Astaxanthin alleviates neuropathic pain by inhibiting the MAPKs and NF-κB pathways.

Abstract

Neuropathic pain is a complex condition that usually lasts a lifetime and has a major negative impact on life after injury. Improving pain management is an important and unmet need. Astaxanthin (AST) is a natural marine medicine with effective antioxidant and anti-inflammatory properties and neuroprotective effects. However, few mechanisms can explain the role of AST in the treatment of neuropathic pain. In the present study, we examined its potential to eliminate spinal nerve ligation (SNL) damage by inhibiting the phosphorylation of extracellular signal-regulated kinase (ERK)1/2, phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK), nuclear factor-κB (NF-κB) p65 and the inflammatory response. The results of behavior tests indicated the promising role of AST in analgesic effect in SNL mice. AST decreased the neuronal and non-neuronal activation, the levels of the inflammatory signaling mediators (p-ERK1/2 p-p38 MAPK and NF-κB p65) and inflammatory cytokine expression (interleukin [IL]-1, IL-17, IL-6, and tumor necrosis factor-α [TNF-α]. These results suggest that AST is a promising candidate to reduce nociceptive hypersensitization after SNL.

• Authors: Lin Zhao, Xueshu Tao, Tao Song
• Journal: European journal of pharmacology (Eur J Pharmacol) Vol. 912 Pg. 174575 (Dec 05 2021) ISSN: 1879-0712 [Electronic] Netherlands
• PMID: 34673033 (Publication Type: Journal Article)
• Copyright: Copyright © 2021 The Authors. Published by Elsevier B.V. All rights reserved.

Chemical References

• Analgesics
• Cytokines
• NF-kappa B
• Rela protein, mouse
• Transcription Factor RelA
• Xanthophylls
• astaxanthine
• p38 Mitogen-Activated Protein Kinases

Topics

• Analgesics (pharmacology, therapeutic use)
• Animals
• Behavior, Animal (drug effects)
• Cell Line
• Cytokines (genetics, metabolism)
• MAP Kinase Signaling System (drug effects)
• Male
• Mice, Inbred C57BL
• NF-kappa B (metabolism)
• Neuralgia (drug therapy, metabolism)
• Neuroglia (drug effects)
• Neurons (drug effects)
• Phosphorylation (drug effects)
• Signal Transduction (drug effects)
• Transcription Factor RelA (metabolism)
• Xanthophylls (pharmacology, therapeutic use)
• p38 Mitogen-Activated Protein Kinases (metabolism)
• Mice