Protective Effect of Gomisin N against Endoplasmic Reticulum Stress-Induced Hepatic Steatosis

• Jang Min-Kyung

  Division of Longevity and Biofunctional Medicine, School of Korean Medicine, Pusan National University Healthy Aging Korean Medical Research Center, School of Korean Medicine, Pusan National University

• Yun Ye-Rang

  Division of Longevity and Biofunctional Medicine, School of Korean Medicine, Pusan National University Healthy Aging Korean Medical Research Center, School of Korean Medicine, Pusan National University

• Kim Seon Hoo

  Division of Longevity and Biofunctional Medicine, School of Korean Medicine, Pusan National University

• Kim Ji Ha

  Division of Longevity and Biofunctional Medicine, School of Korean Medicine, Pusan National University Healthy Aging Korean Medical Research Center, School of Korean Medicine, Pusan National University

• Jung Myeong Ho

  Division of Longevity and Biofunctional Medicine, School of Korean Medicine, Pusan National University Healthy Aging Korean Medical Research Center, School of Korean Medicine, Pusan National University

抄録

Gomisin N is a physiological substance derived from Schisandra chinensis. In the present study, the in vitro and in vivo effects of gomisin N on endoplasmic reticulum (ER) stress and hepatic steatosis were investigated. We quantified the expression of markers of ER stress, including glucose regulated protein 78 (GRP78), CCAAT/enhancer binding protein (C/EBP) homolog protein (CHOP), and X-box-binding protein-1 (XBP-1), and triglyceride (TG) accumulation, in HepG2 cells treated with tunicamycin or palmitate. Tunicamycin treatment in HepG2 cells induced expression of markers of ER stress and increased TG levels; Gomisin N reversed these effects, reducing the expression of markers of ER stress and TG levels. Similar effects were seen following palmitate pretreatment of HepG2 cells. The inhibitory effects of gomisin N were further confirmed in mice injected with tunicamycin. Gomisin N reduced expression of markers of ER stress and decreased TG levels in mouse liver after tunicamycin injection. Furthermore, gomisin N decreased expression of inflammatory and lipogenic genes in palmitate-incubated HepG2 cells. These results suggest that gomisin N inhibits ER stress and ameliorates hepatic steatosis induced by ER stress.

収録刊行物

• Ｂｉｏｌｏｇｉｃａｌ　＆　Ｐｈａｒｍａｃｅｕｔｉｃａｌ　Ｂｕｌｌｅｔｉｎ

  Ｂｉｏｌｏｇｉｃａｌ　＆　Ｐｈａｒｍａｃｅｕｔｉｃａｌ　Ｂｕｌｌｅｔｉｎ 39 (5), 832-838, 2016

  公益社団法人 日本薬学会

キーワード

• gomisin N
• endoplasmic reticulum (ER) stress
• hepatic steatosis
• lipogenesis
• inflammation

詳細情報

• CRID: 1390001204633100544
• NII論文ID: 130005149259
• NII書誌ID: AA10885497
• DOI: 10.1248/bpb.b15-01020
• ISSN: 13475215
• ISSN: 09186158
• NDL書誌ID: 027270183
• PubMed: 26860972
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I027270183
• Web Site: https://www.jstage.jst.go.jp/article/bpb/39/5/39_b15-01020/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2017000467
• 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