title: Inhibition of Cardiomyocytes Hypertrophy by Resveratrol Is Associated with Amelioration of Endoplasmic Reticulum Stress.
abstract: OBJECTIVE
  Resveratrol (Res), a polyphenol antioxidant found in red wine, has been shown to play a cardioprotective role. This study was undertaken to investigate whether Res can protect the heart suffering from hypertrophy injuries induced by isoproterenol (ISO), and whether the protective effect is mediated by endoplasmic reticulum (ER) stress.
  
  
  METHODS
  Cardiomyocytes were randomly assigned to the control group, ISO group (100 nM ISO for 48 h), Res + ISO group (50 μM Res and 100 nM ISO for 48 h) and Res group (50 μM Res for 48h only). Hypertrophy was estimated by measuring the cell surface area and the atrial natriuretic peptide (ANP) gene expression. Apoptosis was measured using Hoechst 33258 staining and transmission electron microscopy. Protein expression of ER stress and apoptosis factors was analyzed using Western Blot analysis.
  
  
  RESULTS
  Res effectively suppress the cardiomyocytes hypertrophy and apoptosis induced by ISO, characterized by the reduction of the myocardial cell surface area, the ANP gene expression, the LDH and MDA leakage amount and the rate of cell apoptosis, while decrease of the protein expression of GRP78, GRP94 and CHOP, and reverse the expression of Bcl-2 and Bax.
  
  
  CONCLUSIONS
  In summary, Res treatment effectively suppressed myocardial hypertrophy and apoptosis at least partially via inhibiting ER stress.
authors.affiliation: Department of Pathophysiology, Qiqihar Medical University, Qiqihar, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Lin
authors.forename: Jingbin
authors.initials: J
authors.lastname: Zhu
authors.forename: Xiaojie
authors.initials: X
authors.lastname: Zhang
authors.forename: Jun
authors.initials: J
authors.lastname: Wang
authors.forename: Wei
authors.initials: W
authors.lastname: Xiao
authors.forename: Bo
authors.initials: B
authors.lastname: Li
authors.forename: Li
authors.initials: L
authors.lastname: Jin
authors.forename: Jie
authors.initials: J
authors.lastname: Lian
authors.forename: Li
authors.initials: L
authors.lastname: Zhou
authors.forename: Jicheng
authors.initials: J
authors.lastname: Liu
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D000975:Antioxidants / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects; D009320:Atrial Natriuretic Factor / Q000235:genetics / Q000378:metabolism; D015153:Blotting, Western; D006332:Cardiomegaly / Q000517:prevention & control; D002316:Cardiotonic Agents / Q000494:pharmacology; D048429:Cell Size / Q000187:drug effects*; D002478:Cells, Cultured; D059865:Endoplasmic Reticulum Stress / Q000187:drug effects*; D015870:Gene Expression / Q000187:drug effects; D006360:Heat-Shock Proteins / Q000378:metabolism; D007545:Isoproterenol / Q000494:pharmacology; D046529:Microscopy, Electron, Transmission; D032383:Myocytes, Cardiac / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D017208:Rats, Wistar; D000077185:Resveratrol; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013267:Stilbenes / Q000494:pharmacology*; D051028:bcl-2-Associated X Protein / Q000378:metabolism; D000091342:Endoplasmic Reticulum Chaperone BiP
chemical_list: D000975:Antioxidants; D009320:Atrial Natriuretic Factor; D002316:Cardiotonic Agents; D006360:Heat-Shock Proteins; D007545:Isoproterenol; D019253:Proto-Oncogene Proteins c-bcl-2; D000077185:Resveratrol; D013267:Stilbenes; D051028:bcl-2-Associated X Protein; C494828:Bax protein, rat; C051684:GRP78 protein, rat; D000091342:Endoplasmic Reticulum Chaperone BiP