Interleukin-1 receptor antagonist ameliorates the pain hypersensitivity, spinal inflammation and oxidative stress induced by systemic lipopolysaccharide in neonatal rats.
Animals
Animals, Newborn
Female
Hyperalgesia
/ chemically induced
Inflammation
/ drug therapy
Interleukin 1 Receptor Antagonist Protein
/ pharmacology
Lipopolysaccharides
/ toxicity
Male
Oxidative Stress
/ drug effects
Pain Measurement
/ drug effects
Pregnancy
Rats
Rats, Sprague-Dawley
Receptors, Interleukin-1
/ antagonists & inhibitors
Spinal Cord
/ drug effects
Hyperalgesia
Interleukin-1 receptor antagonist
Lipopolysaccharide
Oxidative stress
Spinal cord inflammation
Journal
Neurochemistry international
ISSN: 1872-9754
Titre abrégé: Neurochem Int
Pays: England
ID NLM: 8006959
Informations de publication
Date de publication:
05 2020
05 2020
Historique:
received:
15
09
2019
revised:
05
01
2020
accepted:
13
01
2020
pubmed:
29
1
2020
medline:
26
1
2021
entrez:
29
1
2020
Statut:
ppublish
Résumé
Perinatal inflammation-induced reduction in pain threshold may alter pain sensitivity to hyperalgesia or allodynia which may persist into adulthood. In this study, we investigated the anti-inflammatory protective effect of interleukin-1 receptor antagonist (IL-1ra), an anti-inflammatory cytokine, on systemic lipopolysaccharide (LPS)-induced spinal cord inflammation and oxidative stress, thermal hyperalgesia, and mechanical allodynia in neonatal rats. Intraperitoneal (i.p.) injection of LPS (2 mg/kg) or sterile saline was performed in postnatal day 5 (P5) rat pups, and IL-1ra (100 mg/kg) or saline was administered (i.p.) 5 min after LPS injection. Pain reflex behavior, spinal cord inflammation and oxidative stress were examined 24 h after LPS administration. Systemic LPS exposure led to a reduction of tactile threshold in the von Frey filament tests (mechanical allodynia) and pain response latency in the tail-flick test (thermal hyperalgesia) of P6 neonatal rats. Spinal cord inflammation was indicated by the increased numbers of activated glial cells including microglia (Iba1+) and astrocytes (GFAP+), and elevated levels of pro-inflammatory cytokine interleukin-1β (IL-1β), cyclooxygenase-2 (COX-2), and prostaglandin E2 (PGE2) 24 h after LPS treatment. LPS treatment induced spinal oxidative stress as evidenced by the increase in thiobarbituric acid reactive substances (TBARS) content in the spinal cord. LPS exposure also led to a significant increase in oligodendrocyte lineage population (Olig2+) and mature oligodendrocyte cells (APC+) in the neonatal rat spinal cord. IL-1ra treatment significantly reduced LPS-induced effects including hyperalgesia, allodynia, the increased number of activated microglia, astrocytes and oligodendrocytes, and elevated levels of IL-1β, COX-2, PGE2, and lipid peroxidation (TBARS) in the neonatal rat spinal cord. These data suggest that IL-1ra provides a protective effect against the development of pain hypersensitivity, spinal cord inflammation and oxidative stress in the neonatal rats following LPS exposure, which may be associated with the blockade of LPS-induced pro-inflammatory cytokine IL-1β.
Identifiants
pubmed: 31987865
pii: S0197-0186(19)30517-0
doi: 10.1016/j.neuint.2020.104686
pmc: PMC7078012
mid: NIHMS1557955
pii:
doi:
Substances chimiques
Interleukin 1 Receptor Antagonist Protein
0
Lipopolysaccharides
0
Receptors, Interleukin-1
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
104686Subventions
Organisme : NIGMS NIH HHS
ID : P20 GM121334
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS080844
Pays : United States
Informations de copyright
Copyright © 2020. Published by Elsevier Ltd.
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