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Molecular Mechanisms and Therapeutic Strategies of Inflammatory Pain
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Molecular Mechanisms and Therapeutic Strategies of Inflammatory Pain

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: 20 October 2024 | Viewed by 2838

Special Issue Editor

Dr. Suk-Yun Kang

E-Mail Website
Guest Editor
KM Science Research Division, Korea Institute of Oriental Medicine, Daejeon 34054, Republic of Korea
Interests: inflammatory pain; mechanisms of pain; alternative medicine; central sensitization
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Inflammation is a defense response of the living body to harmful stimuli, for example, pathogens or injuries. Inflammation removes the cause of cell damage and goes through the steps of removing dead cells and tissues due to injury and inflammatory response; then, it goes through the stage of initial repair, which restores cells or tissues to their original state. Chronic inflammation has a longer course than acute inflammation, and the causes of it are complex and involve the severity of tissue disorders, repetition of inflammatory stimuli, and the reactivity of the body. There are five typical signs: fever, pain, redness, swelling and loss of function. Inflammatory pain is especially characterized by increased sensitivity due to the inflammatory response associated with tissue damage, resulting in increased activity of primary afferent nerves, which, in turn, results in spontaneous pain, hyperalgesia, and allodynia.

Therefore, detailed research is needed to elucidate the exact mechanism for more effective inflammation management and development of anti-inflammatory and analgesic treatment methods for inflammatory pain patients.

The purpose of this Special Issue is to bring together experts in the field of inflammation and pain to investigate precise molecular mechanisms. This Special Issue welcomes original research and review articles.

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

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Keywords

  • inflammation
  • inflammatory pain
  • molecular mechanism
  • central sensitization

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Published Papers (2 papers)

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21 pages, 4856 KiB  
Article
Inhibitory Effects of Reynoutria japonica Houtt. on Pain and Cartilage Breakdown in Osteoarthritis Based on Its Multifaceted Anti-Inflammatory Activity: An In Vivo and In Vitro Approach
by Hee-Geun Jo, Chae Yun Baek, Juni Lee, Yeseul Hwang, Eunhye Baek, Aejin Song, Ho Sueb Song and Donghun Lee
Int. J. Mol. Sci. 2024, 25(19), 10647; https://doi.org/10.3390/ijms251910647 - 3 Oct 2024
Viewed by 484
Abstract
In the past 30 years, the number of years lived with disability due to osteoarthritis (OA) has doubled, making it an increasing global health burden. To address this issue, interventions that inhibit the progressive pathology driven by age-related low-grade inflammation, the primary mechanism [...] Read more.
In the past 30 years, the number of years lived with disability due to osteoarthritis (OA) has doubled, making it an increasing global health burden. To address this issue, interventions that inhibit the progressive pathology driven by age-related low-grade inflammation, the primary mechanism of OA, are being actively pursued. Recent investigations have focused on modulating the age-related low-grade inflammatory pathology of this disease as a therapeutic target. However, no agent has successfully halted the disease’s progression or reversed its irreversible course. Reynoutria japonica Houtt. (RJ), a promising East Asian herbal medicine, has been utilized for several diseases due to its potent anti-inflammatory activity. This study aims to determine RJ’s capacity to inhibit OA symptoms and associated inflammation, exploring its potential for further development. In vivo and in vitro experiments demonstrated RJ’s anti-OA activity and modulation of multifaceted inflammatory targets. RJ significantly inhibited pain, gait deterioration, and cartilage destruction in a monosodium iodoacetate-induced OA rat model, with its analgesic effect further confirmed in an acetic acid-induced writhing model. RJ exhibited consistent anti-inflammatory activity against multiple targets in serum and cartilage of the OA rat model and lipopolysaccharide-induced RAW 264.7 cells. The inhibition of inflammatory cytokines, including interleukin-1β, interleukin-6, matrix metalloproteinase-13, tumor necrosis factor-α, and nitric oxide synthase 2, suggests that RJ’s alleviation of OA manifestations relates to its multifaceted anti-inflammatory activity. These results indicate that RJ merits further investigation as a disease-modifying drug candidate targeting OA’s inflammatory pathology. To further characterize the pharmacological properties of RJ, future studies with expanded designs are warranted. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Strategies of Inflammatory Pain)
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9 pages, 1502 KiB  
Brief Report
Soft Tissue Manipulation Alters RANTES/CCL5 and IL-4 Cytokine Levels in a Rat Model of Chronic Low Back Pain
by Carmela L. Marciano, Taylor A. Hiland, Krista L. Jackson, Sierra Street, Carson Maris, Andrew Ehrsam, Julia M. Hum, Mary Terry Loghmani, Tien-Min G. Chu, Kyung S. Kang and Jonathan W. Lowery
Int. J. Mol. Sci. 2023, 24(18), 14392; https://doi.org/10.3390/ijms241814392 - 21 Sep 2023
Viewed by 1425
Abstract
Low back pain (LBP) is a common musculoskeletal complaint that can impede physical function and mobility. Current management often involves pain medication, but there is a need for non-pharmacological and non-invasive interventions. Soft tissue manipulation (STM), such as massage, has been shown to [...] Read more.
Low back pain (LBP) is a common musculoskeletal complaint that can impede physical function and mobility. Current management often involves pain medication, but there is a need for non-pharmacological and non-invasive interventions. Soft tissue manipulation (STM), such as massage, has been shown to be effective in human subjects, but the molecular mechanisms underlying these findings are not well understood. In this paper, we evaluated potential changes in the soft tissue levels of more than thirty pro- or anti-inflammatory cytokines following instrument-assisted STM (IASTM) in rats with chronic, induced LBP using Complete Freund’s Adjuvant. Our results indicate that IASTM is associated with reduced soft tissue levels of Regulated on Activation, Normal T cell Expressed and Secreted (RANTES)/Chemokine (C-C motif) ligand 5 (CCL5) and increased soft tissue levels of Interleukin (IL)-4, which are pro-inflammatory and anti-inflammatory factors, respectively, by 120 min post-treatment. IASTM was not associated with tissue-level changes in C-X-C Motif Chemokine Ligand (CXCL)-5/Lipopolysaccharide-Induced CXC Chemokine (LIX)–which is the murine homologue of IL-8, CXCL-7, Granulocyte-Macrophage-Colony Simulating Factor (GM-CSF), Intercellular Adhesion Molecule (ICAM)-1, IL1-Receptor Antagonist (IL-1ra), IL-6, Interferon-Inducible Protein (IP)-10/CXCL-10, L-selectin, Tumor Necrosis Factor (TNF)-α, or Vascular Endothelial Growth Factor (VEGF) at either 30 or 120 min post-treatment. Combined, our findings raise the possibility that IASTM may exert tissue-level effects associated with improved clinical outcomes and potentially beneficial changes in pro-/anti-inflammatory cytokines in circulation and at the tissue level. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Strategies of Inflammatory Pain)
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