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

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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 October 2021) | Viewed by 25931

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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. 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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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

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, the aim of this Special Issue is to 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. Tullia Maraldi
Prof. Dr. Cristina Angeloni
Guest Editors

Manuscript Submission Information

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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.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

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

Published Papers (9 papers)

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Editorial

Jump to: Research, Review

5 pages, 226 KiB

Open AccessEditorial

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

by Cecilia Prata, Tullia Maraldi and Cristina Angeloni

Int. J. Mol. Sci. 2022, 23(12), 6439; https://doi.org/10.3390/ijms23126439 - 09 Jun 2022

Cited by 1 | Viewed by 1200

Abstract

The great increase in life expectancy is linked to the necessity of counteracting chronic-degenerative diseases, e [...] Full article

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

Research

Jump to: Editorial, Review

20 pages, 5747 KiB

Open AccessArticle

Chitin-Derived AVR-48 Prevents Experimental Bronchopulmonary Dysplasia (BPD) and BPD-Associated Pulmonary Hypertension in Newborn Mice

by Pragnya Das, Suchismita Acharya, Varsha M. Prahaladan, Ogan K. Kumova, Shadi Malaeb, Sumita Behera, Beamon Agarwal, Dale J. Christensen, Alison J. Carey and Vineet Bhandari

Int. J. Mol. Sci. 2021, 22(16), 8547; https://doi.org/10.3390/ijms22168547 - 09 Aug 2021

Cited by 7 | Viewed by 2861

Abstract

Bronchopulmonary dysplasia (BPD) is the most common complication of prematurity and a key contributor to the large health care burden associated with prematurity, longer hospital stays, higher hospital costs, and frequent re-hospitalizations of affected patients through the first year of life and increased resource utilization throughout childhood. This disease is associated with abnormal pulmonary function that may lead to BPD-associated pulmonary hypertension (PH), a major contributor to neonatal mortality and morbidity. In the absence of any definitive treatment options, this life-threatening disease is associated with high resource utilization during and after neonatal intensive care unit (NICU) stay. The goal of this study was to test the safety and efficacy of a small molecule derivative of chitin, AVR-48, as prophylactic therapy for preventing experimental BPD in a mouse model. Two doses of AVR-48 were delivered either intranasally (0.11 mg/kg), intraperitoneally (10 mg/kg), or intravenously (IV) (10 mg/kg) to newborn mouse pups on postnatal day (P)2 and P4. The outcomes were assessed by measuring total inflammatory cells in the broncho-alveolar lavage fluid (BALF), chord length, septal thickness, and radial alveolar counts of the alveoli, Fulton’s Index (for PH), cell proliferation and cell death by immunostaining, and markers of inflammation by Western blotting and ELISA. The bioavailability and safety of the drug were assessed by pharmacokinetic and toxicity studies in both neonatal mice and rat pups (P3-P5). Following AVR-48 treatment, alveolar simplification was improved, as evident from chord length, septal thickness, and radial alveolar counts; total inflammatory cells were decreased in the BALF; Fulton’s Index was decreased and lung inflammation and cell death were decreased, while angiogenesis and cell proliferation were increased. AVR-48 was found to be safe and the no-observed-adverse-effect level (NOAEL) in rat pups was determined to be 100 mg/kg when delivered via IV dosing with a 20-fold safety margin. With no reported toxicity and with a shorter half-life, AVR-48 is able to reverse the worsening cardiopulmonary phenotype of experimental BPD and BPD-PH, compared to controls, thus positioning it as a future drug candidate. Full article

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

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16 pages, 1706 KiB

Open AccessArticle

Muscle Damage in Systemic Sclerosis and CXCL10: The Potential Therapeutic Role of PDE5 Inhibition

by Clarissa Corinaldesi, Rebecca L. Ross, Giuseppina Abignano, Cristina Antinozzi, Francesco Marampon, Luigi di Luigi, Maya H. Buch, Valeria Riccieri, Andrea Lenzi, Clara Crescioli and Francesco Del Galdo

Int. J. Mol. Sci. 2021, 22(6), 2894; https://doi.org/10.3390/ijms22062894 - 12 Mar 2021

Cited by 7 | Viewed by 2315

Abstract

Skeletal muscle damage is a common clinical manifestation of systemic sclerosis (SSc). C-X-C chemokine ligand 10 (CXCL10) is involved in myopathy and cardiomyopathy development and is associated with a more severe SSc prognosis. Interestingly, the phosphodiesterase type 5 inhibitor (PDE5i) sildenafil reduces CXCL10 sera levels of patients with diabetic cardiomyopathy and in cardiomyocytes. Here, we analyzed the levels of CXCL10 in the sera of 116 SSc vs. 35 healthy subjects and explored differences in 17 SSc patients on stable treatment with sildenafil. CXCL10 sera levels were three-fold higher in SSc vs. healthy controls, independent of subset and antibody positivity. Sildenafil treatment was associated with lower CXCL10 sera levels. Serum CXCL10 strongly correlated with the clinical severity of muscle involvement and with creatine kinase (CK) serum concentration, suggesting a potential involvement in muscle damage in SSc. In vitro, sildenafil dose-dependently reduced CXCL10 release by activated myocytes and impaired cytokine-induced Signal transducer and activator of transcription 1 (STAT1), Nuclear factor-κB (NFκB) and c-Jun N-terminal kinase (JNK) phosphorylation. This was also seen in cardiomyocytes. Sildenafil-induced CXCL10 inhibition at the systemic and human muscle cell level supports the hypothesis that PDE5i could be a potential therapeutic therapy to prevent and treat muscle damage in SSc. Full article

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

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18 pages, 4557 KiB

Open AccessArticle

Small Immunomodulatory Molecules as Potential Therapeutics in Experimental Murine Models of Acute Lung Injury (ALI)/Acute Respiratory Distress Syndrome (ARDS)

by Dilip Shah, Pragnya Das, Suchismita Acharya, Beamon Agarwal, Dale J. Christensen, Stella M. Robertson and Vineet Bhandari

Int. J. Mol. Sci. 2021, 22(5), 2573; https://doi.org/10.3390/ijms22052573 - 04 Mar 2021

Cited by 13 | Viewed by 2997

Abstract

Background: Acute lung injury (ALI) or its most advanced form, acute respiratory distress syndrome (ARDS) is a severe inflammatory pulmonary process triggered by a variety of insults including sepsis, viral or bacterial pneumonia, and mechanical ventilator-induced trauma. Currently, there are no effective therapies available for ARDS. We have recently reported that a novel small molecule AVR-25 derived from chitin molecule (a long-chain polymer of N-acetylglucosamine) showed anti-inflammatory effects in the lungs. The goal of this study was to determine the efficacy of two chitin-derived compounds, AVR-25 and AVR-48, in multiple mouse models of ALI/ARDS. We further determined the safety and pharmacokinetic (PK) profile of the lead compound AVR-48 in rats. Methods: ALI in mice was induced by intratracheal instillation of a single dose of lipopolysaccharide (LPS; 100 µg) for 24 h or exposed to hyperoxia (100% oxygen) for 48 h or undergoing cecal ligation and puncture (CLP) procedure and observation for 10 days. Results: Both chitin derivatives, AVR-25 and AVR-48, showed decreased neutrophil recruitment and reduced inflammation in the lungs of ALI mice. Further, AVR-25 and AVR-48 mediated diminished lung inflammation was associated with reduced expression of lung adhesion molecules with improvement in pulmonary endothelial barrier function, pulmonary edema, and lung injury. Consistent with these results, CLP-induced sepsis mice treated with AVR-48 showed a significant increase in survival of the mice (80%) and improved lung histopathology in the treated CLP group. AVR-48, the lead chitin derivative compound, demonstrated a good safety profile. Conclusion: Both AVR-25 and AVR-48 demonstrate the potential to be developed as therapeutic agents to treat ALI/ARDS. Full article

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

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12 pages, 4246 KiB

Open AccessArticle

The Interplay between HGF/c-met Axis and Nox4 in BRAF Mutated Melanoma

by Francesca Beretti, Francesca Farnetani, Luca Reggiani Bonetti, Luca Fabbiani, Manuela Zavatti, Antonino Maiorana, Giovanni Pellacani and Tullia Maraldi

Int. J. Mol. Sci. 2021, 22(2), 761; https://doi.org/10.3390/ijms22020761 - 13 Jan 2021

Cited by 3 | Viewed by 2191

Abstract

Background: Melanoma is the leading cause of death due to cutaneous malignancy and its incidence is on the rise. Several signaling pathways, including receptor tyrosine kinases, have a role in the development and progression of melanocytic lesions and malignant melanoma. Among those, the hepatocyte growth factor (HGF)/c-met axis is emerging as a critical player because it can play a role in drug resistance. Indeed, 50% of melanoma patients present BRAF mutations, however, all responders develop resistance to the inhibitors typically within one year of treatment. Interestingly, BRAF inhibitors induce reactive oxygen species (ROS) in melanoma cells, therefore, the aim of this study was to investigate a possible interplay between HGF/c-met and ROS sources, such as NADPH oxidases (Nox). Methods: The expression of c-met and Nox were quantified in 60 patients with primary cutaneous melanoma. In vitro experiments on melanoma primary cells and the cell line were performed to dissect the underpinned molecular mechanism. Results: The outcome of interest was the correlation between the high positivity for both Nox4 and c-met and metastasis occurring at least 1 year later than melanoma diagnosis in BRAF mutated patients, in contrast to nonmutated. In vitro experiments demonstrated that the axis HGF/c-met/Nox4/ROS triggers the epithelial-mesenchymal transition. Conclusions: The observed correlation suggests an interplay between c-met and Nox4 in promoting the onset of metastasis. This study suggests that Nox4 inhibitors could be associated to the current therapy used to treat melanoma patients with BRAF mutations. Full article

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

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Review

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13 pages, 540 KiB

Open AccessReview

The Use of Natural Compounds as a Strategy to Counteract Oxidative Stress in Animal Models of Diabetes Mellitus

by Marcela Salazar-García and Juan Carlos Corona

Int. J. Mol. Sci. 2021, 22(13), 7009; https://doi.org/10.3390/ijms22137009 - 29 Jun 2021

Cited by 14 | Viewed by 2241

Abstract

Diabetes mellitus (DM) is a chronic metabolic disease characterised by insulin deficiency, resulting in hyperglycaemia, a characteristic symptom of type 2 diabetes mellitus (DM2). DM substantially affects numerous metabolic pathways, resulting in β-cell dysfunction, insulin resistance, abnormal blood glucose levels, impaired lipid metabolism, inflammatory processes, and excessive oxidative stress. Oxidative stress can affect the body’s normal physiological function and cause numerous cellular and molecular changes, such as mitochondrial dysfunction. Animal models are useful for exploring the cellular and molecular mechanisms of DM and improving novel therapeutics for their safe use in human beings. Due to their health benefits, there is significant interest in a wide range of natural compounds that can act as naturally occurring anti-diabetic compounds. Due to rodent models’ relatively similar physiology to humans and ease of handling and housing, they are widely used as pre-clinical models for studying several metabolic disorders. In this review, we analyse the currently available rodent animal models of DM and their advantages and disadvantages and highlight the potential anti-oxidative effects of natural compounds and their mechanisms of action. Full article

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

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20 pages, 961 KiB

Open AccessReview

Bladder Hyperactivity Induced by Oxidative Stress and Bladder Ischemia: A Review of Treatment Strategies with Antioxidants

by Yi-Hsuan Wu, Kuang-Shun Chueh, Shu-Mien Chuang, Cheng-Yu Long, Jian-He Lu and Yung-Shun Juan

Int. J. Mol. Sci. 2021, 22(11), 6014; https://doi.org/10.3390/ijms22116014 - 02 Jun 2021

Cited by 18 | Viewed by 4636

Abstract

Overactive bladder (OAB) syndrome, including frequency, urgency, nocturia and urgency incontinence, has a significantly negative impact on the quality-of-life scale (QoL) and can cause sufferer withdrawal from social activities. The occurrence of OAB can result from an imbalance between the production of pro-oxidants, such as free radicals and reactive species, and their elimination through protective mechanisms of antioxidant-induced oxidative stress. Several animal models, such as bladder ischemia/reperfusion (I/R), partial bladder outlet obstruction (PBOO) and ovarian hormone deficiency (OHD), have suggested that cyclic I/R during the micturition cycle induces oxidative stress, leading to bladder denervation, bladder afferent pathway sensitization and overexpression of bladder-damaging molecules, and finally resulting in bladder hyperactivity. Based on the results of previous animal experiments, the present review specifically focuses on four issues: (1) oxidative stress and antioxidant defense system; (2) oxidative stress in OAB and biomarkers of OAB; (3) OAB animal model; (4) potential nature/plant antioxidant treatment strategies for urinary dysfunction with OAB. Moreover, we organized the relationships between urinary dysfunction and oxidative stress biomarkers in urine, blood and bladder tissue. Reviewed information also revealed the summary of research findings for the effects of various antioxidants for treatment strategies for OAB. Full article

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

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18 pages, 2399 KiB

Open AccessReview

Pleiotropic Effects of Isoflavones in Inflammation and Chronic Degenerative Diseases

by Jurga Bernatoniene, Jurga Andreja Kazlauskaite and Dalia Marija Kopustinskiene

Int. J. Mol. Sci. 2021, 22(11), 5656; https://doi.org/10.3390/ijms22115656 - 26 May 2021

Cited by 20 | Viewed by 3308

Abstract

Isoflavones are phytoestrogens of plant origin, mostly found in the members of the Fabaceae family, that exert beneficial effects in various degenerative disorders. Having high similarity to 17-β-estradiol, isoflavones can bind estrogen receptors, scavenge reactive oxygen species, activate various cellular signal transduction pathways and modulate growth and transcription factors, activities of enzymes, cytokines, and genes regulating cell proliferation and apoptosis. Due to their pleiotropic activities isoflavones might be considered as a natural alternative for the treatment of estrogen decrease-related conditions during menopause. This review will focus on the effects of isoflavones on inflammation and chronic degenerative diseases including cancer, metabolic, cardiovascular, neurodegenerative diseases, rheumatoid arthritis and adverse postmenopausal symptoms. Full article

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

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27 pages, 1238 KiB

Open AccessReview

A State of the Art of Antioxidant Properties of Curcuminoids in Neurodegenerative Diseases

by Serena Silvestro, Cinzia Sindona, Placido Bramanti and Emanuela Mazzon

Int. J. Mol. Sci. 2021, 22(6), 3168; https://doi.org/10.3390/ijms22063168 - 20 Mar 2021

Cited by 18 | Viewed by 2843

Abstract

Neurodegenerative diseases represent a set of pathologies characterized by an irreversible and progressive, and a loss of neuronal cells in specific areas of the brain. Oxidative phosphorylation is a source of energy production by which many cells, such as the neuronal cells, meet their energy needs. Dysregulations of oxidative phosphorylation induce oxidative stress, which plays a key role in the onset of neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS). To date, for most neurodegenerative diseases, there are no resolute treatments, but only interventions capable of alleviating the symptoms or slowing the course of the disease. Therefore, effective neuroprotection strategies are needed. In recent years, natural products, such as curcuminoids, have been intensively explored and studied for their therapeutic potentials in several neurodegenerative diseases. Curcuminoids are, nutraceutical compouns, that owen several therapeutic properties such as anti-oxidant, anti-inflammatory and neuroprotective effects. In this context, the aim of this review was to provide an overview of preclinical and clinical evidence aimed to illustrate the antioxidant effects of curcuminoids in neurodegenerative diseases. Promising results from preclinical studies encourage the use of curcuminoids for neurodegeneration prevention and treatment. Full article

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

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