Possible involvement of the HMGB1/RAGE signaling mechanism in the induction of central post-stroke pain induced by acute global cerebral ischemia

Shinichi Harada, Wataru Matsuura, Keyue Liu, Masahiro Nishibori, Shogo Tokuyama

研究成果査読

7 被引用数 (Scopus)

抄録

Central post-stroke pain (CPSP) is one of the most under-recognized consequences of cerebral stroke, but the development of an effective treatment strategy is urgent. High-mobility group box 1 (HMGB1) and the receptor for advanced glycation end products (RAGE, one of the receptors of HMGB1) have recently been shown to be critical in the modulation of nociceptive transduction following peripheral neuropathy. The aim of this study was to determine the interactions between CPSP and HMGB1/RAGE signaling. Male ddY mice were subjected to 30 min of bilateral carotid artery occlusion (BCAO). The development of hind paw mechanical allodynia was measured after BCAO using the von Frey test. Neuronal damage was estimated by histological analysis on day 3 after BCAO. The expression levels of the HMGB1 protein in the spinal cord and the sciatic nerve were significantly increased on day 3 after BCAO, although no effects of BCAO were noted on RAGE protein expression. BCAO-induced mechanical allodynia was significantly decreased by the intravenous and intrathecal administration of anti-HMGB1 monoclonal antibody. The BCAO-induced increase of phosphorylation of extracellular signal-regulated kinase (ERK) was canceled by the administration of anti-HMGB1 monoclonal antibody. In addition, BCAO-induced mechanical allodynia was significantly decreased by intrathecal administration of U0126, an inhibitor of ERK. The results showed that BCAO-induced mechanical allodynia can be regulated by the activation of HMGB1/RAGE signaling.

本文言語English
ページ(範囲)433-440
ページ数8
ジャーナルBrain Research
1646
DOI
出版ステータスPublished - 9月 1 2016
外部発表はい

ASJC Scopus subject areas

  • 神経科学(全般)
  • 分子生物学
  • 臨床神経学
  • 発生生物学

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