Topic Editors

Department of Scienze della Vita e dell’Ambiente, Sezione di Scienze del Farmaco, University of Cagliari, Via Ospedale 72, 09124 Cagliari, Italy
Department of Scienze della Vita e dell’Ambiente, Sezione di Scienze del Farmaco, University of Cagliari, Via Ospedale 72, 09124 Cagliari, Italy
Department of Scienzedella Vita e dell’Ambiente, Sezione di Scienze del Farmaco, University of Cagliari, Via Ospedale 72, 09124 Cagliari, Italy
Biomedical & Tissue Engineering Laboratory, Fundacion Investigacion Hospital General Universitario Valencia, Valencia, Spain
1. Departamento de Farmacia y Tecnología Farmacéutica y Parasitología, Facultad de Farmacia, Universitat de València, Av. Vicente Andrés Estellés s/n, Burjassot, 46100 Valencia, Spain
2. Instituto Interuniversitario de Investigación de Reconocimiento Molecular y Desarrollo Tecnológico (IDM), Universitat Politècnica de València, Universitat de València, 46100 Valencia, Spain

Oxidative Stress and Inflammation, 2nd Volume

Abstract submission deadline
29 February 2024
Manuscript submission deadline
31 May 2024
Viewed by
5952

Topic Information

Dear Colleagues,

Oxidative stress is viewed as an imbalance between the production of reactive oxygen species (ROS) and their elimination by protective mechanisms, which can lead to chronic inflammation. The incorrect lifestyle and the intake of external unhealthy chemicals are the major causes of age-related chronic diseases and cancer. Their study includes diseases pathology pathway, lifestyle, treatment, protection, and prevention of oxidative stress and inflammation. ROS are normally produced within the body in limited amount and are essential compounds involved in the regulation of processes capable of maintaining cell homeostasis and functions (signal transduction, gene expression, and activation of receptors). This imbalance may cause oxidative stress, which can lead to lipid peroxidation, gene mutation, inflammation and other complications. The harmful oxidative activity of ROS can be counteracted only by antioxidant/anti-inflammatory compounds, which may be both synthetic and natural, but are often characterized by several stability issues, such as poor water solubility and low bioavailability, that compromise their in vivo activities. The research papers of this Topic are looked forward to providing an overview of the status of research on both natural and synthetic products with antioxidant properties and capable of counteracting inflammatory diseases, including, but not necessarily restricted to, chemical compounds synthetic or of natural origin, vitamins, peptides, micronutrients, non-starch polysaccharides, probiotics, postbiotics, prebiotics formulations containing functional foods or nutraceutical or cosmeceutical products and their innovative oral, systemic or topical delivery capable to overcome their stability issues.

Dr. Maria Letizia Manca
Dr. Amparo Nacher
Dr. Mohamad Allaw
Dr. Matteo Perra
Dr. Ines Castangia
Topic Editors

Keywords

  • oxidative stress
  • inflammation
  • molecular mechanisms
  • antioxidant
  • cosmeceutics
  • nutraceutics
  • mitochondrial oxidative
  • ROS species
  • lifestyle
  • longevity
  • aging
  • drug delivery
  • skin delivery
  • oral delivery

Participating Journals

Journal Name Impact Factor CiteScore Launched Year First Decision (median) APC
Biomedicines
biomedicines
4.7 3.7 2013 15.4 Days CHF 2600 Submit
Cells
cells
6.0 9.0 2012 16.6 Days CHF 2700 Submit
International Journal of Molecular Sciences
ijms
5.6 7.8 2000 16.3 Days CHF 2900 Submit
Life
life
3.2 2.7 2011 17.5 Days CHF 2600 Submit
Oxygen
oxygen
- - 2021 22.7 Days CHF 1000 Submit

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Published Papers (3 papers)

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22 pages, 18029 KiB  
Article
Reactive Oxygen Species-Dependent Activation of EGFR/Akt/p38 Mitogen-Activated Protein Kinase and JNK1/2/FoxO1 and AP-1 Pathways in Human Pulmonary Alveolar Epithelial Cells Leads to Up-Regulation of COX-2/PGE2 Induced by Silica Nanoparticles
Biomedicines 2023, 11(10), 2628; https://doi.org/10.3390/biomedicines11102628 - 25 Sep 2023
Viewed by 886
Abstract
The risk of lung exposure to silica nanoparticles (SiNPs) and related lung inflammatory injury is increasing with the wide application of SiNPs in a variety of industries. A growing body of research has revealed that cyclooxygenase (COX)-2/prostaglandin E2 (PGE2) up-regulated [...] Read more.
The risk of lung exposure to silica nanoparticles (SiNPs) and related lung inflammatory injury is increasing with the wide application of SiNPs in a variety of industries. A growing body of research has revealed that cyclooxygenase (COX)-2/prostaglandin E2 (PGE2) up-regulated by SiNP toxicity has a role during pulmonary inflammation. The detailed mechanisms underlying SiNP-induced COX-2 expression and PGE2 synthesis remain unknown. The present study aims to dissect the molecular components involved in COX-2/PGE2 up-regulated by SiNPs in human pulmonary alveolar epithelial cells (HPAEpiCs) which are one of the major targets while SiNPs are inhaled. In the present study, we demonstrated that SiNPs induced COX-2 expression and PGE2 release, which were inhibited by pretreatment with a reactive oxygen species (ROS) scavenger (edaravone) or the inhibitors of proline-rich tyrosine kinase 2 (Pyk2, PF-431396), epidermal growth factor receptor (EGFR, AG1478), phosphatidylinositol 3-kinase (PI3K, LY294002), protein kinase B (Akt, Akt inhibitor VIII), p38 mitogen-activated protein kinase (MAPK) (p38 MAPK inhibitor VIII), c-Jun N-terminal kinases (JNK)1/2 (SP600125), Forkhead Box O1 (FoxO1, AS1842856), and activator protein 1 (AP-1, Tanshinone IIA). In addition, we also found that SiNPs induced ROS-dependent Pyk2, EGFR, Akt, p38 MAPK, and JNK1/2 activation in these cells. These signaling pathways induced by SiNPs could further cause c-Jun and FoxO1 activation and translocation from the cytosol to the nucleus. AP-1 and FoxO1 activation could increase COX-2 and PGE2 levels induced by SiNPs. Finally, the COX-2/PGE2 axis might promote the inflammatory responses in HPAEpiCs. In conclusion, we suggested that SiNPs induced COX-2 expression accompanied by PGE2 synthesis mediated via ROS/Pyk2/EGFR/PI3K/Akt/p38 MAPK- and JNK1/2-dependent FoxO1 and AP-1 activation in HPAEpiCs. Full article
(This article belongs to the Topic Oxidative Stress and Inflammation, 2nd Volume)
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13 pages, 7445 KiB  
Article
Chlorogenic Acid Alleviates LPS-Induced Inflammation and Oxidative Stress by Modulating CD36/AMPK/PGC-1α in RAW264.7 Macrophages
Int. J. Mol. Sci. 2023, 24(17), 13516; https://doi.org/10.3390/ijms241713516 - 31 Aug 2023
Cited by 2 | Viewed by 964
Abstract
Chlorogenic acid (CGA) is a bioactive substance with anti-inflammatory activities. Clusters of CD36 have been suggested to be widely involved in inflammatory damage. However, the mechanism of CGA protecting against LPS-induced inflammation involving the CD36 regulation is unclear. Here, we demonstrated that CGA [...] Read more.
Chlorogenic acid (CGA) is a bioactive substance with anti-inflammatory activities. Clusters of CD36 have been suggested to be widely involved in inflammatory damage. However, the mechanism of CGA protecting against LPS-induced inflammation involving the CD36 regulation is unclear. Here, we demonstrated that CGA protected against LPS-induced cell death and decreased the production of ROS. Moreover, the SOD, CAT, and GSH-Px activities were also upregulated in CGA-treated cells during LPS stimulation. CGA reduced COX-2 and iNOS expression and IL-1β, IL-6, and TNF-α secretion in LPS-stimulated RAW264.7 macrophages. In addition, CGA treatment widely involved in immune-related signaling pathways, including NF-κB signaling, NOD-like receptor signaling, and IL-17 signaling using transcriptomic analysis and CD36 also markedly reduced during CGA pretreatment in LPS-induced RAW264.7 cells. Furthermore, the CD36 inhibitor SSO attenuated inflammation and oxidative stress by enabling activation of the AMPK/PGC-1α cascade. These results indicate that CGA might provide benefits for the regulation of inflammatory diseases by modulating CD36/AMPK/PGC-1α to alleviate oxidative stress. Full article
(This article belongs to the Topic Oxidative Stress and Inflammation, 2nd Volume)
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16 pages, 1024 KiB  
Review
Antioxidant Therapy as an Effective Strategy against Noise-Induced Hearing Loss: From Experimental Models to Clinic
Life 2023, 13(4), 1035; https://doi.org/10.3390/life13041035 - 17 Apr 2023
Cited by 1 | Viewed by 2777
Abstract
Cochlear redox unbalance is the main mechanism of damage involved in the pathogenesis of noise-induced-hearing loss. Indeed, the increased free radical production, in conjunction with a reduced efficacy of the endogenous antioxidant system, plays a key role in cochlear damage induced by noise [...] Read more.
Cochlear redox unbalance is the main mechanism of damage involved in the pathogenesis of noise-induced-hearing loss. Indeed, the increased free radical production, in conjunction with a reduced efficacy of the endogenous antioxidant system, plays a key role in cochlear damage induced by noise exposure. For this reason, several studies focused on the possibility to use exogenous antioxidant to prevent or attenuate noise-induce injury. Thus, several antioxidant molecules, alone or in combination with other compounds, have been tested in both experimental and clinical settings. In our findings, we tested the protective effects of several antioxidant enzymes, spanning from organic compounds to natural compounds, such as nutraceuticals of polyphenols. In this review, we summarize and discuss the strengths and weaknesses of antioxidant supplementation focusing on polyphenols, Q-Ter, the soluble form of CoQ10, Vitamin E and N-acetil-cysteine, which showed great otoprotective effects in different animal models of noise induced hearing loss and which has been proposed in clinical trials. Full article
(This article belongs to the Topic Oxidative Stress and Inflammation, 2nd Volume)
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