Prevention of Postoperative Fatigue Syndrome in Rat Model by Ginsenoside Rb1 via Down-Regulation of Inflammation along the NMDA Receptor Pathway in the Hippocampus

• Chen Wei-Zhe

  Department of Gastrointestinal Surgery, The First Affiliated Hospital of Wenzhou Medical University

• Liu Shu

  Department of Gastrointestinal Surgery, The First Affiliated Hospital of Wenzhou Medical University

• Chen Fan-Feng

  Department of Gastrointestinal Surgery, The First Affiliated Hospital of Wenzhou Medical University

• Zhou Chong-Jun

  Department of Gastrointestinal Surgery, The First Affiliated Hospital of Wenzhou Medical University

• Yu Jian

  Department of Gastrointestinal Surgery, The First Affiliated Hospital of Wenzhou Medical University

• Zhuang Cheng-Le

  Department of Gastrointestinal Surgery, The First Affiliated Hospital of Wenzhou Medical University

• Shen Xian

  Department of Gastrointestinal Surgery, The First Affiliated Hospital of Wenzhou Medical University

• Chen Bi-Cheng

  Wenzhou Key Laboratory of Surgery, The First Affiliated Hospital of Wenzhou Medical University

• Yu Zhen

  Department of Gastrointestinal Surgery, The First Affiliated Hospital of Wenzhou Medical University Department of Surgery, Shanghai Tenth People’s Hospital Affiliated to TongJi University

書誌事項

タイトル別名

• Prevention of Postoperative Fatigue Syndrome in Rat Model by Ginsenoside Rb1 <i>via</i> Down-Regulation of Inflammation along the NMDA Receptor Pathway in the Hippocampus

抄録

Postoperative fatigue syndrome (POFS) is a common complication which decelerates recovery after surgery. The present study investigated the anti-fatigue effect of ginsenoside Rb1 (GRb1) through the inflammatory cytokine-mediated N-methyl-D-aspartate (NMDA) receptor pathway. A POFS rat model was created by major small intestinal resection and assessed with an open field test. Real-time quantitative polymerase chain reaction, western blot analysis, high performance liquid chromatography and a transmission electron microscopic analysis were used to determine typical biochemical parameters in the hippocampus. Our results showed that POFS rats exhibited fatigue associated with an increased expression of inflammatory cytokines and NMDA receptor 1, higher (kynurenine)/(tryptophan) and (kynurenine)/(kynurenic acid) on postoperative days 1 and 3, and an increased expression of indoleamine 2,3-dioxygenase (IDO) on postoperative day 1. Degenerated neurons were found in the hippocampus of POFS rats. The NMDA receptor antagonist MK801 had a significant effect on central fatigue on postoperative day 1. GRb1 had no effect on IDO or tryptophan metabolism, but exhibited a significant effect on POFS by inhibiting the expression of inflammatory cytokines and NMDA receptor 1. These data suggested that inflammatory cytokines could activate tryptophan metabolism to cause POFS through the NMDA receptor pathway. GRb1 had an anti-fatigue effect on POFS by reducing inflammatory cytokines and NMDA receptors.

収録刊行物

• Ｂｉｏｌｏｇｉｃａｌ　＆　Ｐｈａｒｍａｃｅｕｔｉｃａｌ　Ｂｕｌｌｅｔｉｎ

  Ｂｉｏｌｏｇｉｃａｌ　＆　Ｐｈａｒｍａｃｅｕｔｉｃａｌ　Ｂｕｌｌｅｔｉｎ 38 (2), 239-247, 2015

  公益社団法人 日本薬学会

キーワード

• ginsenoside Rb1
• postoperative fatigue syndrome
• <i>N</i>-methyl-D-aspartate receptor
• inflammatory cytokine
• tryptophan

詳細情報

• CRID: 1390282679609814656
• NII論文ID: 130004872253
• NII書誌ID: AA10885497
• DOI: 10.1248/bpb.b14-00599
• ISSN: 13475215
• ISSN: 09186158
• NDL書誌ID: 026069765
• PubMed: 25747983
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I026069765
• Web Site: https://www.jstage.jst.go.jp/article/bpb/38/2/38_b14-00599/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2015279173
• 本文言語コード: en
• データソース種別:
  • JaLC
  • NDL
  • Crossref
  • PubMed
  • CiNii Articles
• 抄録ライセンスフラグ: 使用不可