giulia Feliziani, Gaia de Simone, Chiara Rucci and Rosita Gabbianelli
Antioxidants 2024, 13(9), 1061; https://doi.org/10.3390/antiox13091061 - 30 Aug 2024
Cited by 2 | Viewed by 1438
Abstract
Trimethylamine (TMA), a byproduct of gut microbiota metabolism from dietary precursors, is not only the precursor of trimethylamine-N-oxide (TMAO) but may also affect gut health. An in vitro model of intestinal epithelium of Caco-2 cells was used to evaluate the impact of TMA [...] Read more.
Trimethylamine (TMA), a byproduct of gut microbiota metabolism from dietary precursors, is not only the precursor of trimethylamine-N-oxide (TMAO) but may also affect gut health. An in vitro model of intestinal epithelium of Caco-2 cells was used to evaluate the impact of TMA on inflammation, paracellular permeability, epigenetics and mitochondrial functions. The expression levels of pro-inflammatory cytokines (IL-6, IL-1β) increased significantly after 24 h exposure to TMA 1 mM. TMA exposure was associated with an upregulation of SIRT1 (TMA 1 mM, 400 μM, 10 μM) and DNMT1 (TMA 1 mM, 400 µM) genes, while DNMT3A expression decreased (TMA 1 mM). In a cell-free model, TMA (from 0.1 µM to 1 mM) induced a dose-dependent reduction in Sirtuin enzyme activity. In Caco-2 cells, TMA reduced total ATP levels and significantly downregulated ND6 expression (TMA 1 mM). TMA excess (1 mM) reduced intracellular mitochondrial DNA copy numbers and increased the methylation of the light-strand promoter in the D-loop area of mtDNA. Also, TMA (1 mM, 400 µM, 10 µM) increased the permeability of Caco-2 epithelium, as evidenced by the reduced transepithelial electrical resistance values. Based on our preliminary results, TMA excess might promote inflammation in intestinal cells and disturb epigenetic and mitochondrial homeostasis. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation as Targets for Novel Preventive and Therapeutic Approaches in Non-Communicable Diseases: 4th Edition)
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16 pages, 5952 KiB  
Article
Sex Differences in Hepatic Inflammation, Lipid Metabolism, and Mitochondrial Function Following Early Lipopolysaccharide Exposure in Epileptic WAG/Rij Rats
by Stefania Melini, Giovanna Trinchese, Adriano Lama, Fabiano Cimmino, Filomena Del Piano, Federica Comella, Nicola Opallo, Antonio Leo, Rita Citraro, Luigia Trabace, Giuseppina Mattace Raso, Claudio Pirozzi, Maria Pina Mollica and Rosaria Meli
Antioxidants 2024, 13(8), 957; https://doi.org/10.3390/antiox13080957 - 7 Aug 2024
Viewed by 1638
Abstract
Among the non-communicable neurological diseases, epilepsy is characterized by abnormal brain activity with several peripheral implications. The role of peripheral inflammation in the relationship between seizure development and nonalcoholic fatty liver disease based on sex difference remains still overlooked. Severe early-life infections lead [...] Read more.
Among the non-communicable neurological diseases, epilepsy is characterized by abnormal brain activity with several peripheral implications. The role of peripheral inflammation in the relationship between seizure development and nonalcoholic fatty liver disease based on sex difference remains still overlooked. Severe early-life infections lead to increased inflammation that can aggravate epilepsy and hepatic damage progression, both related to increased odds of hospitalization for epileptic patients with liver diseases. Here, we induced a post-natal-day 3 (PND3) infection by LPS (1 mg/kg, i.p.) to determine the hepatic damage in a genetic model of young epileptic WAG/Rij rats (PND45). We evaluated intra- and inter-gender differences in systemic and liver inflammation, hepatic lipid dysmetabolism, and oxidative damage related to mitochondrial functional impairment. First, epileptic rats exposed to LPS, regardless of gender, displayed increased serum hepatic enzymes and altered lipid profile. Endotoxin challenge triggered a more severe inflammatory and immune response in male epileptic rats, compared to females in both serum and liver, increasing pro-inflammatory cytokines and hepatic immune cell recruitment. Conversely, LPS-treated female rats showed significant alterations in systemic and hepatic lipid profiles and reduced mitochondrial fatty acid oxidation. The two different sex-dependent mechanisms of LPS-induced liver injury converge in increased ROS production and related mitochondrial oxidative damage in both sexes. Notably, a compensatory increase in antioxidant defense was evidenced only in female rats. Our study with a translational potential demonstrates, for the first time, that early post-natal infections in epileptic rats induced or worsened hepatic disorders in a sex-dependent manner, amplifying inflammation, lipid dysmetabolism, and mitochondrial impairment. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation as Targets for Novel Preventive and Therapeutic Approaches in Non-Communicable Diseases: 4th Edition)
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