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Special Issue "Antioxidants in Chronic Pain Volume 3"

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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 7533

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Dr. Olga Pol

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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
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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

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Keywords

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

Published Papers (6 papers)

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Research

Open AccessArticle

Honokiol-Rich Magnolia officinalis Bark Extract Attenuates Trauma-Induced Neuropathic Pain

Vittoria Borgonetti

and

Nicoletta Galeotti

Antioxidants 2023, 12(8), 1518; https://doi.org/10.3390/antiox12081518 - 28 Jul 2023

Viewed by 500

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 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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Open AccessArticle

Protective and Pain-Killer Effects of AMC3, a Novel N-Formyl Peptide Receptors (FPRs) Modulator, in Experimental Models of Rheumatoid Arthritis

Maria Paola Giovannoni

Lorenzo Di Cesare Mannelli

and

Carla Ghelardini

Antioxidants 2023, 12(6), 1207; https://doi.org/10.3390/antiox12061207 - 02 Jun 2023

Viewed by 781

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 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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Open AccessArticle

Association of Oxidative-Stress-Related Gene Polymorphisms with Pain-Related Temporomandibular Disorders and Oral Behavioural Habits

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

Viewed by 662

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 = 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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Open AccessArticle

New Treatment for the Cognitive and Emotional Deficits Linked with Paclitaxel-Induced Peripheral Neuropathy in Mice

Ignacio Martínez-Martel

Xue Bai

Gerard Batallé

and

Olga Pol

Antioxidants 2022, 11(12), 2387; https://doi.org/10.3390/antiox11122387 - 01 Dec 2022

Viewed by 1120

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 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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Open AccessArticle

Treatment with Hydrogen-Rich Water Improves the Nociceptive and Anxio-Depressive-like Behaviors Associated with Chronic Inflammatory Pain in Mice

Santiago Coral-Pérez

Ignacio Martínez-Martel

Maria Martínez-Serrat

Gerard Batallé

Xue Bai

Christie R. A. Leite-Panissi

and

Olga Pol

Antioxidants 2022, 11(11), 2153; https://doi.org/10.3390/antiox11112153 - 30 Oct 2022

Viewed by 1615

Abstract

Chronic inflammatory pain is manifested in many diseases. The potential use of molecular hydrogen (H₂) as a new therapy for neurological disorders has been demonstrated. Recent studies prove its analgesic properties in animals with neuropathic pain, but the possible antinociceptive, antidepressant, and/or anxiolytic actions of H₂ during persistent inflammatory pain have not been investigated. Therefore, using male mice with chronic inflammatory pain incited by the subplantar injection of complete Freud’s adjuvant (CFA), we assessed the actions of hydrogen-rich water (HRW) systemically administered on: (1) the nociceptive responses and affective disorders associated and (2) the oxidative (4-hydroxy-2-nonenal; 4-HNE), inflammatory (phosphorylated-NF-kB inhibitor alpha; p-IKBα), and apoptotic (Bcl-2-like protein 4; BAX) changes provoked by CFA in the paws and amygdala. The role of the antioxidant system in the analgesia induced by HRW systemically and locally administered was also determined. Our results revealed that the intraperitoneal administration of HRW, besides reducing inflammatory pain, also inhibited the depressive- and anxiolytic-like behaviors associated and the over expression of 4-HNE, p-IKBα, and BAX in paws and amygdala. The contribution of the nuclear factor erythroid 2-related factor 2/heme oxygenase 1 and NAD(P)H: quinone oxidoreductase 1 pathway in the analgesic activities of HRW, systemically or locally administered, was also shown. These data revealed the analgesic, antidepressant, and anxiolytic actions of HRW. The protective, anti-inflammatory, and antioxidant qualities of this treatment during inflammatory pain were also demonstrated. Therefore, this study proposes the usage of HRW as a potential therapy for chronic inflammatory pain and linked comorbidities. Full article

(This article belongs to the Special Issue Antioxidants in Chronic Pain Volume 3)

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Open AccessArticle

Hydrogen-Rich Water as a Novel Therapeutic Strategy for the Affective Disorders Linked with Chronic Neuropathic Pain in Mice

Maria Martínez-Serrat

Ignacio Martínez-Martel

and

Antioxidants 2022, 11(9), 1826; https://doi.org/10.3390/antiox11091826 - 16 Sep 2022

Cited by 2 | Viewed by 2439

Abstract

Neuropathic pain manifested with allodynia and hyperalgesia usually becomes a chronic condition accompanied with mood disorders. Clinical therapies for neuropathic pain are still unsatisfactory with notable side effects. Recent studies have reported the protective role of molecular hydrogen (H₂) in different diseases including neurological disorders, such as Alzheimer’s as well as its antidepressant activities in animals with chronic stress. This study explored the effects of treatment with hydrogen-rich water (HRW) in male mice with neuropathic pain induced by the chronic constriction of the sciatic nerve (CCI) and the accompanying affective deficits. The likely pathways implied in the HRW analgesic activity, as well as the interaction between heme oxygenase 1 (HO-1) enzyme and H₂ during neuropathic pain were also studied. The results showed: (i) the inhibitory effects of the repetitive treatment with HRW on the allodynia and hyperalgesia provoked by CCI; (ii) the anxiolytic and antidepressant actions of HRW in animals with neuropathic pain; (iii) the contribution of the antioxidant enzymes (HO-1 and NAD(P)H: quinone oxidoreductase 1) and the ATP sensitive potassium channels in the painkiller activities of HRW during neuropathic pain; (iv) a positive interaction between the HO-1 and H₂ systems in inhibiting the CCI-induced neuropathy; and (v) the antioxidant, antinociceptive, anti-inflammatory and/or antiapoptotic features of HRW treatment in the dorsal root ganglia and/or amygdala of sciatic nerve-injured mice. This study demonstrates new protective actions of H₂ and suggests that treatment with HRW might be an interesting therapeutic strategy for chronic neuropathic pain and its associated mood disorders. Full article

(This article belongs to the Special Issue Antioxidants in Chronic Pain Volume 3)

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