Testosterone signaling pathways for reducing neuropathic pain in a rat model of spinothalamic tract lesion.

Astrocyte Molecular signaling Neuropathic pain Spinal cord injury Testosterone

Journal

Iranian journal of basic medical sciences
ISSN: 2008-3866
Titre abrégé: Iran J Basic Med Sci
Pays: Iran
ID NLM: 101517966

Informations de publication

Date de publication:
2024
Historique:
received: 02 03 2024
accepted: 10 06 2024
medline: 10 10 2024
pubmed: 10 10 2024
entrez: 10 10 2024
Statut: ppublish

Résumé

Most individuals who suffer from spinal cord injury (SCI) experience neuropathic pain, which currently has no effective treatment. In this study, we examined how testosterone affects neuropathic pain resulting from SCI. We administered three different doses of testosterone (4, 8, 16 mg/kg, intraperitoneal) to male rats after an electrolytic lesion of the spinothalamic tract. We then conducted behavioral tests, including open field and von Frey tests, within 28 days post-SCI. On day 28 after SCI, we analyzed spinal tissue using western blot to measure the levels of ionized calcium binding adaptor molecule 1 (Iba1), glial fibrillary acidic protein (GFAP), phospho-extracellular signal-regulated kinase (p-ERK1/2), and p-P38 at the injury site. The results showed that testosterone significantly improved both motor activity and mechanical allodynia compared to the SCI-only group. Testosterone also inhibited microglia and astrocyte activation. Furthermore, testosterone significantly decreased p-P38 and p-ERK levels. The findings indicate that testosterone may alleviate SCI-induced neuropathic pain by inhibiting the activation of astrocytes and microglia, as well as suppressing MAPK signaling pathways.

Identifiants

pubmed: 39386234
doi: 10.22038/ijbms.2024.78491.16968
pmc: PMC11459344
doi:

Types de publication

Journal Article

Langues

eng

Pagination

1417-1422

Informations de copyright

© 2024 mums.ac.ir All rights reserved.

Déclaration de conflit d'intérêts

The authors declare that there are no conflicts of interest.

Auteurs

Abbas Alimoradian (A)

Department of Pharmacology, School of Medicine, Arak University of Medical Sciences, Arak, Iran.

Fatemeh Abbaszadeh (F)

Neurobiology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Masoumeh Jorjani (M)

Neurobiology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Department of Pharmacology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Classifications MeSH