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Ginsenoside Rb1 Attenuates Acute Inflammatory Nociception by Inhibition of Neuronal ERK Phosphorylation by Regulation of the Nrf2 and NF-kappa B Pathways

Authors
Jang, MinheeLee, Min JungChoi, Jong HeeKim, Eun-JeongNah, Seupg-YeolKim, Hak-JaeLee, SanghyunLee, Sang WonKim, Young OckCho, Ik-Hyun
Issue Date
Mar-2016
Publisher
CHURCHILL LIVINGSTONE
Keywords
Ginsenoside-Rb1; intrathecal introduction; inflammatory nociception; phospho-ERK; nuclear factor erythroid 2-related factor 2; nuclear factor-kappa B
Citation
JOURNAL OF PAIN, v.17, no.3, pp 282 - 297
Pages
16
Journal Title
JOURNAL OF PAIN
Volume
17
Number
3
Start Page
282
End Page
297
URI
https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/7217
DOI
10.1016/j.jpain.2015.10.007
ISSN
1526-5900
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 mu g) 20 minutes before injection of formalin (5%, 50 mu L) into the plantar surface of the hind paws. Lt. 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 It. 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 Rbl might effectively inhibit formalininduced 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. (C) 2016 by the American Pain Society
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