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Strategies to Counteract Oxidative Stress and Inflammation in Chronic-Degenerative Diseases 2.0

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 July 2023) | Viewed by 41589

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Dr. Cecilia Prata

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Department of Pharmacy and Biotechnology, Alma Mater Studiorum—Università di Bologna, Bologna, Italy
Interests: cell biochemistry and nutrition
Special Issues, Collections and Topics in MDPI journals

Dr. Cristina Angeloni

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Department for Life Quality Studies, Alma Mater Studiorum-University of Bologna, Corso D’Augusto 237, 47921 Rimini, Italy
Interests: nutritional biochemistry; neurodegenerative diseases; oxidative stress; inflammation; nutraceuticals; ageing
Special Issues, Collections and Topics in MDPI journals

Dr. Tullia Maraldi

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Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41125 Modena, Italy
Interests: stem cells and age-related disorders
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Special Issue Information

Dear Colleagues,

The great increase of life expectancy is linked to the necessity of counteracting chronic-degenerative diseases, e.g., cancer, metabolic syndrome, type 2 diabetes, cardiovascular, and neurodegenerative diseases that affect a high percentage of the population. Since oxidative stress and inflammation are common features of these diseases and impact differently on function and structure of organs and tissues.

As volume 1 of the Special Issue “Strategies to Counteract Oxidative Stress and Inflammation in Chronic-Degenerative Diseases” has been successful, we will be exploring this issue further in the International Journal of Molecular Sciences (ISSN 1422-0067, IF 5.923, JCR Category Q1). In this second Special Issue, we collect original articles and reviews on this multifaceted topic that still remains largely unexplored, in order to provide support for the development of novel potential therapeutic approaches.

Suggested topics include but are not limited to:

Cellular and molecular mechanisms to counteract oxidative stress and inflammation in aging and chronic diseases;
Dietetic strategies for prevention of chronic diseases: oxidative stress as a target for interventions;
Association of drugs with antioxidant or anti-inflammatory compounds for the therapy of chronic diseases.

Dr. Cecilia Prata
Dr. Cristina Angeloni
Dr. Tullia Maraldi
Guest Editors

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

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Keywords

chronic-degenerative diseases
oxidative stress
inflammation
nutrition
nutraceuticals
stem cell therapy

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Published Papers (9 papers)

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Editorial

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4 pages, 180 KiB

Open AccessEditorial

Strategies to Counteract Oxidative Stress and Inflammation in Chronic-Degenerative Diseases 2.0

by Cecilia Prata, Cristina Angeloni and Tullia Maraldi

Int. J. Mol. Sci. 2024, 25(9), 5026; https://doi.org/10.3390/ijms25095026 - 4 May 2024

Viewed by 2395

Abstract

Oxidative stress and inflammation are recognized as pivotal contributors and common features of several chronic degenerative diseases, including cancer, metabolic syndrome, type 2 diabetes, cardiovascular diseases and neurodegenerative disorders, affecting a high percentage of the population [...] Full article

(This article belongs to the Special Issue Strategies to Counteract Oxidative Stress and Inflammation in Chronic-Degenerative Diseases 2.0)

Research

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19 pages, 3568 KiB

Open AccessArticle

Antioxidant and Anti-Inflammatory Mechanisms of Cardamonin through Nrf2 Activation and NF-kB Suppression in LPS-Activated BV-2 Microglial Cells

by Kimberly Barber, Patricia Mendonca, Jasmine A. Evans and Karam F. A. Soliman

Int. J. Mol. Sci. 2023, 24(13), 10872; https://doi.org/10.3390/ijms241310872 - 29 Jun 2023

Cited by 15 | Viewed by 2973

Abstract

Chronic oxidative stress (OS) and inflammation are implicated in developing and progressing neurodegenerative diseases (NDs). The chronic activation of microglia cells leads to the overproduction of several substances, including nitric oxide and reactive oxygen species, which can induce neurodegeneration. Natural compounds have recently been investigated for their potential to protect cells from OS and to improve many disease-related conditions. Cardamonin (CD) is a bioactive compound in many plants, such as Alpinia katsumadai and Alpinia conchigera. The present study examined the effects of CD on LPS-activated BV-2 microglial cells. The cell viability results showed that the increasing concentrations of CD, ranging from 0.78 to 200 µM, induced BV-2 cell cytotoxicity in a dose–response manner. In the nitric oxide assay, CD concentrations of 6.25 to 25 µM reduced the release of nitric oxide in LPS-activated BV-2 cells by 90% compared to those treated with LPS only (p ≤ 0.0001). CD (6.25 µM) significantly decreased the cellular production of SOD (3-fold (p ≤ 0.05)) and increased the levels of expression of CAT (2.5-fold (p ≤ 0.05)) and GSH (2-fold (p ≤ 0.05)) in the LPS-activated BV-2 cells. Furthermore, on RT-PCR arrays, CD (6.25 µM) downregulated mRNA expression of CCL5/RANTES (5-fold), NOS2 (2-fold), SLC38A1 (3-fold), TXNIP (2-fold), SOD1 (2-fold), SOD2 (1.5-fold) and upregulated GSS (1.9-fold), GCLC (1.7-fold) and catalase (2.9-fold) expression, indicating CD efficacy in modulating genes involved in OS and inflammation. Furthermore, CD (6.25 µM) increased the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and lowered the levels of Kelch-like ECH-associated protein 1 (Keap1), indicating that this may be the signaling responsible for the elevation of antioxidant factors. Lastly, the results showed that CD (6.25 µM) modulated genes and proteins associated with the NF-kB signaling, downregulating genes related to excessive neuroinflammation. These results imply that CD may be a potential compound for developing therapeutic and preventive agents in treating neurodegeneration induced by excessive OS and inflammation. Full article

(This article belongs to the Special Issue Strategies to Counteract Oxidative Stress and Inflammation in Chronic-Degenerative Diseases 2.0)

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14 pages, 3594 KiB

Open AccessArticle

Shedding Light on Osteosarcoma Cell Differentiation: Impact on Biomineralization and Mitochondria Morphology

by Francesca Rossi, Giovanna Picone, Concettina Cappadone, Andrea Sorrentino, Marta Columbaro, Giovanna Farruggia, Emilio Catelli, Giorgia Sciutto, Silvia Prati, Robert Oliete, Alice Pasini, Eva Pereiro, Stefano Iotti and Emil Malucelli

Int. J. Mol. Sci. 2023, 24(10), 8559; https://doi.org/10.3390/ijms24108559 - 10 May 2023

Cited by 3 | Viewed by 2616

Abstract

Osteosarcoma (OS) is the most common primary malignant bone tumor and its etiology has recently been associated with osteogenic differentiation dysfunctions. OS cells keep a capacity for uncontrolled proliferation showing a phenotype similar to undifferentiated osteoprogenitors with abnormal biomineralization. Within this context, both conventional and X-ray synchrotron-based techniques have been exploited to deeply characterize the genesis and evolution of mineral depositions in a human OS cell line (SaOS-2) exposed to an osteogenic cocktail for 4 and 10 days. A partial restoration of the physiological biomineralization, culminating with the formation of hydroxyapatite, was observed at 10 days after treatment together with a mitochondria-driven mechanism for calcium transportation within the cell. Interestingly, during differentiation, mitochondria showed a change in morphology from elongated to rounded, indicating a metabolic reprogramming of OS cells possibly linked to an increase in glycolysis contribution to energy metabolism. These findings add a dowel to the genesis of OS giving new insights on the development of therapeutic strategies able to restore the physiological mineralization in OS cells. Full article

(This article belongs to the Special Issue Strategies to Counteract Oxidative Stress and Inflammation in Chronic-Degenerative Diseases 2.0)

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25 pages, 6407 KiB

Open AccessArticle

Monoterpenoid Epoxidiol Ameliorates the Pathological Phenotypes of the Rotenone-Induced Parkinson’s Disease Model by Alleviating Mitochondrial Dysfunction

by Yulia Aleksandrova, Kirill Chaprov, Alexandra Podturkina, Oleg Ardashov, Ekaterina Yandulova, Konstantin Volcho, Nariman Salakhutdinov and Margarita Neganova

Int. J. Mol. Sci. 2023, 24(6), 5842; https://doi.org/10.3390/ijms24065842 - 19 Mar 2023

Cited by 7 | Viewed by 2390

Abstract

Parkinson’s disease is the second most common neurodegenerative disease. Unfortunately, there is still no definitive disease-modifying therapy. In our work, the antiparkinsonian potential of trans-epoxide (1S,2S,3R,4S,6R)-1-methyl-4-(prop-1-en-2-yl)-7-oxabicyclo [4.1.0]heptan-2,3-diol (E-diol) was analyzed in a rotenone-induced neurotoxicity model using in vitro, in vivo and ex vivo approaches. It was conducted as part of the study of the mitoprotective properties of the compound. E-diol has been shown to have cytoprotective properties in the SH-SY5Y cell line exposed to rotenone, which is associated with its ability to prevent the loss of mitochondrial membrane potential and restore the oxygen consumption rate after inhibition of the complex I function. Under the conditions of rotenone modeling of Parkinson’s disease in vivo, treatment with E-diol led to the leveling of both motor and non-motor disorders. The post-mortem analysis of brain samples from these animals demonstrated the ability of E-diol to prevent the loss of dopaminergic neurons. Moreover, that substance restored functioning of the mitochondrial respiratory chain complexes and significantly reduced the production of reactive oxygen species, preventing oxidative damage. Thus, E-diol can be considered as a new potential agent for the treatment of Parkinson’s disease. Full article

(This article belongs to the Special Issue Strategies to Counteract Oxidative Stress and Inflammation in Chronic-Degenerative Diseases 2.0)

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14 pages, 3379 KiB

Open AccessArticle

PPAR Pan Agonist MHY2013 Alleviates Renal Fibrosis in a Mouse Model by Reducing Fibroblast Activation and Epithelial Inflammation

by Minjung Son, Ga Young Kim, Yejin Yang, Sugyeong Ha, Jeongwon Kim, Doyeon Kim, Hae Young Chung, Hyung Ryong Moon and Ki Wung Chung

Int. J. Mol. Sci. 2023, 24(5), 4882; https://doi.org/10.3390/ijms24054882 - 2 Mar 2023

Cited by 1 | Viewed by 2446

Abstract

The peroxisome proliferator-activated receptor (PPAR) nuclear receptor has been an interesting target for the treatment of chronic diseases. Although the efficacy of PPAR pan agonists in several metabolic diseases has been well studied, the effect of PPAR pan agonists on kidney fibrosis development has not been demonstrated. To evaluate the effect of the PPAR pan agonist MHY2013, a folic acid (FA)-induced in vivo kidney fibrosis model was used. MHY2013 treatment significantly controlled decline in kidney function, tubule dilation, and FA-induced kidney damage. The extent of fibrosis determined using biochemical and histological methods showed that MHY2013 effectively blocked the development of fibrosis. Pro-inflammatory responses, including cytokine and chemokine expression, inflammatory cell infiltration, and NF-κB activation, were all reduced with MHY2013 treatment. To demonstrate the anti-fibrotic and anti-inflammatory mechanisms of MHY2013, in vitro studies were conducted using NRK49F kidney fibroblasts and NRK52E kidney epithelial cells. In the NRK49F kidney fibroblasts, MHY2013 treatment significantly reduced TGF-β-induced fibroblast activation. The gene and protein expressions of collagen I and α-smooth muscle actin were significantly reduced with MHY2013 treatment. Using PPAR transfection, we found that PPARγ played a major role in blocking fibroblast activation. In addition, MHY2013 significantly reduced LPS-induced NF-κB activation and chemokine expression mainly through PPARβ activation. Taken together, our results suggest that administration of the PPAR pan agonist effectively prevented renal fibrosis in both in vitro and in vivo models of kidney fibrosis, implicating the therapeutic potential of PPAR agonists against chronic kidney diseases. Full article

(This article belongs to the Special Issue Strategies to Counteract Oxidative Stress and Inflammation in Chronic-Degenerative Diseases 2.0)

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16 pages, 3003 KiB

Open AccessArticle

Natural Astaxanthin Is a Green Antioxidant Able to Counteract Lipid Peroxidation and Ferroptotic Cell Death

by Nicola Rizzardi, Laura Pezzolesi, Chiara Samorì, Federica Senese, Chiara Zalambani, Walter Pitacco, Natalia Calonghi, Christian Bergamini, Cecilia Prata and Romana Fato

Int. J. Mol. Sci. 2022, 23(23), 15137; https://doi.org/10.3390/ijms232315137 - 1 Dec 2022

Cited by 10 | Viewed by 4403

Abstract

Astaxanthin is a red orange xanthophyll carotenoid produced mainly by microalgae but which can also be chemically synthesized. As demonstrated by several studies, this lipophilic molecule is endowed with potent antioxidant properties and is able to modulate biological functions. Unlike synthetic astaxanthin, natural astaxanthin (NAst) is considered safe for human nutrition, and its production is considered eco-friendly. The antioxidant activity of astaxanthin depends on its bioavailability, which, in turn, is related to its hydrophobicity. In this study, we analyzed the water-solubility of NAst and assessed its protective effect against oxidative stress by means of different approaches using a neuroblastoma cell model. Moreover, due to its highly lipophilic nature, astaxanthin is particularly protective against lipid peroxidation; therefore, the role of NAst in counteracting ferroptosis was investigated. This recently discovered process of programmed cell death is indeed characterized by iron-dependent lipid peroxidation and seems to be linked to the onset and development of oxidative-stress-related diseases. The promising results of this study, together with the “green sources” from which astaxanthin could derive, suggest a potential role for NAst in the prevention and co-treatment of chronic degenerative diseases by means of a sustainable approach. Full article

(This article belongs to the Special Issue Strategies to Counteract Oxidative Stress and Inflammation in Chronic-Degenerative Diseases 2.0)

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Review

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55 pages, 3447 KiB

Open AccessReview

Molecular Basic of Pharmacotherapy of Cytokine Imbalance as a Component of Intervertebral Disc Degeneration Treatment

by Natalia A. Shnayder, Azamat V. Ashkhotov, Vera V. Trefilova, Zaitun A. Nurgaliev, Maxim A. Novitsky, Marina M. Petrova, Ekaterina A. Narodova, Mustafa Al-Zamil, Galina A. Chumakova, Natalia P. Garganeeva and Regina F. Nasyrova

Int. J. Mol. Sci. 2023, 24(9), 7692; https://doi.org/10.3390/ijms24097692 - 22 Apr 2023

Cited by 5 | Viewed by 2939

Abstract

Intervertebral disc degeneration (IDD) and associated conditions are an important problem in modern medicine. The onset of IDD may be in childhood and adolescence in patients with a genetic predisposition. With age, IDD progresses, leading to spondylosis, spondylarthrosis, herniated disc, spinal canal stenosis. One of the leading mechanisms in the development of IDD and chronic back pain is an imbalance between pro-inflammatory and anti-inflammatory cytokines. However, classical therapeutic strategies for correcting cytokine imbalance in IDD do not give the expected response in more than half of the cases. The purpose of this review is to update knowledge about new and promising therapeutic strategies based on the correction of the molecular mechanisms of cytokine imbalance in patients with IDD. This review demonstrates that knowledge of the molecular mechanisms of the imbalance between pro-inflammatory and anti-inflammatory cytokines may be a new key to finding more effective drugs for the treatment of IDD in the setting of acute and chronic inflammation. Full article

(This article belongs to the Special Issue Strategies to Counteract Oxidative Stress and Inflammation in Chronic-Degenerative Diseases 2.0)

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19 pages, 1002 KiB

Open AccessReview

The Influence of Lifestyle and Treatment on Oxidative Stress and Inflammation in Diabetes

by Magdalena Wronka, Julia Krzemińska, Ewelina Młynarska, Jacek Rysz and Beata Franczyk

Int. J. Mol. Sci. 2022, 23(24), 15743; https://doi.org/10.3390/ijms232415743 - 12 Dec 2022

Cited by 50 | Viewed by 6114

Abstract

Diabetes is considered a new pandemic of the modern world, and the number of sufferers is steadily increasing. Sustained hyperglycemia promotes the production of free radicals and leads to persistent, low-grade inflammation. Oxidative stress causes mitochondrial destruction, which along with activation of the hexosamine pathway, nuclear factor-κB (Nf-κb), p38 mitogen-activated protein kinase (p38 MAPK), c-jun NH2 terminal kinase/stress-activated protein kinase (JNK/SAPK) or toll-like receptors (TLRs), leads to pancreatic β-cell dysfunction. However, there is also the protective mechanism that counteracts oxidative stress and inflammation in diabetes, mitophagy, which is a mitochondrial autophagy. An important part of the strategy to control diabetes is to lead a healthy lifestyle based on, among other things, regular physical activity, giving up smoking, eating a balanced diet containing ingredients with antioxidant potential, including vegetables and fruits, and using hypoglycemic pharmacotherapy. Tobacco smoke is a recognized modifiable risk factor for many diseases including diabetes, and it has been shown that the risk of the disease increases in proportion to the intensity of smoking. Physical activity as another component of therapy can effectively reduce glucose fluctuations, and high intensity interval exercise appears to have the most beneficial effect. A proper diet not only increases cellular sensitivity to insulin, but is also able to reduce inflammation and oxidative stress. Pharmacotherapy for diabetes can also affect oxidative stress and inflammation. Some oral drugs, such as metformin, pioglitazone, vildagliptin, liraglutide, and exenatide, cause a reduction in markers of oxidative stress and/or inflammation, while the new drug Imeglimin reverses pancreatic β-cell dysfunction. In studies of sitagliptin, vildagliptin and exenatide, beneficial effects on oxidative stress and inflammation were achieved by, among other things, reducing glycemic excursions. For insulin therapy, no corresponding correlation was observed. Insulin did not reduce oxidative stress parameters. There was no correlation between glucose variability and oxidative stress in patients on insulin therapy. The data used in this study were obtained by searching PubMed online databases, taking into account recent studies. Full article

(This article belongs to the Special Issue Strategies to Counteract Oxidative Stress and Inflammation in Chronic-Degenerative Diseases 2.0)

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28 pages, 1182 KiB

Open AccessReview

Oxidative Stress in Ageing and Chronic Degenerative Pathologies: Molecular Mechanisms Involved in Counteracting Oxidative Stress and Chronic Inflammation

by Thobekile S. Leyane, Sandy W. Jere and Nicolette N. Houreld

Int. J. Mol. Sci. 2022, 23(13), 7273; https://doi.org/10.3390/ijms23137273 - 30 Jun 2022

Cited by 146 | Viewed by 14083

Abstract

Ageing and chronic degenerative pathologies demonstrate the shared characteristics of high bioavailability of reactive oxygen species (ROS) and oxidative stress, chronic/persistent inflammation, glycation, and mitochondrial abnormalities. Excessive ROS production results in nucleic acid and protein destruction, thereby altering the cellular structure and functional outcome. To stabilise increased ROS production and modulate oxidative stress, the human body produces antioxidants, “free radical scavengers”, that inhibit or delay cell damage. Reinforcing the antioxidant defence system and/or counteracting the deleterious repercussions of immoderate reactive oxygen and nitrogen species (RONS) is critical and may curb the progression of ageing and chronic degenerative syndromes. Various therapeutic methods for ROS and oxidative stress reduction have been developed. However, scientific investigations are required to assess their efficacy. In this review, we summarise the interconnected mechanism of oxidative stress and chronic inflammation that contributes to ageing and chronic degenerative pathologies, including neurodegenerative diseases, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD), cardiovascular diseases CVD, diabetes mellitus (DM), and chronic kidney disease (CKD). We also highlight potential counteractive measures to combat ageing and chronic degenerative diseases. Full article

(This article belongs to the Special Issue Strategies to Counteract Oxidative Stress and Inflammation in Chronic-Degenerative Diseases 2.0)

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