title: Protective Effect of Gomisin N against Endoplasmic Reticulum Stress-Induced Hepatic Steatosis.
abstract: 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.
authors: Division of Longevity and Biofunctional Medicine, School of Korean Medicine, Pusan National University.
authors: Min-Kyung
authors: MK
authors: Jang
authors: Ye-Rang
authors: YR
authors: Yun
authors: Seon Hoo
authors: SH
authors: Kim
authors: Ji Ha
authors: JH
authors: Kim
authors: Myeong Ho
authors: MH
authors: Jung
mesh_terms: D000103:Acetyl-CoA Carboxylase / Q000235:genetics; D000818:Animals; D034242:Cyclooctanes / Q000494:pharmacology / Q000627:therapeutic use; D016207:Cytokines / Q000235:genetics; D000091342:Endoplasmic Reticulum Chaperone BiP; D059865:Endoplasmic Reticulum Stress / Q000187:drug effects*; D054890:Fatty Acid Synthase, Type I / Q000235:genetics; D005234:Fatty Liver / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D005992:Glycerol-3-Phosphate O-Acyltransferase / Q000235:genetics; D006360:Heat-Shock Proteins / Q000378:metabolism; D056945:Hep G2 Cells; D006801:Humans; D017705:Lignans / Q000494:pharmacology / Q000627:therapeutic use*; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008810:Mice, Inbred C57BL; D019308:Palmitic Acid; D011083:Polycyclic Compounds / Q000494:pharmacology / Q000627:therapeutic use*; D020011:Protective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D051742:Transcription Factor CHOP / Q000378:metabolism; D014280:Triglycerides / Q000378:metabolism; D014415:Tunicamycin; D000071717:X-Box Binding Protein 1 / Q000378:metabolism
chemical_list: D034242:Cyclooctanes; D016207:Cytokines; C497249:DDIT3 protein, human; D000091342:Endoplasmic Reticulum Chaperone BiP; C000717247:HSPA5 protein, human; D006360:Heat-Shock Proteins; C000717248:Hspa5 protein, mouse; D017705:Lignans; D011083:Polycyclic Compounds; D020011:Protective Agents; D014280:Triglycerides; D000071717:X-Box Binding Protein 1; C000605543:XBP1 protein, human; C015499:schizandrin B; D014415:Tunicamycin; D051742:Transcription Factor CHOP; D019308:Palmitic Acid; D005992:Glycerol-3-Phosphate O-Acyltransferase; C518729:FASN protein, human; D054890:Fatty Acid Synthase, Type I; C000588423:ACACA protein, human; D000103:Acetyl-CoA Carboxylase