Research on Pharmacotherapy for Neuropathic Pain

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (30 June 2024) | Viewed by 569

Special Issue Editor


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Guest Editor
Department of Anesthesiology and Pain Medicine, College of Medicine, The Catholic University of Korea, Seoul St. Mary's Hospital, Seoul 06591, Republic of Korea
Interests: neuropathic; nociceptive; central sensitization pain; post-operative pain; headache; spinal pain; other non-specific pain; pain management; animal study; clinical study; drug delivery; pain intervention
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Special Issue Information

Dear Colleagues,

Neuropathic pain is generally defined as pain resulting from nerve damage or dysfunction of the somatosensory system and can present in the form of hyperalgesia, allodynia, and paroxysmal or spontaneous pain, which are ordinarily intractable. The obvious pathophysiology of neuropathic pain has not yet been fully understood, but various studies have proposed several consistent pathophysiological mechanisms that are related to neurogenic inflammatory responses and central sensitization. Therefore, multimodal analgesia is the currently recommended strategy for neuropathic pain management. However, due to the diversity of mechanisms, neuropathic pain is sometimes difficult to treat. In order to treat neuropathic pain, pharmacotherapy is still challenging and plays a key role.

We are pleased to invite you to contribute to this Special Issue, titled “Research on Pharmacotherapy for Neuropathic Pain”. This Special Issue aims to introduce and highlight all pharmacological treatments for neuropathic pain including biopharmaceutics, biomedical sciences, cell biology, interdisciplinary research, study of alternative targets or novel therapeutic strategies, new pharmaceutical formulations and drug delivery systems as well as drug repositioning approaches, etc., through animal and clinical study.

In this Special Issue, original research articles and reviews are welcome.

We look forward to receiving your contributions.

Dr. Hue Jung Park
Guest Editor

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Keywords

  • neuropathic
  • pain
  • peripheral
  • spinal
  • central
  • sensitization
  • pain management
  • animal study
  • clinical study
  • drug delivery

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Published Papers (1 paper)

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Research

10 pages, 1710 KiB  
Article
Analgesic Effect of SKI306X on Chronic Postischemic Pain and Spinal Nerve Ligation-Induced Neuropathic Pain in Mice
by Jie Quan, Chun Jing He, Ji Yeon Kim, Jin Young Lee, Chang Jae Kim, Young Jae Jeon, Chang Woo Im, Do Kyung Lee, Ji Eun Kim and Hue Jung Park
Biomedicines 2024, 12(7), 1379; https://doi.org/10.3390/biomedicines12071379 - 21 Jun 2024
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Abstract
Neuropathic pain (NP) results from lesions or diseases affecting the peripheral or central somatosensory system. However, there are currently no drugs that are particularly effective in treating this condition. SKI306X is a blend of purified extracts of three oriental herbs (Clematis mandshurica, Trichosanthes [...] Read more.
Neuropathic pain (NP) results from lesions or diseases affecting the peripheral or central somatosensory system. However, there are currently no drugs that are particularly effective in treating this condition. SKI306X is a blend of purified extracts of three oriental herbs (Clematis mandshurica, Trichosanthes kirilowii, and Prunella vulgaris) commonly used to treat osteoarthritis for their chondroprotective effects. Chronic postischemic pain (CPIP) and spinal nerve ligation (SNL) models were created by binding the upper left ankle of mice with an O-ring for 3 h and ligating the L5 spinal nerve, respectively. Mice with allodynia were injected intraperitoneally with 0.9% normal saline (NS group) or different doses (25, 50, or 100 mg/kg) of SKI306X (SKI groups). We assessed allodynia using von Frey filaments before injection and 30, 60, 90, 120, 180, and 240 min and 24 h after injection to confirm the antiallodynic effect of SKI306X. We also measured glial fibrillary acidic protein (GFAP) levels in the spinal cord and dorsal root ganglia to confirm the change of SKI306X administration. Both models exhibited significant mechanical allodynia. The intraperitoneal injection of SKI306X significantly increased the paw withdrawal threshold in a dose-dependent manner, as the paw withdrawal threshold was significantly increased after SKI306X administration compared with at baseline or after NS administration. GFAP levels in the SKI group decreased significantly (p < 0.05). Intraperitoneal administration of SKI306X dose-dependently attenuated mechanical allodynia and decreased GFAP levels, suggesting that GFAP is involved in the antiallodynic effect of SKI306X in mice with CPIP and SNL-induced NP. Full article
(This article belongs to the Special Issue Research on Pharmacotherapy for Neuropathic Pain)
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