Resolvin D1 attenuates mechanical allodynia after burn injury: Involvement of spinal glia, p38 mitogen-activated protein kinase, and brain-derived neurotrophic factor/tropomyosin-related kinase B signaling

Molecular Pain, 2023 · DOI: 10.1177/17448069231159970 · Published: January 25, 2023

Simple Explanation

This study investigates how Resolvin D1 (RvD1) affects pain after burn injuries in rats. They found that RvD1 reduces pain sensitivity. RvD1 seems to work by calming down specific cells in the spinal cord (glia) and reducing certain signals (p38 MAPK and BDNF/TrkB). These findings suggest RvD1 could be a new way to treat burn pain by targeting these specific pathways in the spinal cord.

Study Duration

14 days

Participants

Male Sprague–Dawley (SD) rats (aged 4–5 weeks and weighing 140–150 g)

Evidence Level

Not specified

Key Findings

1
RvD1 attenuates mechanical allodynia after burn injury in rats.
2
RvD1 prevents the activation of spinal microglia and astroglia, and downregulates p-p38 MAPK and BDNF/TrkB following burn injury.
3
Inhibition of p38 MAPK and BDNF/TrkB signaling attenuates mechanical allodynia after burn injury.

Research Summary

This study investigated the effects of Resolvin D1 (RvD1) on mechanical allodynia after burn injury in rats. The researchers found that RvD1 attenuated mechanical allodynia, prevented glial activation, and downregulated p-p38 MAPK and BDNF/TrkB. The study also showed that inhibiting p38 MAPK and BDNF/TrkB signaling reduced mechanical allodynia after burn injury. Furthermore, inhibiting p38 MAPK prevented spinal microglial activation and downregulated BDNF/TrkB. The findings suggest that RvD1 may alleviate mechanical allodynia after burn injury by inhibiting spinal cord glial activation, microglial p38 MAPK, and BDNF/TrkB signaling in the spinal dorsal horn.

Practical Implications

Potential Therapeutic Target

RvD1 could be developed as a novel therapeutic approach for managing burn pain.

Mechanism Elucidation

The study identifies specific signaling pathways (spinal glia, p38 MAPK, and BDNF/TrkB) involved in burn pain, providing targets for future therapies.

Analgesic Development

The findings suggest that targeting glial activation and associated signaling pathways may lead to the development of more effective analgesics for burn injury.

Study Limitations

1
Some critical parameters of the burn model were not assessed, including the release of neuropeptides, TRPV1 activation spontaneous locomotor activity, shaking or licking and Grimace scale score.
2
The sample was relatively small.
3
Not specified

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