Blockade of interleukin-6 signaling aggravates ischemic cerebral damage in mice: Possible involvement of Stat3 activation in the protection of neurons

Toru Yamashita, Kazunobu Sawamoto, Shigeaki Suzuki, Norihiro Suzuki, Kazuhide Adachi, Takeshi Kawase, Masahiko Mihara, Yoshiyuki Ohsugi, Koji Abet, Hideyuki Okano

研究成果: Article査読

156 被引用数 (Scopus)

抄録

Interleukin (IL)-6 expression transiently increases in the acute phase of cerebral ischemia. To investigate the physiological significance of endogenous IL-6 expression and to identify the main signal pathway for the action of IL-6, we administered anti-mouse IL-6 receptor monoclonal antibody (IL-6RA), which blocks IL-6 signaling, to mice immediately after a 45-min period of middle cerebral artery occlusion (MCAO). At 6 h after MCAO, IL-6RA administration had resulted in a significant reduction in the amount of phosphorylated signal transducer and activator of transcription-3 (Stat3) protein in the peri-infarct area of the cortex. At 24 h after MCAO, blockade of IL-6 signaling had led to an increase in number of apoptotic cells in the peri-infarct area and enlargement of the size of the infarct, and it had adversely affected neurological function. These results suggest that endogenous IL-6 plays a critical role in preventing damaged neurons from undergoing apoptosis in the acute phase of cerebral ischemia and that its role may be mediated by Stat3 activation.

本文言語English
ページ(範囲)459-468
ページ数10
ジャーナルJournal of Neurochemistry
94
2
DOI
出版ステータスPublished - 2005 7

ASJC Scopus subject areas

  • 生化学
  • 細胞および分子神経科学

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