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The Interplay of Oxidative Stress and Inflammation: From Mechanisms to Therapeutic Approaches

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (30 November 2022) | Viewed by 27541

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Prof. Dr. Lorenza Speranza

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Department of Medicine and Science of Aging, University "G. D’Annunzio", 66100 Chieti Pescara, Italy
Interests: oxidative stress; cellular biology; disease; network antioxidant; bioactive vegetable; endogenous antioxidant enzymes; inflammation; nutrition; translation medicine; life sciences
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Dr. Sara Franceschelli

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Department of Medicine and Science of Aging, University “G. D’Annunzio”, 66100 Chieti Pescara, Italy
Interests: nutrition; cellular biology; oxidative stress; cardiovascular disease; endogenous antioxidant enzymes; bioactive vegetable; molecules
Special Issues, Collections and Topics in MDPI journals

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Dear Colleagues,

The field of oxidative stress and inflammation encompasses cell biology, biochemistry, chemistry, physiology and pathophysiology, extending to medicine and health and disease research as well. Oxidative stress and inflammation are closely related pathophysiological processes that can trigger one another. Both processes are found in many pathological conditions, including neurodegenerative diseases, diabetes, cardiovascular diseases, liver disease, chronic kidney disease, cancer and aging. Therefore, the screening of bio-compounds that specifically target both inflammation and oxidative stress or the concomitant use of antioxidant and anti-inflammatory agents could provide further mechanistic insight into the molecular switches controlling oxidative stress and inflammatory responses.

For this Special Issue of IJMS, we are inviting submissions in the form of an original article or review on the several molecular pathways that oxidative stress and inflammation can be affect, leading to new preventive or therapeutic approaches for the mentioned diseases.

Prof. Dr. Lorenza Speranza
Prof. Dr. Sara Franceschelli
Guest Editors

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

oxidative stress
inflammation
biocompounds
cardiovascular disease
therapeutic approach
neurodegenerative disease
chronic disease
disease

Published Papers (8 papers)

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Research

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16 pages, 3654 KiB

Open AccessArticle

Investigation of the Effects of Monomeric and Dimeric Stilbenoids on Bacteria-Induced Cytokines and LPS-Induced ROS Formation in Bone Marrow-Derived Dendritic Cells

by Peter Riber Johnsen, Cecilia Pinna, Luce Mattio, Mathilde Bech Strube, Mattia Di Nunzio, Stefania Iametti, Sabrina Dallavalle, Andrea Pinto and Hanne Frøkiær

Int. J. Mol. Sci. 2023, 24(3), 2731; https://doi.org/10.3390/ijms24032731 - 01 Feb 2023

Cited by 2 | Viewed by 1750

Abstract

Stilbenoids are anti-inflammatory and antioxidant compounds, with resveratrol being the most investigated molecule in this class. However, the actions of most other stilbenoids are much less studied. This study compares five monomeric (resveratrol, piceatannol, pterostilbene, pinostilbene, and trimethoxy-resveratrol) and two dimeric (dehydro-δ-viniferin and trans-δ-viniferin) stilbenoids for their capability to modulate the production of bacteria-induced cytokines (IL-12, IL-10, and TNF-α), as well as lipopolysaccharide (LPS)-induced reactive oxygen species (ROS), in murine bone marrow-derived dendritic cells. All monomeric species showed dose-dependent inhibition of E. coli-induced IL-12 and TNF-α, whereas only resveratrol and piceatannol inhibited IL-10 production. All monomers, except trimethoxy-resveratrol, inhibited L. acidophilus-induced IL-12, IL-10, and TNF-α production. The dimer dehydro-δ-viniferin remarkably enhanced L. acidophilus-induced IL-12 production. The contrasting effect of resveratrol and dehydro-δ-viniferin on IL-12 production was due, at least in part, to a divergent inactivation of the mitogen-activated protein kinases by the two stilbenoids. Despite having moderate to high total antioxidant activity, dehydro-δ-viniferin was a weak inhibitor of LPS-induced ROS formation. Conversely, resveratrol and piceatannol potently inhibited LPS-induced ROS formation. Methylated monomers showed a decreased antioxidant capacity compared to resveratrol, also depending on the methylation site. In summary, the immune-modulating effect of the stilbenoids depends on both specific structural features of tested compounds and the stimulating bacteria. Full article

(This article belongs to the Special Issue The Interplay of Oxidative Stress and Inflammation: From Mechanisms to Therapeutic Approaches)

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17 pages, 3405 KiB

Open AccessArticle

Hydroxytyrosol Reduces Foam Cell Formation and Endothelial Inflammation Regulating the PPARγ/LXRα/ABCA1 Pathway

by Sara Franceschelli, Federica De Cecco, Mirko Pesce, Patrizio Ripari, Maria Teresa Guagnano, Arturo Bravo Nuevo, Alfredo Grilli, Silvia Sancilio and Lorenza Speranza

Int. J. Mol. Sci. 2023, 24(3), 2057; https://doi.org/10.3390/ijms24032057 - 20 Jan 2023

Cited by 7 | Viewed by 2764

Abstract

Cholesterol accumulation in macrophages leads to the formation of foam cells and increases the risk of developing atherosclerosis. We have verified whether hydroxytyrosol (HT), a phenolic compound with anti-inflammatory and antioxidant properties, can reduce the cholesterol build up in THP-1 macrophage-derived foam cells. We have also investigated the potential mechanisms. Oil Red O staining and high-performance liquid chromatography (HPLC) assays were utilized to detect cellular lipid accumulation and cholesterol content, respectively, in THP-1 macrophages foam cells treated with HT. The impact of HT on cholesterol metabolism-related molecules (SR-A1, CD36, LOX-1, ABCA1, ABCG1, PPARγ and LRX-α) in foam cells was assessed using real-time PCR (RT-qPCR) and Western blot analyses. Finally, the effect of HT on the adhesion of THP-1 monocytes to human vascular endothelial cells (HUVEC) was analyzed to study endothelial activation. We found that HT activates the PPARγ/LXRα pathway to upregulate ABCA1 expression, reducing cholesterol accumulation in foam cells. Moreover, HT significantly inhibited monocyte adhesion and reduced the levels of adhesion factors (ICAM-1 and VCAM-1) and pro-inflammatory factors (IL-6 and TNF-α) in LPS-induced endothelial cells. Taken together, our findings suggest that HT, with its ability to interfere with the import and export of cholesterol, could represent a new therapeutic strategy for the treatment of atherosclerotic disease. Full article

(This article belongs to the Special Issue The Interplay of Oxidative Stress and Inflammation: From Mechanisms to Therapeutic Approaches)

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22 pages, 5535 KiB

Open AccessArticle

Quercetin Ameliorates Testicular Damage in Zucker Diabetic Fatty Rats through Its Antioxidant, Anti-Inflammatory and Anti-Apoptotic Properties

by Eva Tvrdá, Ján Kováč, Kristína Ferenczyová, Barbora Kaločayová, Michal Ďuračka, Filip Benko, Viera Almášiová and Monika Barteková

Int. J. Mol. Sci. 2022, 23(24), 16056; https://doi.org/10.3390/ijms232416056 - 16 Dec 2022

Cited by 4 | Viewed by 1544

Abstract

The aim of this study was to investigate the effects of quercetin (QUE) on the testicular architecture as well as markers of oxidative, inflammatory, and apoptotic profile of male gonads in Zucker diabetic fatty (ZDF) rats suffering from Type 2 diabetes mellitus in the absence or presence of obesity. QUE was administered orally at a dose of 20 mg/kg/day for 6 weeks. Morphometric analysis revealed that QUE treatment led to an improvement in testicular appearance, particularly in the case of Obese ZDF rats. Furthermore, a significant stabilization of the antioxidant capacity (p < 0.05), superoxide dismutase and catalase activity (p < 0.01), with a concomitant decrease in lipid peroxidation (p < 0.05) were observed in Obese ZDF animals exposed to QUE. Our data also indicate a significant decline in the levels of interleukin (IL)-1 (p < 0.05), IL-6 (p < 0.01) and tumor necrosis factor alpha (p < 0.001) following QUE supplementation to Obese ZDF rats in comparison with their respective control. Finally, a significant down-regulation of the pro-apoptotic BAX protein (p < 0.0001) was observed in Obese ZDF rats administered with QUE, while a significant Bcl-2 protein overexpression (p < 0.0001) was recorded in Lean ZDF animals when compared to their untreated control. As such, our results suggest that QUE is a potentially beneficial agent to reduce testicular damage in ZDF rats with Type 2 diabetes mellitus by decreasing oxidative stress, chronic inflammation, and excessive cell loss through apoptosis. Full article

(This article belongs to the Special Issue The Interplay of Oxidative Stress and Inflammation: From Mechanisms to Therapeutic Approaches)

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Review

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13 pages, 1735 KiB

Open AccessReview

Neuroinflammation and Oxidative Stress in Individuals Affected by DiGeorge Syndrome

by Michela Menghi, Ginevra Micangeli, Francesca Tarani, Carolina Putotto, Federica Pirro, Alessandro Mariani, Carla Petrella, Federica Pulvirenti, Bianca Cinicola, Fiorenza Colloridi, Luigi Tarani and Marco Fiore

Int. J. Mol. Sci. 2023, 24(4), 4242; https://doi.org/10.3390/ijms24044242 - 20 Feb 2023

Cited by 1 | Viewed by 10416

Abstract

DiGeorge syndrome (DGS) is a rare genetic disease caused by microdeletions of the 22q11.2 region (DGS1). A haploinsufficiency at 10p level has been proposed also as a DGS cause (DGS2). Clinical manifestations are variable. The most frequent features are thymic hypoplasia or aplasia with consequent immune deficiency, cardiac malformations, hypoparathyroidism, facial and palatine abnormalities, variable degrees of cognitive impairment and psychiatric disorders. The specific aim of this descriptive report is to discuss the correlation between oxidative stress and neuroinflammation in DGS patients with microdeletions of the 22q11.2 region. The deleted chromosomic region maps various genes involved in mitochondrial metabolisms, such as DGCR8 and TXNRD2, that could lead to reactive oxygen species (ROS) increased production and antioxidant depletion. Furthermore, increased levels of ROS in mitochondria would lead to the destruction of the projection neurons in the cerebral cortex with consequent neurocognitive impairment. Finally, the increase in modified protein belonging to the family of sulfoxide compounds and hexoses, acting as inhibitors of the IV and V mitochondria complex, could result in direct ROS overproduction. Neuroinflammation in DGS individuals could be directly related to the development of the syndrome’s characteristic psychiatric and cognitive disorders. In patients with psychotic disorders, the most frequent psychiatric manifestation in DGS, Th-17, Th-1 and Th-2 cells are increased with consequent elevation of proinflammatory cytokine IL-6 and IL1

β

. In patients with anxiety disorders, both CD3 and CD4 are increased. Some patients with autism spectrum disorders (ASDs) have an augmented level of proinflammatory cytokines IL-12, IL-6 and IL-1

β

, while IFN

γ

and the anti-inflammatory cytokine IL-10 seem to be reduced. Other data proposed that altered synaptic plasticity could be directly involved in DGS cognitive disorders. In conclusion, the use of antioxidants for restoring mitochondrial functionality in DGS could be a useful tool to protect cortical connectivity and cognitive behavior. Full article

(This article belongs to the Special Issue The Interplay of Oxidative Stress and Inflammation: From Mechanisms to Therapeutic Approaches)

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32 pages, 1633 KiB

Open AccessReview

Anti-Inflammatory, Antioxidant, and Neuroprotective Effects of Polyphenols—Polyphenols as an Element of Diet Therapy in Depressive Disorders

by Anna Winiarska-Mieczan, Małgorzata Kwiecień, Karolina Jachimowicz-Rogowska, Janine Donaldson, Ewa Tomaszewska and Ewa Baranowska-Wójcik

Int. J. Mol. Sci. 2023, 24(3), 2258; https://doi.org/10.3390/ijms24032258 - 23 Jan 2023

Cited by 16 | Viewed by 3330

Abstract

Depressive disorders can affect up to 350 million people worldwide, and in developed countries, the percentage of patients with depressive disorders may be as high as 10%. During depression, activation of pro-inflammatory pathways, mitochondrial dysfunction, increased markers of oxidative stress, and a reduction in the antioxidant effectiveness of the body are observed. It is estimated that approximately 30% of depressed patients do not respond to traditional pharmacological treatments. However, more and more attention is being paid to the influence of active ingredients in food on the course and risk of neurological disorders, including depression. The possibility of using foods containing polyphenols as an element of diet therapy in depression was analyzed in the review. The possibility of whether the consumption of products such as polyphenols could alleviate the course of depression or prevent the progression of it was also considered. Results from preclinical studies demonstrate the potential of phenolic compounds have the potential to reduce depressive behaviors by regulating factors related to oxidative stress, neuroinflammation, and modulation of the intestinal microbiota. Full article

(This article belongs to the Special Issue The Interplay of Oxidative Stress and Inflammation: From Mechanisms to Therapeutic Approaches)

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10 pages, 804 KiB

Open AccessReview

Pediatric Multisystem Syndrome Associated with SARS-CoV-2 (MIS-C): The Interplay of Oxidative Stress and Inflammation

by Serafina Perrone, Laura Cannavò, Sara Manti, Immacolata Rullo, Giuseppe Buonocore, Susanna Maria Roberta Esposito and Eloisa Gitto

Int. J. Mol. Sci. 2022, 23(21), 12836; https://doi.org/10.3390/ijms232112836 - 25 Oct 2022

Cited by 9 | Viewed by 1324

Abstract

Pediatric inflammatory multisystem syndrome temporally associated with SARS-CoV-2 (MIS-C) is characterized by persistent fever and evidence of single or multiorgan dysfunction, and laboratory evidence of inflammation, elevated neutrophils, reduced lymphocytes, and low albumin. The pathophysiological mechanisms of MIS-C are still unknown. Proinflammatory mediators, including reactive oxygen species and decreased antioxidant enzymes, seems to play a central role. Virus entry activates NOXs and inhibits Nrf-2 antioxidant response inducing free radicals. The biological functions of nonphagocytic NOXs are still under study and appear to include: defense of epithelia, intracellular signaling mechanisms for growth regulation and cell differentiation, and post-translational modifications of proteins. This educational review has the aim of analyzing the newest evidence on the role of oxidative stress (OS) in MIS-C. Only by relating inflammatory mediators to OS evaluation in children following SARS-CoV-2 infection will it be possible to achieve a better understanding of these mechanisms and to reduce long-term morbidity. The link between inflammation and OS is key to developing effective prevention strategies with antioxidants to protect children. Full article

(This article belongs to the Special Issue The Interplay of Oxidative Stress and Inflammation: From Mechanisms to Therapeutic Approaches)

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12 pages, 953 KiB

Open AccessReview

Inflammation in Pulmonary Hypertension and Edema Induced by Hypobaric Hypoxia Exposure

by Samia El Alam, Eduardo Pena, Diego Aguilera, Patricia Siques and Julio Brito

Int. J. Mol. Sci. 2022, 23(20), 12656; https://doi.org/10.3390/ijms232012656 - 21 Oct 2022

Cited by 12 | Viewed by 3519

Abstract

Exposure to high altitudes generates a decrease in the partial pressure of oxygen, triggering a hypobaric hypoxic condition. This condition produces pathophysiologic alterations in an organism. In the lung, one of the principal responses to hypoxia is the development of hypoxic pulmonary vasoconstriction (HPV), which improves gas exchange. However, when HPV is exacerbated, it induces high-altitude pulmonary hypertension (HAPH). Another important illness in hypobaric hypoxia is high-altitude pulmonary edema (HAPE), which occurs under acute exposure. Several studies have shown that inflammatory processes are activated in high-altitude illnesses, highlighting the importance of the crosstalk between hypoxia and inflammation. The aim of this review is to determine the inflammatory pathways involved in hypobaric hypoxia, to investigate the key role of inflammation in lung pathologies, such as HAPH and HAPE, and to summarize different anti-inflammatory treatment approaches for these high-altitude illnesses. In conclusion, both HAPE and HAPH show an increase in inflammatory cell infiltration (macrophages and neutrophils), cytokine levels (IL-6, TNF-α and IL-1β), chemokine levels (MCP-1), and cell adhesion molecule levels (ICAM-1 and VCAM-1), and anti-inflammatory treatments (decreasing all inflammatory components mentioned above) seem to be promising mitigation strategies for treating lung pathologies associated with high-altitude exposure. Full article

(This article belongs to the Special Issue The Interplay of Oxidative Stress and Inflammation: From Mechanisms to Therapeutic Approaches)

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9 pages, 1248 KiB

Open AccessBrief Report

Hyaluronic Acid Alleviates Oxidative Stress and Apoptosis in Human Tenocytes via Caspase 3 and 7

by Marialucia Gallorini, Cristina Antonetti Lamorgese Passeri, Amelia Cataldi, Anna Concetta Berardi and Leonardo Osti

Int. J. Mol. Sci. 2022, 23(15), 8817; https://doi.org/10.3390/ijms23158817 - 08 Aug 2022

Cited by 8 | Viewed by 1782

Abstract

Rotator cuff tendinopathy (RCT) is the primary reason for shoulder surgery and its clinical management is still challenging. Hyaluronic acid (HA) has been shown to have anti-inflammatory effects in vitro and in vivo under RCT conditions, characterized by an exaggerated oxidative stress (OS). However, molecular mechanisms underlying HA-related effects are still partially disclosed. With these aims, a cell model of RCT was established by exposing primary human tenocytes to H₂O₂ for up to 72 h. Four different HAs by molecular weight were administered to measure nitric oxide (NO) and OS, apoptosis, and collagen 1 expression. In parallel, the well-known antioxidant ascorbic acid was administered for comparison. The present study highlights that HAs characterized by a low molecular weight are able to counteract the H₂O₂-induced OS by decreasing the percentage of apoptotic cells and reversing the activation of caspase 3 and 7. Likewise, NO intracellular levels are comparable to the ones of controls. In parallel, collagen 1 expression was ameliorated by HAs characterized by higher molecular weights compared to AA. These findings confirm that HA plays an antioxidant role comparable to AA depending on the molecular weight, and highlight the molecular mechanisms underlying the HA anti-apoptotic effects. Full article

(This article belongs to the Special Issue The Interplay of Oxidative Stress and Inflammation: From Mechanisms to Therapeutic Approaches)

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