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Antioxidants
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Antioxidants in Chronic Pain Volume 3
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Antioxidants in Chronic Pain Volume 3

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 8694

Special Issue Editor

Dr. Olga Pol

E-Mail Website
Guest Editor
Grup de Neurofarmacologia Molecular, Institut d’Investigació Biomèdica Sant Pau, Hospital de la Santa Creu i Sant Pau, 08041 Barcelona, Spain
Interests: analgesia; anxiety; depression; cannabinoids; carbon monoxide; heme oxygenase 1; hydrogen sulfide; nitric oxide; Nrf2 transcription factor; oxidative stress; pain; opioids
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Chronic pain, defined as a syndrome characterized by persistent suffering for long periods of time, can originate and manifest in different forms, including diabetic neuropathy, osteoarthritic pain, inflammatory pain, or neuropathic pain, and affects a high percentage of people. When pain is prolonged for long periods of time, it is also accompanied by emotional disorders such as depression, anxiety, and cognitive deficits, which exert a negative impact on the perception of pain and can lead to significant deterioration in the patient’s quality of life. The optimum treatment of chronic pain is an unmet medical need and a major challenge in pain research, considering that current therapies have limited effectiveness and significant side effects.

Oxidative stress is highly implicated in the development of chronic pain and the associated emotional disorders. Reactive oxygen species (ROS) are elevated in the central and peripheral nervous system of animals with chronic pain, and ROS scavengers alleviate hyperalgesia. The role of several antioxidants in pain relief, by attenuating ROS generation and/or by activating the endogenous antioxidant system triggered by the nuclear factor erythroid-2 related factor 2 (Nrf2), heme oxygenase 1 (HO-1), NADPH quinone oxidoreductase 1, superoxide dismutase, glutathione peroxidase 1, and/or the catalase signaling pathway, has been demonstrated. Thus, Nrf2/HO-1 activators modulate the pronociceptive responses generated by nerve damage, inflammation, chemotherapeutic agents and/or hyperglycemia, and are regarded as a good therapeutic strategy.

There is a wide variety of antioxidant compounds with different structures and chemical properties whose analgesic properties and mechanisms of action during chronic pain have not been identified. This Special Issue on “Antioxidants in Chronic Pain Volume 3” aims to collect original research papers designed to identify new antioxidant compounds able to efficiently relieve chronic pain, such as potential therapeutic targets. We believe that this Special Issue will help to advance research on new effective strategies in the treatment of chronic pain.

We look forward to your contribution.

Dr. Olga Pol
Guest Editor

Manuscript Submission Information

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. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). 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

  • analgesia
  • antioxidants
  • Heme oxygenase 1
  • neuropathy
  • nociception
  • Nrf2 transcription factor
  • oxidative stress
  • pain

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Published Papers (4 papers)

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Research

16 pages, 4217 KiB  
Article
Honokiol-Rich Magnolia officinalis Bark Extract Attenuates Trauma-Induced Neuropathic Pain
by Vittoria Borgonetti and Nicoletta Galeotti
Antioxidants 2023, 12(8), 1518; https://doi.org/10.3390/antiox12081518 - 28 Jul 2023
Cited by 4 | Viewed by 2297
Abstract
Neuropathic pain (NP) affects about 8% of the general population. Current analgesic therapies have limited efficacy, making NP one of the most difficult to treat pain conditions. Evidence indicates that excessive oxidative stress can contribute to the onset of chronic NP and several [...] Read more.
Neuropathic pain (NP) affects about 8% of the general population. Current analgesic therapies have limited efficacy, making NP one of the most difficult to treat pain conditions. Evidence indicates that excessive oxidative stress can contribute to the onset of chronic NP and several natural antioxidant compounds have shown promising efficacy in NP models. Thus, this study aimed to investigate the pain-relieving activity of honokiol (HNK)-rich standardized extract of Magnolia officinalis Rehder & E. Wilson bark (MOE), well known for its antioxidant and anti-inflammatory properties, in the spared nerve injury (SNI) model. The molecular mechanisms and efficacy toward neuroinflammation were investigated in spinal cord samples from SNI mice and LPS-stimulated BV2 microglia cells. MOE and HNK showed antioxidant activity. MOE (30 mg/kg p.o.) produced an antiallodynic effect in SNI mice in the absence of locomotor impairment, reduced spinal p-p38, p-JNK1, iNOS, p-p65, IL-1ß, and Nrf2 overexpression, increased IL-10 and MBP levels and attenuated the Notch signaling pathway by reducing Jagged1 and NEXT. These effects were prevented by the CB1 antagonist AM251. HNK reduced the proinflammatory response of LPS-stimulated BV2 and reduced Jagged1 overexpression. MOE and HNK, by modulating oxidative and proinflammatory responses, might represent interesting candidates for NP management. Full article
(This article belongs to the Special Issue Antioxidants in Chronic Pain Volume 3)
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19 pages, 5584 KiB  
Article
Protective and Pain-Killer Effects of AMC3, a Novel N-Formyl Peptide Receptors (FPRs) Modulator, in Experimental Models of Rheumatoid Arthritis
by Valentina Ferrara, Alessandra Toti, Elena Lucarini, Carmen Parisio, Laura Micheli, Clara Ciampi, Francesco Margiotta, Letizia Crocetti, Claudia Vergelli, Maria Paola Giovannoni, Lorenzo Di Cesare Mannelli and Carla Ghelardini
Antioxidants 2023, 12(6), 1207; https://doi.org/10.3390/antiox12061207 - 2 Jun 2023
Viewed by 1782
Abstract
Rheumatoid arthritis is an autoimmune disorder that causes chronic joint pain, swelling, and movement impairment, resulting from prolonged inflammation-induced cartilage and bone degradation. The pathogenesis of RA, which is still unclear, makes diagnosis and treatment difficult and calls for new therapeutic strategies to [...] Read more.
Rheumatoid arthritis is an autoimmune disorder that causes chronic joint pain, swelling, and movement impairment, resulting from prolonged inflammation-induced cartilage and bone degradation. The pathogenesis of RA, which is still unclear, makes diagnosis and treatment difficult and calls for new therapeutic strategies to cure the disease. Recent research has identified FPRs as a promising druggable target, with AMC3, a novel agonist, showing preclinical efficacy in vitro and in vivo. In vitro, AMC3 (1–30 µM) exhibited significant antioxidant effects in IL-1β (10 ng/mL)-treated chondrocytes for 24 h. AMC3 displayed a protective effect by downregulating the mRNA expression of several pro-inflammatory and pro-algic genes (iNOS, COX-2, and VEGF-A), while upregulating genes essential for structural integrity (MMP-13, ADAMTS-4, and COLIAI). In vivo, AMC3 (10 mg kg−1) prevented hypersensitivity and restored postural balance in CFA-injected rats after 14 days. AMC3 attenuated joint alterations, reduced joint inflammatory infiltrate, pannus formation, and cartilage erosion. Chronic AMC3 administration reduced transcriptional changes of genes causing excitotoxicity and pain (EAATs and CCL2) and prevented morphological changes in astrocytes, including cell body hypertrophy, processes length, and thickness, caused by CFA in the spinal cord. This study demonstrates the usefulness of AMC3 and establishes the groundwork for further research. Full article
(This article belongs to the Special Issue Antioxidants in Chronic Pain Volume 3)
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18 pages, 861 KiB  
Article
Association of Oxidative-Stress-Related Gene Polymorphisms with Pain-Related Temporomandibular Disorders and Oral Behavioural Habits
by Ema Vrbanović, Marko Zlendić, Koraljka Gall Trošelj, Marko Tomljanović, Kristina Vuković Đerfi and Iva Z. Alajbeg
Antioxidants 2023, 12(6), 1195; https://doi.org/10.3390/antiox12061195 - 31 May 2023
Cited by 2 | Viewed by 1795
Abstract
The frequency of selected polymorphisms, one in each gene coding for proteins with antioxidative properties (CAT(rs1001179), SOD2(rs4880), GPX1(rs1050450), and NQO1(rs689452)), was compared between patients suffering from pain-related temporomandibular disorders (TMDp; n = 85) and control subjects (CTR; n [...] Read more.
The frequency of selected polymorphisms, one in each gene coding for proteins with antioxidative properties (CAT(rs1001179), SOD2(rs4880), GPX1(rs1050450), and NQO1(rs689452)), was compared between patients suffering from pain-related temporomandibular disorders (TMDp; n = 85) and control subjects (CTR; n = 85). The same was evaluated when participants were divided with respect to oral behavioural habits frequency into high-frequency parafunction (HFP; n = 98) and low-frequency parafunction (LFP; n = 72) groups. Another aim was to investigate whether polymorphisms in these genes can be associated with participants’ psychological and psychosomatic characteristics. Polymorphisms were genotyped using the genomic DNA extracted from buccal mucosa swabs and real-time TaqMan genotyping assays. No differences in genotype distribution between TMDp patients and control subjects were found. Still, TMDp patients who were homozygous for minor allele A, related to the GPX1 polymorphism rs1050450, reported significantly more waking-state oral behaviours than GA + GG genotype carriers (score: 30 vs. 23, p = 0.019). The frequency of genotype AA for rs1050450 polymorphism was higher in HFP than in LFP participants (14.3% vs. 4.2%, p  = 0.030). The most important predictors of waking-state oral behaviours were depression, anxiety, AA genotype (rs1050450), and female sex. The explored gene polymorphisms were not found to be significant risk factors for either TMDp or sleep-related oral behaviours. The association of waking-state oral behaviours with selected gene polymorphisms additionally supports previous assumptions that daytime bruxism is more closely linked to various stress manifestations, which might also be reflected through the variability related to the cellular antioxidative activity. Full article
(This article belongs to the Special Issue Antioxidants in Chronic Pain Volume 3)
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17 pages, 14222 KiB  
Article
New Treatment for the Cognitive and Emotional Deficits Linked with Paclitaxel-Induced Peripheral Neuropathy in Mice
by Ignacio Martínez-Martel, Xue Bai, Gerard Batallé and Olga Pol
Antioxidants 2022, 11(12), 2387; https://doi.org/10.3390/antiox11122387 - 1 Dec 2022
Cited by 6 | Viewed by 2242
Abstract
Chemotherapy-provoked peripheral neuropathy and its linked comorbidities severely reduce the quality of a patient’s life. Its therapy is not completely resolved and has become an important clinical challenge. The protective actions of molecular hydrogen (H2) in many neurological disorders have been [...] Read more.
Chemotherapy-provoked peripheral neuropathy and its linked comorbidities severely reduce the quality of a patient’s life. Its therapy is not completely resolved and has become an important clinical challenge. The protective actions of molecular hydrogen (H2) in many neurological disorders have been described, but its effects on memory and the emotional deficits accompanying neuropathic pain induced by chemotherapy remain unknown. In this study, using male mice injected with paclitaxel (PTX), we examined the effects of systemic treatment with hydrogen-rich water (HRW) in: (i) the mechanical and thermal allodynia provoked by PTX and the pathways involved; (ii) the memory deficits, anxiety- and depressive-like behaviors associated with PTX-induced peripheral neuropathy (PIPN); and (iii) the plasticity (p-extracellular signal-regulated protein kinase; p-ERK ½), nociceptive (p-protein kinase B, p-Akt), inflammatory (p-nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha; p-IKBα), and oxidative (4-hydroxynonenal: 4-HNE) alterations provoked by PIPN in the prefrontal cortex (PFC). The results revealed: (1) the antiallodynic actions of HRW administered at one or two times per day during 7 and 3 consecutive days; (2) the participation of Kv7 potassium channels and the Nrf2-heme oxygenase 1-NAD(P)H: quinone oxidoreductase 1 pathway in the painkiller effects of HRW; (3) the inhibition of memory deficits and the anxiodepressive-like behaviors related with PIPN induced by HRW; and (4) the normalization of p-ERK ½, p-Akt and 4-HNE up-regulation and the activation of antioxidant enzymes produced by this treatment in PFC. This study proposes HRW as a possible effective and safe therapy for PIPN and its associated cognitive and emotional deficits. Full article
(This article belongs to the Special Issue Antioxidants in Chronic Pain Volume 3)
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