Highlights
- •Intrathecal introduction of ginsenoside-Rb1 (Rb1) decreased nociceptive behavior.
- •Rb1 decreased activation of the proto-oncogene c-Fos in the spinal dorsal horn.
- •Rb1 inhibited neuronal extracellular signal-regulated kinase phosphorylation.
- •Rb1 activated the nuclear factor erythroid 2-related factor 2 pathway.
- •Rb1 inhibited the nuclear factor kappa B pathway.
Abstract
Ginsenoside-Rb1 (Rb1) has anti-inflammatory effects. However, the potential antinociceptive
value of Rb1 for the treatment of acute inflammatory nociception is still unknown.
In this study, we examined whether Rb1 has any antinociceptive effects on acute inflammatory
nociception in Sprague Dawley rats given intrathecal (i.t.) introduction of Rb1 (2,
10, and 50 μg) 20 minutes before injection of formalin (5%, 50 μL) into the plantar
surface of the hind paws. I.t. introduction of Rb1 significantly decreased nociceptive
behavior during phase II (16–60 minutes), but not phase I (0–10 minutes), after formalin
stimulation, corresponding to the reduced activation of c-Fos in the L4 to L5 spinal
dorsal horn after formalin stimulation. Rb1 also reduced the phosphorylation of extracellular
signal-regulated kinase in the neurons, but not the microglia and astrocytes. Microscopic
examination of the microglia and astrocytes revealed no morphological changes due
to formalin stimulation and i.t. introduction of Rb1. Interestingly, Rb1 activated
the nuclear factor erythroid 2-related factor 2 pathway and inhibited nuclear factor
kappa B pathways.
Perspective
Our findings indicate that i.t. introduction of Rb1 might effectively inhibit formalin-induced
acute inflammatory nociception by inhibition of neuronal extracellular signal-regulated
kinase phosphorylation, which is thought to regulate the nuclear factor erythroid
2-related factor 2 nuclear factor kappa B pathways in the spinal dorsal horn, which
suggests therapeutic potential for suppression of acute inflammatory pain.
Key words
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Article info
Publication history
Published online: November 05, 2015
Accepted:
October 14,
2015
Received in revised form:
October 6,
2015
Received:
April 21,
2015
Footnotes
This study was supported by the Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Education, Science and Technology, Republic of Korea (NRF-2014R1A2A1A11051240) and Cooperative Research Program for Agriculture Science & Technology Development funded by Rural Development Administration, Republic of Korea (PJ011582042015).
The authors have no conflicts of interest to declare.
Identification
Copyright
© 2016 American Pain Society. Published by Elsevier Inc. All rights reserved.
