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Targeting the D Series Resolvin Receptor System for the Treatment of Osteoarthritis Pain
Junting Huang1, James J Burston1, Li Li1
1University of Nottingham, Nottingham, UK.
Objective:
Pain is a major symptom of osteoarthritis (OA); currently available analgesics either do not provide adequate pain relief or are associated with serious side effects. The aim of this study was to investigate the therapeutic potential of targeting the resolvin receptor system to modify OA pain and pathology.
Methods:
Gene expression of 2 resolvin receptors (ALX and ChemR23) was quantified in synovium and medial tibial plateau specimens obtained from patients with OA at the time of joint replacement surgery. Two models of OA joint pain were used for the mechanistic studies. Gene expression in the joint and central nervous system was quantified. The effects of exogenous administration of the D series resolvin precursor 17(R)-hydroxy-docosahexaenoic acid (17[R]-HDoHE) on pain behavior, joint pathology, spinal microglia, and astroglyosis were quantified. Plasma levels of relevant lipids, resolvin D2, 17(R)-HDoHE, and arachidonic acid, were determined in rats, using liquid chromatography tandem mass spectrometry.
Results:
There was a positive correlation between resolvin receptor and interleukin-6 (IL-6) expression in human OA synovial and medial tibial plateau tissue. In rats, synovial expression of ALX was positively correlated with expression of IL-1β, tumor necrosis factor, and cyclooxygenase 2. Treatment with 17(R)-HDoHE reversed established pain behavior (but not joint pathology) in 2 models of OA pain. This was associated with a significant elevation in the plasma levels of resolvin D2 and a significant reduction in astrogliosis in the spinal cord in the monosodium iodoacetate-induced OA rat model.
Conclusion:
Our preclinical data demonstrate the robust analgesic effects of activation of the D series resolvin pathways in 2 different animal models of OA. Our data support a predominant central mechanism of action in clinically relevant models of OA pain.
Insights
Targeting resolvin pathways shows promise for osteoarthritis pain relief. Preclinical studies demonstrate significant pain reduction by activating these pathways, suggesting a central mechanism for pain management.
Area of Science:
- Biomedical Science
- Pharmacology
- Pain Research
Background:
- Osteoarthritis (OA) pain significantly impacts quality of life.
- Current OA pain management options have limitations in efficacy and safety.
Purpose of the Study:
- To investigate the therapeutic potential of the resolvin receptor system for OA pain and pathology.
- To explore targeting resolvin pathways for novel OA pain management strategies.
Main Methods:
- Quantified gene expression of resolvin receptors (ALX, ChemR23) in human OA tissues.
- Utilized two OA rat models to study pain behavior and joint pathology.
- Administered 17(R)-hydroxy-docosahexaenoic acid (17[R]-HDoHE) and assessed effects on pain, pathology, and central nervous system markers.
Main Results:
- Positive correlation between resolvin receptor and IL-6 expression in human OA.
- 17(R)-HDoHE treatment reversed established OA pain behavior in rats.
- Observed reduced spinal cord astrogliosis and elevated resolvin D2 levels post-treatment.
Conclusions:
- Activation of D series resolvin pathways demonstrates robust analgesic effects in OA models.
- Preclinical data support a predominant central mechanism of action for OA pain relief.
