Special Issues

Modulation of Oxidative Stress as a Pharmacological Strategy
Editor: Luciano Saso, Brigitta Buttari and Marzia Arese

Submission Deadline: 31 January 2024 (Status: Open)

Special Issue Editors

Prof. Luciano Saso      Email   |   Website
Department of Physiology and Pharmacology "Vittorio Erspamer", Sapienza University, Rome, Italy
Interests: modulation of oxidative stress; NRF2; antioxidants; pro-oxidants; pharmacology

Dr. Brigitta Buttari      Email   |   Website
Department of Cardiovascular and Endocrine-metabolic Diseases, and Aging, Istituto Superiore di Sanità, Rome, Italy
Interests: modulation of oxidative stress; NRF2; antioxidants; immunology

Prof. Marzia Arese      Email   |   Website
Department of Biochemical Science "A. Rossi Fanelli", Sapienza University, Rome, Italy
Interests: Nitric oxide signaling; mitochondrial pathophysiology; oxidative stress responses

Special Issue Information

Dear Colleagues,

Oxidative stress (OS) is considered a key element driving pathophysiological processes that play a role in the onset and progression of various non-communicable diseases. According to its widely endorsed definition, OS arise from an imbalance between oxidants and antioxidants in favor of the oxidants, associated with the disruption of the physiological redox signaling pathways and leading to molecular/ macromolecular damage.

Through protein modifications, DNA lesions and lipid peroxidation, OS may alter multiple biological processes, such as the induction of inflammation, apoptosis and endoplasmic reticulum stress, as well as the deregulation of autophagy, impairment of mitochondrial function/metabolism, promoting dysfunctional immune responses, and accelerating all mechanisms involved in the pathological progression and exacerbation of symptoms. However, recent research has shown that OS byproducts, such as hydrogen peroxide, hydrogen sulfide and nitric oxide, are crucial effectors of the redox signal. The Nuclear factor erythroid-2-Related Factor 2 (NRF2) is a transcription factor activated in response to oxidative stress to control fundamental cellular processes such as apoptosis, autophagy, angiogenesis, proliferation, prevent cell damage and suppresses pro-inflammatory cytokines. Multiple genes encoding for cytoprotective proteins, including antioxidant, anti-inflammatory, and detoxifying enzymes, as well as proteins that assist in the repair or removal of damaged macromolecules are regulated directly by the NRF2 signaling pathway or by a complex relationship with other signaling pathways. Considering the fundamental role of NRF2 in the modulation of inflammatory and oxidative processes, a great interest is assigned to the study of natural and synthetic substances capable of activating the NRF2 pathway to design new therapeutic strategies to treat oxidative stress and inflammatory diseases.

We invite researchers in this field and participants of the COST Action CA20121, Bench to Bedside Transition for Pharmacological regulation of NRF2 in non-communicable diseases (BenBedPhar) to submit their contributions (original articles, reviews, or perspectives) relevant to the scope of the Special Issue, including, but not limited to modulators of oxidative stress as potential therapeutic strategies for controlling disease or as a preventive measure.

Luciano Saso, Brigitta Buttari and Marzia Arese
Guest Editors


oxidative stress; antioxidants; hydrogen peroxide; hydrogen sulfide; Nuclear factor erythroid-2-Related Factor 2 (NRF2); modulation; pharmacology

Manuscript Submission Information

Manuscripts should be submitted via our online editorial system at https://www.biolifesas.org/journalx_brha/authorLogOn.action by registering and logging in to this website. Once you are registered, click here to start your submission. Manuscripts can be submitted now or up until the deadline. All papers will go through peer-review process. Accepted papers will be published in the journal (as soon as accepted) and meanwhile listed together on the special issue website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts will be thoroughly refereed through a double-blind peer-review process. Please visit the Instruction for Authors page before submitting a manuscript. Submitted manuscripts should be well formatted in good English.

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  • Article
    José-Luis Rodríguez, Zoyla-Mirella Clavo, Mariella Ramos-Gonzalez, Max De La Cruz, Luis Inostroza-Ruiz, Wendy Bada-Laura, Olga Palomino, Maria S. Fernández-Alfonso, Raquel Mateos, Luis Goya
    Journal of Biological Regulators and Homeostatic Agents. 2023, 37(11): 6179-6192. https://doi.org/10.23812/j.biol.regul.homeost.agents.20233711.590
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    Background: Oxidative stress is a potential cause of cardiovascular pathologies, so the protection of endothelial cells and vascular tissues is essential to avoid such conditions, perhaps with the use of natural compounds rich in phenolic compounds with a proven high antioxidant capacity. The present study was designed to show the cytoprotective capacity of phenolic extracts from the plant Brunfelsia grandiflora, as well as describe its antioxidant defense mechanisms and the expression of some molecular markers involved in cellular protection.

    Methods: Human EA.hy926 cells were exposed to Brunfelsia grandiflora (B. grandiflora) extract (1, 10, 25, 50, 100, and 200 μg/mL) in co-treatment (22 h with 100 μM tert-Butyl hydroperoxide (t-BOOH) and B. grandiflora concentrations) and pre-treatment (18 h of B. grandiflora concentrations and then 200 μM t-BOOH for 4 h). Cell viability, reactive oxygen species (ROS) production, nitric oxide (NO) levels, caspase 3/7 activity, malondialdehyde (MDA) concentration, and reduction in reduced glutathione (GSH) levels, glutathione peroxidase (GPx), and glutathione reductase (GR) activity were measured, and real-time PCR molecular assays superoxide dismutase (SOD2), nuclear factor E2-related factor (NRF2), BCL-2-associated X protein (BAX), and B-cell lymphoma 2 (BCL2) were performed. Data were analyzed via one-way ANOVA followed by Tukey's post hoc test.

    Results: B. grandiflora bark extract, mainly at concentrations of 25, 50, 100, and 200 μg/mL, significantly (p < 0.05) reversed (pre-treatment and co-treatment) the deleterious effects of t-BOOH on EA.hy926 endothelial cells, which were significantly decreased cell viability, GSH activity, and SOD2 and NRF2 expression (p < 0.05); and significantly increased levels of ROS, NO, MDA, caspase-3/7 activity, GPx activity, GR activity, and the BAX/BCL2 ratio (p < 0.05).

    Conclusions: B. grandiflora extract was able to reduce the deleterious effects of t-BOOH on EA.hy926 endothelial cells, which may indicate its potential phytotherapeutic benefit against cytotoxic damage caused by chemical agents.